MEDICAL-SURGICAL 2 : PTM1 Care of Clients with Gastrointestinal Disorders Abdominal Pain O - Onset: “When did the pain begin?” L - Location: “Please point where exactly you fee the pain.” D - Duration: “How long does the pain last?” C - Characteristic: “Please describe the pain you feel in your abdomen.” A - Aggravating: “What triggers the pain?” R - Relieving: “What relieves the pain?” T - Timing: “When does the pain occur?” S - Severity: “Please rate your pain from 110” Dyspepsia • Upper abdominal discomfort associated with eating • Most common symptom of patients with GI dysfunction • Typically caused by fatty foods, salads, coarse vegetables, and highly seasoned foods Intestinal Gas • Accumulation of gas in GI tract • Belching: expulsion of gas from stomach through the mouth • Flatulence: expulsion of gas from the rectum • May indicate food intolerance or gallbladder Disease Nausea and Vomiting • Nausea is a vague, uncomfortable sensation of sickness that may or may not be followed by vomiting • Vomiting is a physiologic protective response that limits the effects of noxious agents by emptying the stomach contents and secretions of small intestine • Triggers: odors, activity, medications, food Intake Change in Bowel Habits • Diarrhea: an abnormal increase in frequency and liquidity of stool or in daily stool weight or volume • Commonly occurs when the contents move so rapidly through the intestine and colon that there is inadequate time for the GI secretions and oral contents to be absorbed. • Constipation: a decrease in frequency of stool, or stools that are hard, dry, and of smaller volume than typical Change in Stool Characteristics • Normal stool: light to dark brown • Melena: Black tarry stool indicative of upper GI bleeding • Hematochezia: Bright red blood in stool • Steatorrhea: Fatty stool • Acholic stool: light- gray or clay- colored stool resulting from decreased or absent conjugated bilirubin Diagnostic Tests for GI Disorders Fecal Occult Blood Test (FOBT)/ Guaiac Test • Stool for occult blood • Done to detect GI bleeding • Preparation: • High fiber diet for 48-72 hours • Avoid red meat, poultry, turnips, horse radish, • cauliflower, and melon – false positive result • Avoid vitamin C – false negative result • Hold 48hrs prior: steroids, iron, indomethacin, colchicine • 3 stool specimens will be collected for three consecutive days Stool for Ova, Parasites, and E. histolytica (OPEH) • Clean technique • Send fresh, warm specimen (within 30 mins) Stool for Culture and Sensitivity • Identifies microorganism and determines appropriate antibiotic therapy • Sterile technique • Use sterile collection tube and sterile cotton- tipped applicator to collect Specimen Abdominal Ultrasound (UTZ) • Ultrasonography is a noninvasive diagnostic technique in which highfrequency sound waves are passed into the internal body structures, and the ultrasonic echoes are recorded on an oscilloscope as they strike tissues of different densities. • Used to detect: • Enlargement of gallbladder, pancreas, presence of gallstones, ectopic pregnancy, appendicitis • Sound waves cannot travel through bones, gas, or fluid • Nursing interventions: • NPO 8 to 12 hours prior to UTZ • If for gallbladder studies, fat-free meal the • evening before • Schedule barium studies after • ultrasonography since barium interferes with • sound wave transmission UGI Tract Study (Barium Swallow) • Visualizes esophagus, stomach, duodenum, and jejunum • Contrast medium: Barium sulfate – white, chalky substance • X-rays are taken on standing, and lying Position • Nursing interventions: • Pre procedure: • NPO 6-8 hours • Post procedure: • Laxatives, as ordered • Increase OFI • Inform client that stool may become white • for 24-72 hours LGI Tract Study (Barium Enema) • Visualization of colon through x- rays after rectal installation of barium • Barium enema is C/I for patients with active inflammatory diseases, fistula, or suspected perforation of colon. • Diatrizoic acid is used instead (water-soluble iodinated contrast medium) • Nursing interventions: • Low- residue diet 1 to 2 days before • Clear liquid diet and laxative the evening • before • NPO post-midnight • Cleansing enema until clear in AM of • procedure • Schedule before any upper GI studies Computed Tomography (CT) Scan • Provides cross- sectional images of abdominal organs and structures. • Used to detect and localize many inflammatory conditions in the colon (appendicitis, diverticulitis, regional enteritis, and ulcerative colitis) • Painless procedure, but uses radiation • Nursing interventions: • Clear liquid diet in AM • If using contrast medium: • NPO 2-4 hours • Check for allergies to seafood and iodine • Assess for claustrophobia • Instruct client to remain still during entire procedure Magnetic Resonance Imaging (MRI) • Noninvasive technique that uses magnetic fields and radiowaves to produce images of area being studied • Used to evaluate abdominal soft tissues as well as blood vessels, abscesses, fistulas, neoplasms, and other sources of bleeding • Nursing Interventions: • Pre- procedure: • NPO 6-8 hours • Remove all jewelries and other metals • Inform patient and family that procedure lasts • for 60 to 90 minutes, inform that the MRI • machine will make a knocking sound during • the procedure • Assess for claustrophobia • Contraindications: • Pacemakers • • Aneurysm clips Orthopedic screws Upper GI Endoscopy • Direct visualization of esophagus, stomach, and duodenum • Nursing interventions (Pre op): • Obtain written consent • NPO 6-8 hours • Administer Atropine sulfate, as ordered • Administer sedatives/narcotics/tranquilizers, as ordered • Remove dentures or bridges • Lidocaine spray is applied to the posterior pharynx to depress gag reflex. • Instruct not to swallow saliva • Nursing Interventions (Post op): • Position to side- lying position • NPO until gag reflex returns • NSS gargle • Monitor VS • Assess: bleeding, crepitus, fever, neck/throat • pain, dyspnea, dysphagia, back/shoulder pain Lower GI Endoscopy • Proctosigmoidoscopy: Direct visualization of sigmoid and rectum • Colonoscopy: Direct visualization of the colon • Nursing Interventions (Pre op) • Obtain written consent • Clear liquid diet 24 hours before procedure • Administer laxative/cathartic, as ordered • Cleansing enema until clear • Position to knee-chest/lateral position during procedure • Assess for vasovagal stimulation • Nursing Interventions (Post op): • Position to supine for a few minutes • Assess for signs of perforation – bleeding, pain, fever • Hot Sitz bath to relieve discomfort in anorectal area Common Nursing Procedures for Clients with GI Disorders • Gastrointestinal Decompression • Enteral Feeding (NGT, PEG/PEJ) • Parenteral Nutrition Gastric and Intestinal Decompression • The removal of gas or fluid to prevent gastric and intestinal distention • Achieved through the use of nasogastric tubes (NGT) or nasoenteric tubes Nasoenteric Tubes Nursing interventions: • After insertion of nasoenteric tubes, turn patient to the RIGHT side. This facilitates passage of tube to the duodenum. • Shortening of length of tube from the outside indicates passage of tube to duodenum Enteral Feeding Nasogastric Tube Feeding • Also called gastric gavage • Feeding formula should be at ROOM TEMPERATURE. Cold formula causes cramps. • Position: semi- fowler’s to high- fowler’s • Check NGT placement: • BEST- xray • Check pH of Gastric secretions (Should be acidic with pH of 1-3) • Note color of aspirate (greenish or yellowish) • Introduce 10 mL of air into NGT and auscultate epigastric area for gurgling sounds • After each feeding, instill 30 to 60 mL of water • Have the client remain in semi- to highfowler’s position for 30 to 60 minutes after feeding Gastrostomy/Jejunostomy Feeding • Gastrostomy: stoma is in the stomach • A procedure in which an opening is created into the stomach either for the purpose of administering nutrition, fluids, and medications via a feeding tube, or for gastric decompression. • Preferred way of enteral feeding for nutritional support of greater than 4 weeks • Jejunostomy: stoma is in the jejunum • A surgically placed opening in the jejunum for the purpose of administering nutrition, fluids, and medications • Indicated when gastric route is not accessible, or to decrease aspiration risk when stomach is not functioning adequately to process and empty food or fluids vein • Type of solution: hypertonic (25% to 35%) • Nursing interventions: • Administer TPN at ROOM TEMPERATURE • Consume TPN within 24 hours • Change IV tubing every 24 hours • Use an infusion pump to maintain a steady infusion rate • If infusion is delayed, DO NOT catch up. Notify physician. • Monitor urine and blood glucose levels. • Provide skin care on the catheter insertion site Care of Clients with Upper Gastrointestinal Disorders • Feeding should be at ROOM temperature • Position: semi- to high- fowler’s position • Check patency: • Instill 15 to 30 ml of water • Have the client remain in semi- to highfowler’s position for 30 to 60 mins after feeding Parenteral Nutrition • A method of providing nutrients to the body by an IV route • Goals: • To improve nutritional status • Establish a positive nitrogen balance • Maintain muscle mass • Promote weight maintenance or gain • Enhance healing process Positive Nitrogen Balance • Positive nitrogen balance is necessary to create an anabolic environment, allowing the body to build new muscle Total Parenteral Nutrition (TPN) • Primary purpose: to administer glucose • Indications: • Clients who need extensive nutritional support over an extended period of time • Site of catheter insertion: SUBCLAVIAN Stomatitis • A painful disorder characterized by inflammation and ulcerations in the mouth, including the lips, tongue, and mucous membranes Herpetic Stomatitis • Causative agent: Herpes simplex virus (HSV) type 1 • Clinical manifestations: • Diffuse, shiny erythematous involvement of the gingiva with edema and gingival bleeding • Initially, lesions appear as spherical • gray vesicles dispersed in different areas • After 24 hours, the vesicles rupture and form painful small ulcers with a red, elevated halo- like margins and a depressed yellow and grayish- white center. Aphthous Stomatitis (Canker sores) • Cause: Not well- understood • Local altered immune response • Systemic: Iron deficiency, vitamin B6 or B12 deficiency, DM, inflammatory bowel disease, immunosuppression • Clinical Manifestations • Small, white painful ulcers • Well- circumscribed lesion Other Causes of Stomatitis • Radiation therapy • Chemotherapy Medical Management: • Lidocaine hydrochloride (Xylocaine): topical anesthetic • Acyclovir (Zovirax), if cause is HSV • Analgesics, as ordered Nursing Management • Monitor caloric and food intake • Provide soft, bland foods during acute episodes • Diet as tolerated (DAT) as the sores heal • Encourage small, frequent feedings • Encourage to drink room temperature liquids • Provide/Assist with mouth care: • Let patient rinse mouth with NSS after • eating • Avoid alcohol- based mouthwash • Use soft- bristled toothbrush Esophageal Varices Varices (sing. Varix) • an enlarged, tortuous vein usually occurring in the distal esophagus • Cause: • Portal hypertension •Complications: • Rupture of varices • UGI Bleeding •Clinical Manifestations: • Generally asymptomatic • GI bleeding manifestations: • Hematemesis • Coffee- ground emesis • Melena • Abdominal bloating • Hypotension, tachycardia Medical Management: • Octreotide acetate (Sandostatin) IV • Given to control bleeding by decreasing blood flow to the GI tract, thus lowering pressure in the portal system • Balloon tamponade • Uses Sengstaken-Blakemore tub Balloon Tamponade • The tube is passed into the esophagus where a balloon will be inflated to put direct pressure onto the bleeding varices • The balloon is periodically deflated to prevent esophageal necrosis •Nursing Responsibilities: • Keep patient on NPO • Elevate HOB to 30 to 45 degrees • WOF: dyspnea • Prepare at bedside: scissors • If w/ respiratory distress, cut the tube as this is a medical emergency Medical Management: • Sclerotherapy • A procedure in which a caustic substance is injected into the varix. • An esophagogastroduodenoscopy (EGD) is performed and a sclerosing agent will be injected using a special needle • Several treatment sessions are needed to create a scar tissue that will permanently stop the bleeding • Esophageal ligation • This procedure involves placing a rubber band or O- ring on the varix • An EGD is performed to guide the placement of the bands Surgical Management: • Portacaval shunt (aka portosystemic shunt) • Relieves the pressure on the • esophageal veins by redirecting blood • from the portal vein to the inferior vena • cava • Some blood bypasses the liver and reenters the circulatory system General Nursing Management: • Place patient on bed rest if with active bleeding • May perform out of bed activities if no bleeding but avoid strenuous activity and Valsalva maneuvers Hiatal Hernia Hiatal Hernia (Diaphragmatic Hernia) • The opening of the diaphragm through which the esophagus passes becomes enlarged, and part of the upper stomach moves up into the lower portion of the thorax • Women >Men • Sliding hiatal hernia (Type 1) • Occurs when the upper stomach and the gastroesophageal junction are displaced upward and slide in and out of the thorax • 95% of hiatal hernia cases • Primary cause: muscle weakness in the esophageal hiatus – caused by aging, congenital muscle weakness, obesity, trauma, surgery, or prolonged increases in intraabdominal pressure • Paraesophageal hernia/Rolling hernia (Type 2) • Occurs when all or part of the stomach pushes through the diaphragm beside the esophagus • Most often the fundus and greater curvature of the stomach • Primary cause: anatomical Defect • Clinical Manifestations: • 91% are asymptomatic (Smith & Shahjehan, 2021) • Pyrosis: heartburns • Dysphagia (difficulty swallowing), odynophagia (painful swallowing) due to compression of esophagus • Dyspnea • Abdominal pain • Nausea and vomiting • Gastric distention, belching, flatulence • Diagnostics: • Barium swallow: confirmatory test • Esophagogastroduodenoscopy (EGD): the passage of fiberoptic tube through the mouth and throat into the digestive tract for visualization of the esophagus, stomach, and small intestine • Chest CT scan • Complication • Erosive esophagitis • Esophageal cancer • Medical Management: • Antiemetics- to relieve n&v • Metoclopramide (Plasil) • Ondansetron (Zofran) • Promethazine (Phenergan) • Antacids- neutralizes the acid in the stomach • Aluminum hydroxide • Magnesium hydroxide • H2- receptor antagonist- to suppress secretion of gastric acid • Cimetidine (Tagamet) • Ranitidine (Zantac) • Famotidine (Pepcid) • Proton pump inhibitors- to suppress gastric acid secretions • Esomeprazole (Nexium) • Lansoprazole (Prevacid) • Omeprazole (Losec) Surgical Management: • Nissen Fundoplication • Reserved for extreme cases which involves gastric outlet obstruction or suspected strangulation • The upper part of the stomach is wrapped around the LES to strengthen the sphincter, prevent acid reflux, and repair a hiatal hernia. • “Gastric wrap- around” • Nursing Management: • Relieve pain through antacids • Modify diet: • High- protein diet to enhance LES pressure • Small frequent feedings- prevent gastric distention and prevents further protrusion of stomach into thoracic cavity • Instruct client to eat slowly and chew food properly • Avoid foods and beverages that decrease LES pressure such as fatty • • • • foods, cola beverages, coffee, tea, chocolate, alcohol Let the client assume upright position before and after eating for 1 to 2 hours Instruct client to avoid eating at least 3 hours before bedtime Advise client to reduce body weight, if obese. Advise client to promote lifestyle changes: • Elevate HOB 6 to 12 inches for sleep • Avoid factors that increase abdominal pressure • like use of constrictive clothing, straining at stool, heavy lifting, bending, stooping, vigorous coughing • Avoid cigarette smoking as smoking causes rapid and significant drop in LES pressure Gastroesophageal Reflux Disease (GERD) • A disorder characterized by backflow of gastric or duodenal contents into the esophagus. • Causes: • Incompetent LES • Pyloric stenosis • Hiatal hernia • Motility disorder of esophagus • Risk Factors: • Aging • Smoking • Coffee drinking • Alcohol consumption • Gastric infection with Helicobacter pylori • Clinical Manifestations: • Pyrosis (described as burning sensation in the esophagus) • Dyspepsia • Regurgitation (spitting up of food from the esophagus or stomach without nausea or forceful contractions of the abdominal muscles) • Dysphagia and odynophagia • Complications: • Dental erosion • Ulceration of the pharynx and esophagus • Pulmonary complication (aspiration pneumonia) • Diagnostics: • Barium swallow- to evaluate damage to esophageal mucosa • Ambulatory 12- to 36- hour esophageal pH monitoring- to evaluate degree of acid reflux Medical Management: • Antacids- neutralizes the acid in the stomach • Aluminum hydroxide • Magnesium hydroxide • H2- receptor antagonist- to suppress secretion of gastric acid • Cimetidine (Tagamet) • Ranitidine (Zantac) • Famotidine (Pepcid) • Proton pump inhibitors- to suppress gastric acid secretions • Esomeprazole (Nexium) • Lansoprazole (Prevacid) • Omeprazole (Prilosec) • Nursing Management: • Low fat diet • Avoid caffeine, tobacco, beer, milk, and other stimulating foods • Avoid eating or drinking 2 hours before bedtime • Encourage to maintain normal body weight • Avoid tight- fitting clothes • Elevate HOB by at least 30 degrees Gastritis • Inflammation of the gastric mucosa • Affects men and women equally Acute Gastritis • Lasts for several hours to few days • May be erosive or non- erosive • Erosion loss of epithelium no mucus • Caused by local irritants: • Aspirin and NSAIDs • Alcohol • Gastric radiation therapy • Caused by Helicobacter pylori • Releases toxins which are associated with stomach mucosal inflammation and host tissue damage (Malik et al., 2021) • Clinical Manifestations: • Gastrointestinal Symptoms: • Hematemesis • Epigastric pain (rapid onset) • Melena • Anorexia • Nausea and vomiting • Systemic manifestations: • Possible signs of shock • Collaborative Management • Reduce irritation of gastric mucosa • Relief of symptoms Medical Management: • H2- receptor antagonist • Proton- pump inhibitors • Antiemetic, if with n&v • Antibiotic therapy if with H. pylori Nursing Management: • Maintain on NPO until acute symptoms subsides • Maintain IV fluids, as ordered • In severe cases, NG tube may be used to monitor for bleeding, to lavage precipitating agent from stomach, or to keep stomach empty and free of noxious stimuli • Monitor VS and check vomitus for blood Chronic Gastritis • Results from repeated exposure to irritating agents or recurring episodes of acute gastritis • Gastric epithelial and mucosal cell atrophy • More common in older adults • Causes (ABC): • Autoimmune- Hashimoto’s thyroiditis, Grave’s Disease • Bacterial- chronic H. pylori infection • Chemical- long term aspirin/NSAID therapy • Clinical Manifestations: • Gastrointestinal Symptoms: • Vague epigastric discomfort relieved by eating • Intolerance to spicy or fatty foods • Nausea and vomiting • Early satiety • Pyrosis • Belching • Sour taste in mouth • Systemic manifestations: • Pernicious Anemia • Fatigue • Collaborative Management • Eliminate specific cause Medical Management: • Control underlying pathology • Discontinue irritating medications • Antibiotic combinations for Chronic H. pylori gastritis • Vitamin B12 therapy, if with pernicious anemia Nursing Management: • Non- irritating diet (no spices, non fatty) • Provide small frequent feedings • Advice client about smoking cessation and reduction of alcohol consumption • Stress management Peptic Ulcer Disease (PUD) • A condition characterized by erosion of the GI mucosa resulting from digestive action of HCl acid and pepsin. • Commonly occurs in the stomach (gastric ulcer) and proximal duodenum (duodenal ulcer) • Precipitating factors: • Helicobacter pylori infection • Gram- negative bacillus found within gastric epithelial cells. • Releases toxins which are associated with stomach mucosal inflammation and host tissue damage (Malik et al., 2021) • Accounts for 90% of duodenal ulcers and 70% to 90% of gastric ulcers • Non- steroidal Anti-inflammatory Drugs (NSAIDs) • Prostaglandin normally protects the gastric mucosa • NSAIDs block prostaglandin synthesis by inhibiting the COX-1 enzyme, resulting in decreased gastric mucus and bicarbonate production and a decrease in mucosal blood flow. • Medications • Steroids, Fluorouracil, KCl • Zollinger- Ellison Syndrome • Benign or malignant tumor in the pancreas or duodenum causes increase in gastric acid secretion • Stress • Stress stimulates SNS. However, constant exposure to stress exhausts the SNS and activates. Parasympathetic Nervous System which increases gastric motility and HCl production. • Fatty, spicy, highly acidic foods • Type A Personality • Perfectionist, workaholics – have increased gastric motility and HCl acid secretion • Type O Blood • Individuals with type O blood have higher pepsinogen levels which is activated into pepsin. Pepsin +HCl= aggressor to the GI mucosa • Diagnostics: • Upper GI endoscopy: • Allows direct visualization of inflammatory changes, ulcers, and lesions • Urea breath test: • Detects the presence of H. pylori Urea Breath Test • The test is based on the principle that orally administered urea becomes broken down into ammonia and bicarbonate through the action of an enzyme urease which is produced in large amounts by H. pylori. • Uses 14C- urea as tracer which will be taken by the patient PO • • Taken on an empty stomach S/E: diarrhea, abdominal cramps, confusion, dizziness, weakness • Administer cimetidine and antacids 1 hour apart as antacids decrease the absorption of oral cimetidine • Cytoprotective agents: coats ulcers and enhances prostaglandin synthesis • DOC: Sucralfate (Carafate) • Administer on an empty stomach • S/E: constipation • Administer 1 hour apart from antacids • H. pylori treatment: • Triple therapy • Quadruple therapy Triple Therapy for H. pylori: • PPI BID • Clarithromycin 500 mg BID • Amoxicillin 500 mg BID or Metronidazole (Flagyl) 500 mg BID • Taken for 10-14 days Gastric vs Duodenal Ulcers • Clinical Manifestations: • Dull, aching, gnawing epigastric pain Medical Management: • Antacids: neutralizes HCl • Best administered 1 to 2 hours after eating as this is the peak time of HCl secretion • Aluminum- Magnesium hydroxide (Maalox) • Milk of Magnesia • Aluminum- Magnesium Trisilicate (Gaviscon) • • Calcium carbonate (Tums) • H2- receptor blockers: reduces HCl secretions •Quadruple Therapy for H. pylori: • Bismuth subsalicylate 525mg QID • Tetracycline 500 mg BID • Metronidazole 250 mg QID • PPI OD • Taken for 10-14 days Surgical Management: • Recommended for patient with intractable ulcers (those failing to heal after 12 to 16 weeks of medical treatment), lifethreatening hemorrhage, perforation, or obstruction or those with Zollinger-Ellison Syndrome that is unresponsive to medications. • Vagotomy: Severing of the vagus nerve. • Decreases gastric acid by diminishing cholinergic stimulation to the parietal cells, making them less responsive to gastrin • Pyloroplasty: surgical dilatation of the pyloric sphincter to treat bleeding duodenal ulcers • Longitudinal incision is made into the pylorus and transversely sutured closed to enlarge the outlet and relax the muscle • • • • Antrectomy: surgical removal of the antrum portion of the stomach (50%) with anastomosis to either duodenum or jejunum • Billroth I (Gastroduodenostomy): removal of the lower portion of the stomach (which contains cells that secrete gastrin) as well as a small portion of the duodenum and pylorus. The remaining segment is anastomosed to the duodenum. • Billroth II (Gastrojejunostomy): removal of the lower portion of the stomach with anastomosis to the jejunum. A duodenal stump remains and is oversewn. • Subtotal gastrectomy: removal of 75% of the distal stomach with Billroth I or II repair. • Nursing Management: • Relieve pain through medications, as ordered • Encourage client to adhere to dietary modifications •Dietary modifications: • DAT when asymptomatic • Bland diet during exacerbation • • Advise client to eat slowly and chew food properly Small, frequent feeding during exacerbation Instruct to avoid the following: • Fatty foods, coffee, tea, chocolate, cola drinks, spices, alcohol • Bedtime snacks • Binge eating • Large quantities of milk Encourage client to quit smoking Enhance coping through stress therapy: • Develop recreation and hobbies • Have regular pattern of exercise • Stress reduction at home and at work Clients Having Gastric Surgeries • Preop Care • Provide psychosocial support • Teach client DBCT • Provide nutritional support as ordered • Ensure consent form is signed • Inform client and family on post op measures (e.g., presence of NGT, oxygen therapy, blood transfusion, TPN) • Post op Care • Promote patent airways and ventilation • Position to semi- fowler’s position • Reinforce DBCT exercises and incentive spirometry • Administer analgesics before activities, as ordered • Splint incisions • Facilitate early ambulation • Prevent potential complications: • Prevent bleeding which is highest during the first 24 hours and on the 4th to 7th day post op due to non healing • Monitor NGT drainage. Reddish for the first 12 hours then becomes dark red • Avoid unnecessary irrigation or repositioning of NGT • Leakage from anastomosis • Monitor for signs of leakage (e.g., • dyspnea, pain, and fever when oral fluids are initiated) • Monitor for signs of peritonitis (e.g., severe abdominal pain, abdominal rigidity, fever) Care of Clients with Lower Gastrointestinal Disorders Dumping Syndrome • A group of unpleasant vasomotor and GI symptoms caused by rapid emptying of gastric contents into the jejunum. • Common cause: • Billroth II procedure • Clinical Manifestations: • Early Signs (5-30 mins pc) • Diarrhea • Weakness • Abdominal cramps • Tachycardia • Pallor • Diaphoresis • Nausea • Late Signs (2 to 3 hours pc) • Hyperglycemia (initially) • Hypoglycemia • Collaborative Management: • Position patient to LEFT SIDE- LYING after meals • Provide small, frequent feedings • HIGH- PROTEIN DIET. Protein empties in the stomach lowly. • Limit carbohydrates • Instruct patient to drink water AFTER MEALS not within meals • Octreotide- decrease GI symptoms • Acarbose- for clients with late dumping • Billroth II to Billroth I conversion • • • • • • • • • • Jejunum Ileum Cecum Appendix Ascending colon Transverse colon Descending colon Sigmoid colon Rectum Anus Function of Small Intestines Main function: absorption of nutrients • Duodenum- mixing with biliary and pancreatic secretions • Jejunum- CHO, CHON, fats, sodium, chloride • Ileum- Vitamin B12 and bile Salts Function of Large Intestines Main function: Reabsorption of water and electrolytes • Done through a slow, weak peristaltic movement • Intermittent, strong peristaltic waves may occur after a meal is eaten Acute Abdomen • “Surgical abdomen” • Sudden onset of abdominal pain without traumatic etiology and requires swift surgical intervention to prevent peritonitis, sepsis, and septic shock. • Causes: • Appendicitis • Diverticulitis • Intestinal Obstruction Appendix • The appendix is a small wormlike appendage that is attached to the cecum. It measures about 3 to 4 inches long. • Normally, it fills with by products of digestion and empties regularly into the cecum; however, this emptying process is ineffective making it at risk for obstruction and infection. Appendicitis • Inflammation of the appendix • Causes: • Obstruction of the appendix by: • Fecalith • Foreign bodies • Infection • • • • • • • • Clinical Manifestations: • Diffuse abdominal pain that eventually becomes localized to RLQ • (+) McBurney’s Sign: rebound tenderness on RLQ Anorexia, nausea and vomiting Rigid abdomen, guarding behavior (+) Rovsing’s sign: RLQ pain upon deep palpation of LLQ • Decreased or absent bowel sounds • High grade fever: 38̊C- 38.5 ̊C • (+) Psoas sign: Pain on passive extension of the right thigh. Patient lies on left side. Examiner extends patient's right thigh while applying counter resistance to the right hip. • (+) Obturator sign: Pain on passive internal rotation of the flexed thigh. Examiner moves lower leg laterally while applying resistance to the lateral side of the knee, resulting in internal rotation of the femur. Diagnostics: • Abdominal CT Scan: (+) enlargement and inflammation of appendix (enlargement of at least 6mm is suggestive), Confirmatory test • Complete Blood Count (CBC): • (+) Leukocytosis: • WBC> 10,000/mm3; • WBC> 20,000/mm3 indicates peritonitis • Pregnancy Test (for females): • To rule out ectopic pregnancy • Urinalysis: • To rule out UTI Complications • Rupture of appendix • Peritonitis Collaborative Management: • Decrease peristalsis • Bed rest • Maintain NPO • Provide pain relief by COLD application • Avoid factors that increase peristalsis: • Hot compress over abdomen • Laxatives • Enema • Initiate and maintain IV therapy • Administer antibiotics, as ordered Surgical Management: • Appendectomy • Surgical removal of the appendix by laparotomy or laparoscopy Appendectomy • Method of Anesthesia: Spinal anesthesia • Flat on bed 6 to 8 hours post op to prevent spinal headache • Monitor return of sensation in the lower extremities • Post op nursing care: • Facilitate early ambulation (Day 0- day of surgery) • Post op position: HIGH- FOWLER to reduce tension on incision and abdominal organs • DAT if bowel sounds are present • Instruct to avoid heavy lifting post op, but can resume normal activity within 2 to 4 weeks Ruptured Appendicitis Clinical Manifestations: • Sudden relief of abdominal pain followed by onset of intense abdominal pain • Abdominal rigidity • Leukocytosis (WBC >20,000/mm3) Surgical Management: • Exploratory Laparotomy Appendectomy Diverticular Diseases • Diverticulum- saclike herniation of the lining of the bowel that extends through a defect in the muscle layer • Diverticulosis- presence of multiple diverticula without inflammation or symptoms • Diverticulitis- a diverticulum that becomes inflamed, causing perforation and potential complications • Commonly occurs in the sigmoid colon • Commonly affects older population • Risk Factors: • Age • Low fiber diet (a.k.a. low residue diet) • Obesity • History of cigarette smoking • (+) family history • Clinical Manifestations: (Diverticulosis) • Asymptomatic • Chronic constipation with episodes of diarrhea • Anorexia • Nausea • Abdominal distention • LLQ pain (70% of cases) • Low grade fever • Diagnostics: • Colonoscopy • Screening test • Permits visualization of the extent of diverticular disease • Abdominal CT Scan w/ contrast • Confirmatory test • CBC: • (+) leukocytosis • Low Hgb, especially if with frank blood in stool • Complications: • Abscess • Obstruction • Fistula • Peritonitis • Hemorrhage Medical Management: • Hinchey Classification: • Guide to determine treatment of diverticulitis • Stage I: • Outpatient treatment • Rest, oral fluids, analgesic • Clear liquid diet until inflammation subsides; then a high- fiber, low fat diet • Stage II: • May require hospitalization • NPO • Nasogastric suctioning if with vomiting or distention • IV fluids, as prescribed • Broad-spectrum antibiotics, as ordered DOC: Ampicillin- sulbactam (Unasyn) • Analgesics, as ordered DOC: (Oxycodone) • Stage III or IV: • Surgical candidates • Hartmann procedure: • Resection of the colon Hartmann procedure • One- stage resection: • The inflamed area is removed and a primary end-toend anastomosis is completed • Multi- stage resection: • Used for diverticulitis with complications • Stage 1- colostomy creation • Stage 2- colostomy take down and anastomosis • Nursing Management: • High- fiber diet • Bulk- forming laxatives, as ordered • DOC: Psyllium fiber • Liberal fluid intake of 2,000 mL/day • Avoid nuts and seeds (sesame seeds, cucumber, tomatoes, popcorn) • Encourage an individualized exercise program Intestinal Obstruction • Exists when a blockage prevents the normal flow of intestinal contents through the intestinal tract • Etiology may be mechanical or functional • Mechanical obstruction: • Obstruction results from pressure in the intestinal wall • Causes: • Surgical adhesions- most common cause • Hernia • Chron’s disease • Intussusception • Volvulus • Neoplasm • Functional (paralytic) obstruction: • Intestinal musculature cannot propel the contents along the bowel • Causes: Paralytic ileus (lack of intestinal peristalsis and bowel sounds) • Most common and may result after an abdominal surgery, hypokalemia, and thoracic and lumbar spinal fractures Small Bowel Obstruction (SBO) • Clinical Manifestations: • Crampy, wavelike and colicky pain above and below the blockage • Absent fecal matter and flatus, but may pass blood and/or mucus • Reflux vomiting • Dehydration: extreme thirst, drowsiness, generalized malaise, aching, parched tongue and mucus membranes • Diagnostics: • Abdominal x- ray and CT scan: • (+) abnormal quantities of gas, fluid, or both in the intestines and sometimes collapsed distal bowel • CBC • High Hct (hematocrit is the percentage of RBC in blood) • Possibly increased WBC • Electrolytes • Hypokalemia • Low hydrogen ions Medical Management: • Rest the bowel! • NG decompression x 3 days Surgical Management: • Dependent on the cause • Hernia- herniorrhaphy • Adhesions- adhesiolysis • Nursing Management: • Maintain function of NG tube • Monitor NG output q4H or as ordered • Assess for fluid and electrolyte imbalance • Monitor nutritional status • Assess for manifestations consistent with resolution (normal bowel sounds, decreases distention, verbalization of relief, passage of flatus or stool) • WOF: discrepancies in I &O, worsening of pain or distention, and increased NG output Large Bowel Obstruction (LBO) • Clinical manifestations: • Slow onset of symptoms • Constipation- may be the only presenting symptom for weeks • Altered stool shape (ribbon- like) • Bleeding • Abdominal distention (late sign) • Diagnostics: • Abdominal x-ray and abdominal CT or MRI • (+) distended colon • Pinpoints the site of the obstruction Medical Management: • IV fluids to restore fluid and electrolyte balance • NG aspiration and decompression • Surgical Management: • Colonoscopy: performed to untwist and decompress the bowel • Cecostomy: surgical opening into the cecum for patients who are poor surgical risks; provides an outlet for releasing gas and a small amount of drainage. • Nursing Management: • Monitor for worsening of symptoms • Administer IV fluids and electrolytes, as ordered • Prepare patient for surgery if unresponsive to non-surgical interventions Peritonitis • Inflammation of the peritoneum (serous membrane lining the abdominal cavity) • Causes: • Bacteria (E. coli and Klebsiella, Proteus, Pseudomonas, and Streptococcus species) • Fungal • External causes: abdominal surgery or trauma (GSW, stab wound) • Categories of Peritonitis: • Primary peritonitis: • Occurs as a result of spontaneous bacterial infection of ascitic fluid • Most commonly affects adults with liver failure • Secondary peritonitis: • Occurs secondary to perforation of abdominal organs with spillage that infects the serous peritoneum • Tertiary peritonitis: • Occurs as a result of suprainfection in a patient who is immunocompromised Clinical Manifestations: • Abdominal pain: initially diffuse but eventually localizes and becomes more intense over the site of maximal peritoneal irritation • Abdominal guarding and rigidity (“boardlike abdomen”) • Anorexia, nausea and vomiting • Diminished peristalsis leading to paralytic ileus • Fever (37.8 to 38.5) • Signs of early shock: restlessness, tachycardia, hypotension, weakness, pallor, diaphoresis, oliguria Diagnostics: • CBC • Leukocytosis with increase in immature neutrophils (bands) • Low hgb and hct, if with blood loss • Abdominal UTZ • (+) Abscess (localized collection of purulent material surrounded by inflamed tissues) and fluid collections • CT scan • (+) abscess formation • Peritoneal aspiration and culture and sensitivity of aspirated fluid • Reveals infection and identify causative organism Medical Management: • Fluid replacement with isotonic fluids • Analgesics for pain • Antiemetics • NPO • Intestinal intubation and suctioning • Oxygen therapy • I.V. Broad- spectrum antibiotics Surgical Management: • Directed toward excision, resection with or without anastomosis, repair, and drainage Nursing Management: • Monitor VS, I&O • Bed rest in semi- fowler’s position • Encourage DBE to prevent respiratory complications Acute Gastroenteritis • Inflammation of the mucosa of the stomach and small intestine • Mainly characterized by sudden onset diarrhea accompanied by nausea, vomiting, and abdominal cramping • Cause: Ingestion of infectious organism • Virus- Rotavirus, Norovirus • Bacteria- E. coli, Shigella, Salmonella, C. difficile • Parasite- Giardia lamblia, Entameoba histolytica • Diagnostics: • Stool culture- indicated ONLY for diarrhea > 3-5 days • Stool for OPEH Medical Management - Rehydration • Oral rehydration salts (ORS) • Hydrite- volume per volume • replacement. • Electrolyte drinks • Gatorade • Pocari sweat • IV rehydration, as ordered Medical Management - Control of diarrhea • Antidiarrheal agents, as ordered • Loperamide (Diatabs/Imodium)inhibits peristalsis, delays transit of intestinal contents, increases absorption of water from stools • Diphenoxylate with atropine (Lomotil)Decreases peristalsis and intestinal motility Medical Management- Eliminate causative organism • Rifaximin, as ordered • Nonabsorbable antibiotic used to treat E. coli traveller's diarrhea • C. difficile infection • Metronidazole (Flagyl)- first- line drug for mild cases • Vancomycin (Vancocin)- used for severe infections Nursing management: • Observe contact precaution, especially for C. difficilediarrhea (handwashing, gloves, and gown) • Place patient with C. difficile in private rooms, and use disposable thermometers and stethoscopes • Encourage oral fluids • Maintain IV-line patency • Encourage bed rest- to rest bowel • BRAT diet- Banana, Rice, Applesauce, and Toast. These foods help thicken stool consistency Irritable Bowel Syndrome (IBS) • A chronic functional disorder characterized by recurrent abdominal pain associated with disordered bowel movements • Affects women > men • Diagnosed in adults younger than 45 years old • Triggers: • Chronic stress • Sleep deprivation • Surgery • Infections • Diverticulitis • Food (milk, yeast products, eggs, wheat products, red meat) • Types of IBS: • IBS- C: main symptom is constipation • IBS- D: main symptom is diarrhea • IBS- M: main symptom is a combination of constipation and diarrhea • Clinical manifestations: • Abdominal pain: • Precipitated by eating • Relieved by defecation • Bloating and distention • Manifestations must be present for at least 3 months • Diagnostics: • Stool diary • Bristol Stool Form Scale Medical Management: • Probiotics (Lactobacillus) for abdominal bloating and gas, as ordered • Dicyclomine (Bentyl) for abdominal pain, as ordered • IBS- C: • Psyllium fiber • IBS-D: • Anti-diarrheal agents • Loperamide • Alosetron (Lotronex): for severe IBS-D that persists for at least 6 months and is unresponsive to therapies Nursing Management: • Lifestyle modification • Emphasize and reinforce good sleep habits and good dietary habits • Encourage to eat at regular times and to avoid food triggers • Do not take fluid with meals as this may result to bloating • Encourage smoking cessation and avoidance of alcoholic beverages Inflammatory Bowel Disease (IBD) • A group of chronic disorders: Chron’s disease and Ulcerative colitis that result in inflammation or ulceration (or both) of the bowel. • Exact cause: UNKNOWN • Risk factors: • (+) family history • Caucasian • Jewish • Living in a northern climate • Living in an urban area • Abdominal CT scan • More sensitive tool for diagnosing Chron’s disease • Highlights bowel wall thickening and mesenteric edema • Abdominal MRI • Sensitive and specific in terms of identifying pelvic and perianal abscess and fistulae • Complications: • Intestinal obstruction • Perianal disease • Enterocutaneous fistula (an abnormal opening between the small bowel and the skin) Chron’s Disease • Regional enteritis • Subacute and chronic inflammation of the GI tract wall that extends through all the layers • Most commonly occurs is the distal ileum and the ascending colon • Characterized by periods of remission and exacerbation • Clinical Manifestations: • Diarrhea • Right lower quadrant pain unrelieved by defecation • Crampy • Occurs after meals • Avoidance behavior: avoids intake of food • Weight loss, malnutrition, anemia • “Cobblestone” appearance of affected bowel • Bowel ulceration separated by edematous patches • Diagnostics: • Barium studies • (+) “string sign”: indicates constriction of a segment of the intestine Ulcerative Colitis • Chronic ulcerative and inflammatory disease of the mucosal and submucosal layers of the colon and rectum • Characterized by unpredictable periods of remission and exacerbation • Inflammatory changes begin in the rectum and progress proximally through the colon • Clinical Manifestations: • Bloody or purulent diarrhea (6 or more Liquid stools/day) • Left lower quadrant pain • Intermittent tenesmus • Anorexia, weight loss, dehydration • Fever • Diagnostics: • Colonoscopy • (+) friable, inflamed mucosa with exudates and ulcerations • Stool analysis • (+) blood • Laboratories • CBC: Low Hgb, low Hct, leukocytosis • Elevated C- reactive protein IBD Management • Dietary Modifications • Diet: low- residue, high- protein, highcalorie diet to rest bowel and meet nutritional needs • Avoid triggers of diarrhea: • Avoid milk, cold foods, and smoking • TPN, as prescribed for severe malnutrition • Pharmacologic Management: • Sulfasalazine (Azulfidine) • Effective for mild or moderate inflammation • Prevent recurrence • Metronidazole (Flagyl) • Used if with complications such as abscess or fistula formation • Corticosteroids • Prednisone PO • Hydrocortisone IV • Immunomodulators • Azathioprine (Imuran) • Used as maintenance regimen to prevent relapse •Surgical Management: • Chron’s Disease Total colectomy with ileostomy Colectomy: excision of the entire colon Ileostomy: surgical opening into the ileum • Stoma is found at the RLQ • Drainage is watery and occurs at frequent intervals • Ulcerative colitis: • Proctocolectomy with ileostomy Proctocolectomy: complete excision of colon, rectum, and anus Hernias • A hernia occurs when the wall of a muscle weakens, and the intestine protrudes through the muscle wall of a cavity Umbilical Hernias • A portion of the intestine protrudes through the umbilicus • Risk factors: • Multiparity • Liver cirrhosis • Ascites Abdominal Hernias • Occurs in the midline of the abdomen between the umbilicus and the xiphoid process. Inguinal Hernias • Most common type • Occurs in the groin area • Clinical Manifestations: (Hernias) • Bulging over herniated area which appears when patient stands or strains, and disappears when supine • Pain (may or may not be present) Hernia Complications • Incarcerated hernia • Hernias that do not return to the abdominal cavity with rest or manipulation and cause complete bowel obstruction • Strangulated hernia • Similar characteristic with incarcerated hernias but blood supply to hernia is cut off Medical Management • Hernia truss • A device that applies pressure to the hernia, thus keeping the intestine in the abdominal cavity. Surgical Management • Herniorrhaphy • Involves making an incision in the abdominal wall, replacing the contents of the hernial sac, repairing the weakened tissue, and closing the opening. • Hernioplasty • Involves replacing the hernia into the abdomen and reinforcing the weakened muscle wall with wire, mesh, or fascia Hemorrhoids • Dilated portions of veins in the anal canal • May be internal or external Types: • Internal hemorrhoids- located above the internal sphincter • First degree: do not prolapse and protrude into anal canal • Second degree: prolapse outside the anal canal during defecation but reduce spontaneously • Third degree: prolapsed to the extent that they require manual reduction • Fourth degree: prolapsed to the extent that they not be reduced • External hemorrhoids • Appear outside the external sphincter • Causes: • Constipation- most common • Pregnancy • Obesity • Liver cirrhosis • Right- sided heart failure • Clinical Manifestations: • Constipation • Anal pain • Rectal bleeding with defecation (hematochezia) • Anal itchiness Collaborative Management: • High- residue diet and increased oral fluid intake • Bulk- forming laxatives, as ordered. DOC: Psyllium • Cold packs to anal area followed by warm sitz bath • Astringents, as ordered to reduce engorgement. DOC: witch hazel • Sclerotherapy • Sclerosing agent: 5% phenol in saline • The sclerosing agent is injected into the base of the hemorrhoid to cause blood vessel thrombosis, which helps prevent prolapse. • Rubber band ligation • Hemorrhoid is visualized through an anoscope, and the proximal portion is grasped with an instrument • A small rubber band is then slipped over the hemorrhoid. • Tissue distal to the rubber band becomes necrotic after several days and sloughs off • Hemorrhoidectomy: • Surgical excision of hemorrhoids • Rectal sphincter is dilated digitally • Hemorrhoids are removed with a clamp and cautery, or are ligated and then excised • Pre- op: • Low residue diet to reduce bulk of Feces • Post- op: • Administer analgesics, as ordered • Assist client to side- lying or prone position • Apply ice packs over dressing for the first 12 hours to prevent bleeding • Warm sitz bath 12 to 24 hours post op. Best time to do sitz bath is after every bowel movement. • • Administer stool softeners, as ordered Encourage increase oral fluids and high-residue diet • WOF: rectal bleeding, suppurative drainage, continued pain on defecation, continued constipation Care of Clients with Fecal Diversions (Ostomy) • Monitor for fecal drainage. Fecal Diversion • Reroutes the flow of feces when the normal functioning of the bowel is hindered by disease, obstruction, or traumatic injury • May be temporary or permanent Ostomy • A surgically created procedure to divert fecal stream of the intestinal tract through the abdominal wall or into an artificially created reservoir • Ileostomy: surgical creation of an opening into the ileum or small intestine • Colostomy: surgical opening into the colon by means of a stoma to allow drainage of contents of the colon Indications: • IBD • Diverticulitis • Colorectal cancer Nursing Care: • Preoperative preparation: • Routine preop care • Postoperative Care: • Encourage early ambulation • Administer analgesics, as ordered • Monitor stoma for color and size • Normal: pink to bright red and shiny • Slight edema for 5 to 7 days • Should protrude ½ to ¾ inch over the abdomen • Abnormal: cyanotic/pale/ashen/dusky • Stoma Care: • Gently ask the client to look at the stoma. If the client refuses to do so, encourage him/her the verbalize feelings • Inform client that the stoma ha no touch or pain sensation • Cleanse stoma initially with sterile NSS until healed • Instruct to report discoloration ASAP to physician. • Skin Care: • Ileostomy: • Instruct client to wear pouch at all times. • Stoma should be rechecked 3 weeks post op and final size and type of appliance is selected in 3 months • Ileostomy and Colostomy: • Wash the skin around the stoma with warm water and mild soap. Pat dry. • When pouch seal leaks, change pouch immediately • Use skin barrier (Karaya paste) to protect peristomal skin from irritation • Promoting Nutrition • Low residue diet for the first 6 to 8 weeks • Strained fruits and vegetable are recommended • Avoid foods that are high in fiber or hard-to-digest kernels (popcorn, coconut) • Encourage increase oral fluids especially during summertime for • clients with ileostomy. Sport drinks may be used • If fecal drainage is too watery, restrict fiber • If fecal drainage is excessively dry, increase salt intake • Supporting a positive self- concept: • Encourage client to verbalize feelings, fears, and concerns about stoma • Encourage client to participate in stoma care. When the client starts to ask about the ostomy and ostomy care, that signals readiness for health education. • Preventing sexual dysfunction: • Advise couple on the following: • Explore positions the minimize stress and pressure on the pouch • Empty and clean the pouch before sexual activity • Used smaller- sized pouch or pouch cover during sexual activity • Use an abdominal binder to hold pouch secure MEDICAL-SURGICAL 2 : PTM2 Hepato-Biliary and Pancreatic Disorders Hepatobiliary System • Liver • Intrahepatic bile ducts • Extrahepatic bile ducts • Gall bladder Functions of the liver • Glucose metabolism • Glycogenesis- conversion of glucose into glycogen • Glycogenolysis- reverse conversion of glycogen into glucose • Ammonia conversion • Fat metabolism • Vitamin and Iron storage- liver stores vitamins A, B, and D, iron, copper • Bile formation • Bilirubin excretion • Drug metabolism Liver Function Tests Jaundice Jaundice- yellowish or greenish-yellow discoloration of body tissues due to increased blood bilirubin concentration Causes: • Liver disease • Obstruction of bile flow • Excessive RBC destruction Gall Bladder • Pear-shaped, hollow, saclike organ • Composed mostly of smooth muscles • Has a capacity of 30 to 50 mL • Functions as storage depot for bile Bile • Composed of water and electrolytes (Na+, K+, Ca++, Cl-, HCO3-) as well as significant amounts of lecithin, fatty acids, cholesterol, bilirubin, and bile salts • Helps in emulsification of fats Gall Bladder Stones Cholelithiasis – gall bladder stones Choledocholithiasis – stones in the common bile duct (CBD) • Made up of cholesterol crystals • Form in sterile gall bladder Risk Factors (5Fs): • F- Female • F- Fat • F- Forty • F- Fertile • F- Fregnant Clinical Manifestations • May be asymptomatic • Biliary colic- excruciating pain associated with the temporary obstruction of the cystic duct or CBD • Trigger: heavy meal • Location: RUQ • Characteristics: radiates to back or right shoulder, associated with nausea and vomiting • (+) Murphy’s sign - increased discomfort or inspiratory arrest (a catching of the breath) during deep inspiration when the examiner palpates the RUQ • Fever • Jaundice • Dark colored urine • Acholic stool – grayish or clay colored stool • Vitamin deficiency of fat- soluble vitamins Types of Gall Bladder Stones Pigment stones • Made up of calcium bilirubinate • Brown pigment stones – form in infected bile • Black pigment stones – form in sterile gall bladder Cholesterol stones Diagnostics: Abdominal ultrasound –diagnostic procedure of choice • More accurate if patient is placed on NPO overnight to distend the gallbladder Endoscopic Retrograde Cholangiopancreatography (ERCP) • Diagnostic: permits the direct visualization of the hepatobiliary system using a flexible fiberoptic endoscope • Therapeutic: treatment of confirmed choledocholithiasis • Initial position: Left semi- prone ERCP- Nursing Care Before the procedure: • Facilitate signing of consent • Reinforce instructions on procedure and how he/she can cooperate • Place on NPO as ordered • Monitor patient closely, esp. if moderate sedation is used After the procedure: • Monitor vital signs • Assess for signs of perforation or infection • Monitor for side effects of medications used during procedure • Monitor for return of gag and cough reflex Management Goals: • Reduce incidence of acute episodes of gallbladder pain and cholecystitis Strategies: • Dietary and supportive management • Pharmacotherapy • Endoscopic or surgical procedures Acute episodes: • Rest • IV fluids • Nasogastric suctioning • NPO • Analgesics, as ordered • Meperidine (Demerol)- drug of choice for acute cholecystitis • NSAIDs – for biliary colic • Antibiotics, as ordered Diet after an acute episode: • Low- fat liquid (e.g., protein- and carbohydrate- rich powdered supplements stirred into skim milk) • Cooked fruits, rice or tapioca, lean meats, mashed potatoes, non–gas-forming vegetables, bread, coffee, or tea may be added as tolerated. • Avoid eggs, cream, pork, fried foods, cheese, rich dressings, gas- forming vegetables, and alcohol Pharmacotherapy • Ursodeoxycholic acid (UDCA) • Indication: • Small, radiolucent cholesterol stones • Patients who refuse surgery • Patients who is a contraindication to surgery • MOA: inhibits cholesterol synthesis and secretion, thereby desaturating bile Laparoscopic Cholecystectomy • Gallbladder removal through a small incision made through the abdominal wall at the umbilicus • Standard therapy for symptomatic gallstones • ERCP may be done prior to procedure if CBD is obstructed by gallstones. Preoperative Care • Facilitate signing of consent • Reinforce education on: • Possible open abdominal approach • Type of anesthesia: general • Turning, deep- breathing exercises, and early ambulation • Inform on possible necessity of drainage tubes and NGT and suction during the postoperative period Postoperative Care • Monitor v/s and I&O • Facilitate turning, DBE, and early ambulation • Diet: • Immediate post op: low fat, high protein, high carbohydrate diet • Upon discharge: no special dietary instructions but to avoid excessive fats x 4 to 6 weeks • Instruct that BM may increase in frequency (1-3 x a day) and diminishes over a period of weeks to months Pancreas • A J-shaped, soft, lobulated, retroperitoneal organ. • It lies transversely, although a bit obliquely, on the posterior abdominal wall behind the stomach • Has both exocrine and endocrine functions • Exocrine Pancreas • Produces highly alkaline secretions • Amylase: CHO digestion • Trypsin: CHON digestion • Lipase: Fat digestion • Secretin increases HCO3- secretion from pancreas • Cholecystokinin (CCK) stimulate release of digestive enzymes Pancreatitis • Pancreatitis- inflammation of the pancreas • Types: • Acute pancreatitis- medical emergency with high mortality rate • Chronic pancreatitis- undetectable in early stage Acute Pancreatitis • Interstitial Edematous Pancreatitis • Most common type • (-) necrosis but pancreas become enlarged due to inflammatory edema • Milder form but places patient at risk for hypovolemic shock, fluid and electrolyte imbalance, and sepsis • Necrotizing Pancreatitis • Necrosis is evident in peripancreatic parenchyma or in tissue surrounding gland • More widespread and complete enzymatic digestion of gland • Causes: “I GET SMASHED” • I - Idiopathic • G - Gall stones • E - Ethanol (Alcohol) • T - Trauma • S - Steroids • M - Mumps/Malignancy • A - Autoimmune • S - Scorpion stings • H-Hypercalcemia/Hypertriglyceridemia • E - ERCP • D – Drugs • Clinical Manifestations • Severe abdominal pain – major symptom • Diffuse and difficult to localize • Typically occurs in midepigastrium 24 to 48 hours after a very heavy meal or alcohol ingestion • Unrelieved by antacids and vomiting • Accompanied by abdominal distention, poorly defined palpable abdominal mass, and decreased peristalsis • Board- like abdomen – indicative of peritonitis • Cullen’s sign – hemorrhagic discoloration of umbilical area due to intraperitoneal hemorrhage • Grey Turner’s sign – discoloration of left flank • Nausea and vomiting – may be bile stained • Fever, jaundice, mental confusion, agitation • Hypotension • Tachycardia • Cyanosis • Cold, clammy extremities • • Elevated serum amylase and lipase within 24 hour of the onset of symptoms Hyperglycemia, hypocalcemia • Complications • Local: • Pancreatic cysts or abscess • Acute fluid collections in or near the pancreas • Systemic: • Pulmonary insufficiency with hypoxia • Shock • Kidney disease • GI bleeding Medical Management • NPO – to inhibit pancreatic stimulation • Nasogastric suction if with abdominal distention and paralytic ileus • Enteral feeding – preferred route to meet nutritional needs • Total Parenteral Nutrition (TPN), if enteral route is not tolerated • Pain control using opioids (i.e., morphine, fentanyl, hydromorphone) • Antibiotics, if with infection only • Intensive insulin therapy/Continuous insulin infusion if with hyperglycemia • IV Calcium gluconate if with tetany • If shock is present: • Give plasma or plasma volume expanders (e.g., dextran or albumin) • Dopamine IV – to increase SVR • PLR – fluid of choice to correct electrolyte imbalance Surgical Management • ERCP with/without lap chole if gall stones are the cause • Laparotomy • Performed by making a large incision in the abdomen to gain access to the peritoneal cavity. • Done to assist in diagnosis, establish pancreatic drainage, • Pancreatic Surgery • Resect or debride an infected, necrotic pancreas Nursing Management • Pain Control • Assess pain score regularly • Administer opioids, as ordered • Institute non- pharmacologic pain relief interventions • Facilitate and maintain NPO • Institute bed rest - to decrease the metabolic rate and reduce the secretion of pancreatic and gastric enzymes. • Refer increasing severity of pain to physician ASAP • Improving breathing pattern • Place in semi- Fowler’s position - to decrease pressure on the diaphragm by a distended abdomen and to increase respiratory expansion. • Change positions frequently – to prevent atelectasis and pooling of secretions • Facilitate DBE and coughing, instruct on use of incentive spirometry • Improving nutritional status • Monitor daily weights • Administer enteral/parenteral nutrition, as prescribed • Monitor blood glucose q4-6H or as ordered • Facilitate high protein, low fat diet once acute symptoms subside • Instruct to avoid heavy meals and alcoholic beverages • Maintaining skin integrity • Assess surgical wound, drainage sites, and skin for signs of infection, inflammation, and breakdown • Provide wound care as prescribed • Prevent contact of intact skin with drainage • Facilitate turning to sides q2H • Use specialty beds as indicated to prevent skin breakdown Chronic Pancreatitis • Clinical Manifestations • Recurring attacks of severe upper abdominal and back pain, accompanied by vomiting • • • • • • Unresponsive to opioids Triggered by food Frequency and duration increases over time Weight loss – due to anorexia and/or fear that eating will precipitate an attack Impaired protein and fat digestion Steatorrhea – stools with high fat content MEDICAL-SURGICAL 2 : PTM3 Care of Clients with Endocrine Disorders Overview of the Endocrine System • Endocrine system plays a vital role in orchestrating cellular interactions, metabolism, growth, reproduction, aging and response to adverse conditions. • The system uses chemical transmitters known as hormones to regulate and integrate body functions by acting on local or distant target sites • Negative feedback mechanism is deployed to maintain homeostasis • Disorders of the endocrine system are manifested as hyperfunction or hypofunction of a specific endocrine gland Pituitary Gland (Hypophysis) • Master gland of the body • Divided into the anterior PG (adenohypophysis) and posterior PG (neurohypophysis) • Controlled by the hypothalamus Anterior Pituitary Gland (Adenohypophysis) • Growth hormone (GH) • Also known as somatotropin • Stimulates growth of bone and muscle • Promotes protein synthesis and fat metabolism • Decreases carbohydrate metabolism • Insulin antagonist • Adrenocorticotropic hormone (ACTH) • Stimulates synthesis and secretion of adrenal cortical hormones • Thyroid- stimulating hormone (TSH) • Stimulates synthesis and secretion of thyroid hormones • Follicle Stimulating hormone (FSH) • Female: stimulates growth of ovarian follicle • Male: stimulates sperm production • Luteinizing hormone (LH) • Female: stimulates development of corpus luteum; release of oocyte • Male: stimulates secretion of testosterone • Prolactin • Prepares female breast for breastfeeding Posterior Pituitary Gland (Neurohypophysis) • Antidiuretic Hormone (ADH) • Increases water reabsorption by kidney • Oxytocin • Stimulate contraction of pregnant uterus • Milk ejection Thyroid Gland • Thyroid hormones: triiodothyronine (T3) and thyroxine (T4) • Increase metabolic rate • Increase responsiveness to catecholamines • • Stimulate SNS activity Necessary for fetal growth and development • Calcitonin (Thyrocalcitonin) • Lowers blood calcium and phosphate level • When calcitonin is high, serum calcium is low • When calcitonin is low, serum calcium is high Parathyroid Gland • Parathyroid hormone (PTH) • Regulates serum calcium • PTH elevates serum calcium but LOWERS phosphorus level • Increase PTH, hypercalcemia • Decreased PTH, hypocalcemia Pancreas • Endocrine function is performed by the islets of Langerhans Adrenal Glands • Located atop the kidneys • Divided into the adrenal cortex and adrenal medulla • Adrenal cortex= adrenocortical hormones • Adrenal medulla= adrenomedullary hormones Adrenocortical Hormones: Sugar, Salt, Sex • Glucocorticoids (Cortisol: Sugar) • Regulate blood glucose level • Enhance gluconeogenesis • Insulin antagonist • Has anti- inflammatory effect • Decrease T- lymphocyte participation in cell-mediated immunity • Increase gastric acid and pepsin production • Mineralocorticoids (Aldosterone: Salt) • Increases sodium retention • Increases potassium and hydrogen • excretion • “pro- sodium, anti- potassium” • Sex hormones (Androgen and estrogen) • Responsible for some secondary sex characteristics in females, but works as gonadal steroids in males • Insulin • Secreted by beta cells • Lowers blood glucose by facilitating glucose transport across cell membranes of muscle, liver, and adipose tissues • Promotes glycogenesis • Glucagon • Secreted by alpha cells • Increases blood glucose concentration by stimulation of glycogenolysis and gluconeogenesis Adrenomedullary Hormones • Epinephrine and norepinephrine • Serves as neurotransmitters for the SNS Disorders of the Pituitary Gland Disorders of the Anterior Pituitary Gland • Acromegaly • Hypopituitarism Disorders of the Posterior Pituitary Gland • Diabetes insipidus (DI) • Syndrome of Inappropriate Antidiuretic Hormone (SIADH) • • Normal: GH <0.4 mcg/L Acromegaly: GH > 0.4 mcg/L Disorders of the Anterior Pituitary Gland Acromegaly • A rare condition characterized by overproduction of growth hormone (GH). • Prevalence rate: 28-137 cases/million population (Kamusheva et al., 2020) • Cause: • Idiopathic hyperplasia of the APG • Pituitary tumor (adenoma)- most common • Clinical Manifestations: • A - Arthralgia/Arthritis • B - Blood pressure raised • C - Carpal Tunnel Syndrome • D - Diabetes • E - Enlarged organs, head, hand, face, feet • F - Field defect (visual impairment) • G - Gynecomastia • Prognosis: Shorter than average life span • Diagnostic tests: • Serum Growth Hormone • Diagnostic Criteria> 0.4 mcg/L • Insulin- like Growth Factor 1 (IGF-1) • Mediates peripheral action of GH • Normal: 135-449 ng/mL • Elevated IGF-1 is diagnostic of acromegaly • Oral Glucose Tolerance Test (OGTT) • GH secretion is normally inhibited by glucose • Baseline GH levels are obtained before ingestion of 75- or 100- gm oral glucose • GH levels are then measured at 30, 60, 90, and 120 minutes Medical Management • Octreotide acetate (Sandostatin) • Somatostatin analogue • Reduces GH and IGF-1 to normal • Given SQ 3x a week • GH levels are measured every 2 weeks to guide drug dosing, and then every 6 months until desired response is obtained Surgical Therapy • Transsphenoidal hypophysectomy: • Removal of the pituitary gland • Treatment of choice for small pituitary tumors Incision is made in the inner aspect of the upper lip and gingiva. The sella turcica is entered through the floor of the nose and the sphenoid sinuses. Postoperative nursing care: • Position: Low- fowlers position (30degrees) at all times to reduce pressure on sella turcica and decrease headaches • Provide mouth care q4H to keep surgical area clean and free of debris • Avoid toothbrushing for at least 10 days to protect suture line • Instruct patient to avoid vigorous coughing, sneezing, and straining at stool to prevent cerebrospinal fluid leakage • WOF: clear nasal discharge, persistent and severe generalized or supraorbital headache • CSF leak usually resolves within 72 hours when treated with head elevation and bed rest • Report to physician increasing urine output and low specific gravity as they may indicate the development of diabetes insipidus • Essential hormones of target organs are replaced postoperatively, as ordered Radiation Therapy • Used when surgery failed to produce a cure or patients are poor candidates • Given in combination with medications • May also be used to shrink tumor prior to surgery • Panhypopituitarism (Simmond’s disease) • Total failure of the pituitary gland that results to deficiency of all pituitary hormones • Sheehan’s syndrome • Hypopituitarism caused by postpartum pituitary necrosis • Causes: • Pituitary tumor- most common • Autoimmune disease • Infection • Pituitary infarction • Destruction/Removal of pituitary gland • Clinical Manifestations: • Early (associated with spaceoccupying lesion): • Headache • Visual changes • Loss of smell • Nausea and vomiting • Seizures Acromegaly vs Gigantism • Management: • Surgical removal of tumor • Radiation therapy • Lifelong hormone replacement therapy Disorders of the Posterior Pituitary Gland Hypopituitarism • A rare disorder that involves a decrease in one or more of the pituitary hormones. Types: • Selective hypopituitarism • Deficiency of one pituitary hormone Diabetes Insipidus (DI) • Most common disorder of the neurohypophysis • Characterized by a deficiency in antidiuretic hormone (ADH) • Clinical Manifestations: • Polyuria: Large urine volume • UO= 2 to 20L/day • Very dilute urine • Urine Specific Gravity: 1.001 to 1.005 • Polydipsia, craves cold water (2 to 20L) • Hypovolemia • Thirst • Tachycardia • Hypotension Urine Osmolality • A measure of the number of dissolved particles in a fluid. • Used to evaluate the balance between water and dissolved particles in the urine • Measurement of concentration • Normal: 250-900 mOsm/kg Urine Specific Gravity • A measure of the concentration of particles in urine and the density of urine compared with density of water. • Provides information on the kidney’s ability to concentrate urine • Normal: 1.010 to 1.020 • Diagnostics: • Fluid Deprivation Test • Urine osmolality are measured at the beginning and end of test • Fluids are withheld for 8 to 12 hours or until 3% to 5% of body weight is lost • Desmopressin acetate (DDAVP) is given intranasally or SQ Central DI Management: • Desmopressin (DDAVP) • A synthetic vasopressin • Given intranasally q12 to 24 hours • Caution: CAD • Chlorpropamide (Diabinese) and • Carbamazepine (Tegretol) • Helps decrease thirst associated with central DI • During acute episodes: • Hypotonic IV fluids or D5 Water, as ordered to replace urine output • Encourage increased oral fluids as tolerated • Monitor VS, urine output and specific gravity • Monitor level of consciousness and for signs of dehydration Nephrogenic DI Management: • Low- sodium diet (no more than 3g/day) helps decrease urine output • Thiazide diuretics, as ordered • Hydrochlorothiazide, Chlorothiazide • Reduces flow to the ADHsensitive distal nephrons • Indomethacin (Indocin), as ordered • NSAID • Helps increase renal responsiveness to ADH Syndrome of Inappropriate Antidiuretic Hormone (SIADH) • Excessive secretion of ADH from the pituitary gland even in the face of subnormal serum osmolality • Provide frequent oral care and distractions to decrease discomfort r/t thirst from fluid restrictions Management (Severe hyponatremia): • Seizure precautions • IV Hypertonic (3%) saline solution (administer slowly), as ordered • Furosemide (Lasix), as ordered • Loop diuretic • Promotes diuresis • Used ONLY if serum sodium is at least 125 mEq/L • Fluid restriction of 500mL/day, as ordered • Obtain daily weights • Clinical Manifestations: • Dilutional hyponatremia (Na <135 mEq/L) • Headache- earliest sign • Serum hypo- osmolality • Concentrated urine • Oliguria • Weight gain • Diagnostics • Serum Na <135 meq/L • Serum osmolality <280 mOsm/kg • Urine Specific Gravity > 1.025 Management (Mild/mod hyponatremia) • Fluid restriction to 800 to 1000 mL/day, as ordered • Obtain daily weights • Position HOB flat or elevated no more than 10 degrees (to enhance venous return to heart and increase left atrial filling pressure, thereby reducing release of ADH) • Place on seizure precautions Management: • Tolvaptan (Samsca) • Vasopressin V2 receptor antagonists • It works by increasing the amount of water released from the body as urine. Removing fluid from the body helps to increase the level of sodium in the blood. • Used to treat euvolemia-hyponatremia in HOSPITALIZED patients • Monitor closely to prevent rapid correction of serum sodium Management (Chronic SIADH): • Demeclocycline (Declomycin) • Inhibits ADH- induced water reabsorption and promotes water diuresis • Typically used when patients find severe fluid restriction unacceptable and the underlying disorder cannot be corrected • Use ice chips or sugarless gum to decrease thirst • Teach patient to supplement diet with sodium and potassium, especially when loop diuretics are prescribed Disorders of the Thyroid Gland Thyroid Hormones • Triiodothyronine (T3) • Thyroxine (T4) • Calcitonin Thyroid Hormone Synthesis Regulation of Thyroid Hormones Euthyroid: thyroid hormone level is within normal Goiter • A goiter is an enlarged thyroid gland • Cause: • Iodine deficiency • Goitrogens- foods or drugs that contain thyroid inhibiting agents • Thyroid cells are stimulated to grow which may result to an overactive (hyperthyroidism) or underactive (hypothyroidism) thyroid • Types: • Nontoxic goiter: • Diffuse enlargement of the thyroid gland that does not result from a malignancy or inflammatory process • Thyroid hormones are normal • Nodular goiter: • Thyroid- hormone secreting nodules that function independent of TSH stimulation • Benign nodules • May be multinodular goiter (multiple nodules) or solitary autonomous nodule (single nodule) • Toxic nodular goiter: • Nodular goiters associated with hyperthyroidism • Prevention: • Iodine supplementation • Use of iodized salt • Limit intake of goitrogenic foods • ASIN law (RA 8172) • Act for Salt Iodization Nationwide (ASIN) • Requires the addition of iodine to all salt intended for animal and human consumption in order to eliminate micronutrient malnutrition in the country Management: • Thyroid hormone replacement to prevent further enlargement • Levothyroxine (Synthroid) • Surgery is required to remove large goiters Hyperthyroidism • A form of thyrotoxicosis resulting from an excessive synthesis and secretion of endogenous and exogenous thyroidhormones by the thyroid • Causes: • Grave’s disease - most common • Toxic nodular goiter • Toxic adenoma • Thyroiditis • Excessive ingestion of thyroid hormone Grave’s Disease • An autoimmune disorder that results from an excessive output of thyroid hormones caused by an abnormal stimulation of the thyroid gland by circulating immunoglobulins • Affects women> men • Occurs between 30-40 years old • May be precipitated by emotional shock, stress, or infection • Clinical Manifestations: • Basic concept: Everything is HIGH, FAST, and WET • Presenting symptom: nervousness Ophthalmopathy • Exophthalmos- protrusion of eyeballs resulting from fluid accumulation at the fatpads behind the eyelids • Dalyrimple’s sign (Thyroid stare)bright- eyed stare and infrequent blinking • Von Graafe’s sign (lid lag)- long and deep palpebral fissure that is still evident even when looking down • Jeffrey’s sign- forehead remains smooth when patient looks up Dermopathy • Thickened and hyperpigmened skin at the pretibial area • Assessment and Diagnostics: • Enlarged thyroid; soft and may pulsate • Decreased TSH, Increase Free T4 • Normal TSH: 0.5 -5.0 mIU/L • Normal free T4: 0.9 to 1.7 ng/dL • Radioactive iodine uptake: • Measures the rate of iodine uptake by the thyroid • Uses Iodine123 (I123) and a count is made over the thyroid gland using a scintillation counter • Scintillation counter detects the gamma rays released from the breakdown of I123 • Hyperthyroidism: HIGH uptake of I123 Medical Management: • Radioactive Iodine Therapy • Goal: eliminate the hyperthyroid state with the administration of sufficient radiation in a single dose. • Agent: Iodine 131 (I131) • Contraindicated in pregnancy and lactation • Mechanism of action: • The radioactive isotope of iodine becomes concentrated inside the thyroid gland destroying ONLY the thyroid cells without jeopardizing other radiosensitive tissues • Pre- treatment: • Methimazole • Anti-thyroid • Started 4 to 6 weeks prior to treatment • Stopped 3 days before and resumed 3 days after RAI Therapy • Nursing Interventions: • PATIENTS IS RADIOACTIVE and may contaminate others through saliva, urine, or radiation emitting from the body • Isolate patient • Anti- thyroid medications • Mechanism of action: prevents formation of thyroid hormones by blocking iodine utilization • DOC: • Propylthiouracil (PTU) • Methimazole (Tapazole) • Nursing Management: • Instruct to take medication early in the morning on an empty stomach 30 minutes before eating to avoid decrease in absorption • Advise patient that it may take weeks until symptom relief occurs • WOF: fever and sore throat • Adjunctive therapy • Beta- blockers • • Propranolol, metoprolol Decreases HR, systolic blood pressure, and anxiety Eye Care for Exophthalmos: • Artificial tears to prevent excessive dryness • Tinted eyeglasses • Eye shield Surgical management • Indications: • Pregnant women who are allergic to antithyroid medications • Large goiters • Patients who are unable to take antithyroids Subtotal Thyroidectomy • Surgical removal of about 5/6 of the thyroid tissue • Requires a euthyroid state prior to conduct • Pre-medications: • Anti-thyroid • Iodine compounds • Potassium iodide (KI), Lugol’s solution, Saturated Solution of Potassium iodide (SSKI) • MOA: reduce the size and vascularity of thyroid gland • Administer with milk or fruit juice to increase palatability • Administer using a straw to prevent staining of teeth • Post operative Care: • POSITION: semi-fowler’s with head, neck, and shoulders erect • Monitor surgical site for bleeding and edema: • Check dressing and back of neck • WOF: respiratory distress • Prepare at bedside: tracheostomy set, oxygen, and suction equipment • Assess for laryngeal nerve damage • Let client speak q hourly • Expected: mild hoarseness • Abnormal: Severe hoarseness with high-pitched voiced and stridor • Monitor for signs of hypocalcemia and tetany: • WOF: • (+) Trousseau’s sign • (+) Chvostek’s sign • Nursing responsibility: Prepare Calcium gluconate at bedside Thyrotoxicosis (Thyroid Storm) • A form of severe, life- threatening hyperthyroidism • Causes: stress (surgery, RAI), infection • Clinical Manifestations: • Hyperpyrexia (T >38.5C) • Extreme tachycardia (HR > 130 bpm) • Exaggerated symptoms of hyperthyroidism • Altered mental status (delirium, psychosis, coma) Management: • Ice packs, paracetamol • Humidified oxygen • IV fluids with dextrose • Propylthiouracil (PTU), Lugol’ssolution, dexamethasone Hypothyroidism • Results from suboptimal levels of thyroid hormones • Affects women > men • Commonly occurs between 40 to 70 years old • Types: • Primary hypothyroidism- dysfunction of the thyroid gland • Secondary hypothyroidism- the dysfunction originates from the pituitary gland • Cretinism- hypothyroidism in children • Causes: • Hashimoto’s thyroiditis (most common): • An autoimmune form of thyroiditis in which the person’s own immune system attacks the thyroid gland • Atrophy of thyroid gland with aging • RAI therapy, thyroidectomy • Medications (Lithium, iodine compounds, and anti- thyroids) • Head and neck radiation therapy • Diagnostics: • Clinical Manifestations • Basic concept: “Everything is low, slow, and dry” • Early: • Hoarseness of voice • Extreme fatigue • Loss of libido • Amenorrhea • Skin dryness • Late: • Cold intolerance • Hypothermia • Expressionless and masklike facie • Weight gain even without increase in food intake • Bradycardia • Alopecia • Constipation • Apathy • Sensitivity to opioids is increased • Atherosclerosis • Myxedema: accumulation of mucopolysaccharides in the subcutaneous tissue Myxedema Coma • A rare life- threatening condition • Decompensated state of severe hypothyroidism • Common among undiagnosed hypothyroidisms • Precipitated by: • Infection • Opioids • Clinical Manifestations: • Altered mental status (initial manifestation) • Respiratory depression • Hyponatremia, hypoglycemia • Hypotension, bradycardia, hypothermia Medical management • Goal: restore normal metabolic state • • Levothyroxine (Synthroid) • Taken on an empty stomach • Avoid strawberry, peaches, cabbage • Dose is gradually increased to prevents • hyperthyroidism • Caution: may increase oxygen demand which • triggers angina or ACS • Discontinue immediately if with angina or • dysrhythmia T3 and T4 IV replacement for myxedema coma Disorders of the Parathyroid Gland Parathyroid Glands • Embedded in the posterior aspect of the thyroid gland • Secretes parathormone (PTH) • Increases serum calcium level, but decreases phosphorus level • Vitamin D enhances effects of hormone Hyperparathyroidism • Overproduction of parathormone and is characterized by bone decalcification and the development of renal calculi • Types: • Primary hyperparathyroidism • Parathyroid adenoma – most common • Long- term lithium therapy • Secondary hyperparathyroidism • A compensatory response to conditions that induce hypocalcemia • CKD, vitamin D deficiency • • Clinical Manifestations: • Fatigue • Muscle weakness • Constipation • Nausea and vomiting • Dysrhythmias • Hypertension • Kidney stones • Pathologic fractures • Skeletal pain and tenderness • Shortening of body stature • Diagnostics • Serum calcium level • Normal: 8.5-10.5 mg/dL • Hyperparathyroidism: elevated • Intact PTH • Normal: 14-72 pg/mL • Hyperparathyroidism: elevated • Serum phosphorous level • Normal: 2.5- 4.5 mg/dL • Hyperparathyroidism: decreased • Bone Mineral Density (BMD) Hyperparathyroidism: T score of -2.5 or less at any site or previous fragility fracture Medical management • Hydration therapy • Increased fluid intake to 2,000mL or more to prevent renal calculi • PNSS IV- fluid of choice as sodium enhances excretion of calcium • Mobility • Bones subjected to the normal stress of walking give up less calcium. Bed rest increases calcium excretion and the risk of renal calculi. • Gallium nitrate (Ganite) • Anti- hypercalcemic • Alendronate (Fosamax) • Bisphosphonates Inhibit osteoclastic bone resorption, normalizing serum calcium levels Surgical Management: • Parathyroidectomy: • Removal of one or more of the parathyroid glands • Postoperative care: • Position: Semi- Fowler’s • WOF respiratory distress, bleeding at post operative site • Prepare at bedside: tracheostomy set Hypercalcemic Crisis • Occurs with extreme elevation of calcium levels greater than 13 mg/dL • Cause: dehydration Management: • Rapid rehydration with large volume of isotonic fluid • Loop diuretic (e.g., Furosemide) if with edema • Calcitonin- promotes renal excretion of calcium • Corticosteroids- promotes calcium deposition in bone • Dialysis Hypoparathyroidism • Hyposecretion of parathyroid hormone • Cause: • Subtotal thyroidectomy (most common) • Abnormal parathyroid development • Clinical Manifestations: • Hypocalcemia (Ca++ < 8.5mg/dL) • Tetany: general muscle hypertonia, with tremor and spasmodic or uncoordinated contractions occurring with or without efforts to make voluntary movement Latent Tetany: • Numbness, tingling, and cramps in the extremities • Stiffness of hands and feet Overt Tetany: • Bronchospasm • Laryngospasm • (+) Trousseau’s sign: carpopedal spasm resulting from occlusion of the blood flow to the arm for 3 minutes • (+) Chvostek’s sign: sharp tapping over the facial nerve causes spasm or twitching of mouth, nose, eye • Seizures • Dysrhythmias • Photophobia Medical Management: • Goal: increase serum calcium to 8.5 to 10.5 mg/dL • Vitamin D3 (calciferol) • Hydrochlorothiazide (Hydrodiuril)decreases urinary calcium excretion • Calcium gluconate very slow IVTT - if hypocalcemia is after thyroidectomy • Aluminum hydroxide gel (Amphojel) after meals to bind phosphate and promote its excretion through the GI tract • Place patient on seizure precaution • Have a tracheostomy set, oxygen, and suction available at bedside • Provide a high- calcium, low- phosphorus diet • Broccoli, tomato, banana, kidney beans • Avoid cheese, milk and milk products, and egg yolk • Avoid spinach which contains oxalate that forms insoluble calcium substances Disorders of the Adrenal Glands Pheochromocytoma • A tumor of the chromaffin cells of the adrenal medulla (usually benign; 10% malignant) • Peak incidence at 40-50 years old • Affects men and women equally • High familial tendency • Clinical Manifestations: • Headache • Hyperhidrosis • Hypertension • Hypermetabolism • Hyperglycemia • Diagnostics: • Vanillylmandelic Acid (VMA) Test • Measures urinary excretion of catecholamine metabolite • Specimen: 24- hour urine sample • Avoid coffee and tea, banana, chocolate, vanilla, and aspirin • Normal: 1.4-6.5mg/24 hours • Clonidine suppression test • Clonidine suppresses release of neurogenically mediated catecholamines • (+): clonidine does not suppress catecholamine levels Medical Management (ABC): • Alpha- Adrenergic blocker • Phenoxybenzamine (Dibenzyline) • Given 10 to 14 days prior to surgery • S/E: orthostasis, nasal stuffiness, fatigue, retrograde ejaculation • Beta- Adrenergic blocker • Propranolol (Inderal) • Initiated once alpha- adrenergic control is achieved • Calcium Channel Blocker • Nifedipine (Adalat) • Alternative treatment if blood pressure control is inadequate or patient is unable to tolerate side effects Surgical Management: • Adrenalectomy • Removal of one or both adrenal glands • Definitive treatment of pheochromocytoma • Pre-operative preparation: control blood pressure • Complication: • Hypertensive crisis (Intra/Post- Op) • Results from the manipulation of the tumor during surgical excision • Mgt: • Sodium nitroprusside (Nitropress) • Phentolamine (OraVerse) Nursing Management: • Institute bed rest with HOB elevated to promote orthostatic decrease in BP during episodes of hypertension or tachycardia • Monitor vital signs, ECG, fluid and electrolytes, and blood glucose levels Cushing’s Syndrome • A clinical condition that results from chronic exposure to excess corticosteroids, particularly glucocorticoids • Affects women > men • Cause: • Steroids (most common exogenous) • Cushing’s Disease: Presence of ACTHsecreting pituitary adenoma (most common endogenous) • Hyperplasia of adrenal gland (less common) • Ectopic production of ACTH by malignancies • Clinical manifestation: • Moon - face • Buffalo hump • Virilization (women): appearance of masculine traits and recession of feminine traits • Truncal obesity but thin extremities • Purple/Red Striae • • • • • • • Easy bruising Menstrual disorders HTN Unexplained hypokalemia Sleep disturbances Hyperglycemia Osteoporosis, Pathologic fractures • Diagnostics: • Serum cortisol level • Normal: • high in early morning (6 to 8 am): 10-20 mcg/dL; • low in the evening (4 to 6 pm): 3-10 mcg/dL • Abnormal: disruption of normal variation • Dexamethasone suppression test • Dexamethasone 1mg (low dose) or 8 mg (high dose) PO at bedtime, then plasma cortisol and ACTH levels are obtained at 8am the next morning Collaborative Management: • Transsphenoidal hypophysectomy • Done if cause is a pituitary tumor • Adrenalectomy (Laparoscopic): • Done if cause is adrenal hypertrophy • Post operative care: • Symptoms of adrenal insufficiency may appear 12 to 48 hours after surgery • Hydrocortisone is given for several months • Adrenal enzyme inhibitor • Metyrapone (Metopirone), Ketoconazole (Nizoral) • Used if cause is an ectopic ACTH production • Dose reduction • Done if cause of syndrome is the administration of corticosteroids • Dose is tapered to the minimum dosage needed to treat underlying disease process Addison’s Disease • Primary adrenocortical insufficiency • Occurs when the adrenal glands are damaged and cannot secret adrenocortical hormones • Causes: • Autoimmune or idiopathic atrophy • Abrupt withdrawal of corticosteroids • Adrenalectomy • Infections (i.e., tuberculosis and histoplasmosis) • Clinical Manifestations: • Muscle weakness • Anorexia • GI symptoms • Emaciation • Dark pigmentation of knuckles, knees, and elbows, dehydration • Hypoglycemia, hyponatremia, hyperkalemia • Emotional lability • Bronze pigmentation of skin Medical Management: • Hydrocortisone (Solu- cortef), as ordered • Fludrocortisone (Florinef), as ordered • Dietary: • High sodium, low potassium • Small, frequent feedings if with anorexia Addisonian Crisis • Hypotension, cyanosis, fever, n&v, signs of shock • Cause: stress, exposure to cold, acute infection, decreased salt intake, dehydration Management: • High-dose hydrocortisone IV • 5% dextrose in normal saline IV- to reverse hypotension • Vasopressors, if with persistent hypotension Primary Aldosteronism • Excessive production of aldosterone • Cause: • Tumor of the adrenal gland (solitary adrenocortical adenoma) • Clinical Manifestations: • Hypertension • Hypokalemia • Muscle weakness • Fatigue • Dysrhythmias • Diagnostics: • Captopril Challenge Test (CCT) • ACE inhibitors normally block the activity of RAAS • Give 25-50 mg captopril PO after sitting/standing for at least 1 hours with blood samples drawn at time zero and after 2 hours for plasma renin activity (PRC) and plasma aldosterone measurements • (+): Plasma aldosterone is >/= 8.5 ng/dL AND renin remain suppressed Collaborative Management • Laparoscopic adrenalectomy: • Done to achieve total surgical removal of adrenal tumor • Less complications and shorter hospital stay • Spironolactone (Aldactone) • Potassium- sparing diuretic • Controls hypertension without causing further hypokalemia MEDICAL-SURGICAL 2: PTM4 Care of Clients with Diabetes Mellitus Diabetes Mellitus (DM) • A group of metabolic disease characterized by hyperglycemia. • Hyperglycemia- elevated blood glucose level • Normal blood glucose: 80-120 mg/dL • A chronic, multisystem disease related to abnormal insulin production, impaired insulin utilization, or both • A disorder of glucose metabolism related to absence or insufficient insulin supply and/or poor utilization of the insulin • General Risk Factors • Family history • Obesity • Race/Ethnicity (i.e., AfricanAmericans, Hispanics, • Native Americans, Asian American, Pacific Islander) • Age ≥ 45 years old • Previously identified impaired fasting glucose • Hypertension (≥140/90) • Decreased HDL, increased triglycerides • History of gestational diabetes/ delivery of babies over 9lbs • Types: • Type I Diabetes Mellitus • Juvenile- onset diabetes • Insulin- dependent diabetes mellitus (IDDM) • Type II Diabetes Mellitus • Adult- onset diabetes • Non-Insulin- Dependent Diabetes Mellitus (NIDDM) • Classical Signs • Polyuria: increased frequency and volume of urine • Polydipsia: increased thirst sensation • Polyphagia: increased hunger sensation Type 1 Diabetes Mellitus • Characteristics: • Acute onset • Usually before 30 years old • Patient is thin • Etiology: • Destruction of beta cells by • Genetics • Immunologic • Environmental Type 2 Diabetes Mellitus • Characteristics: • Most prevalent type • Slow onset • Usually after 30 years old • Common among obese • Risk Factors: • Overweight/Obesity • Old age • Family history of DM type 2 • African Americans, Asian Americans, Hispanics, Native Hawaiians or other Pacific Islanders, and Native Americans • Etiology: • Insulin resistance: decreased tissue sensitivity to insulin • Unknown cause • Impaired insulin secretion Medical Management • Goal: Achieve euglycemia without episodes of hypoglycemia while maintaining a high quality of life Insulin Therapy • Historically, insulin was derived from beef and pork pancreas • Recent insulin preparations are genetically engineered human insulins derived from E.coli or yeast cells using recombinant DNA technology • Commonly given subcutaneously, butregular insulin may be given IV/SQ • Dose is prepared in “units” Insulin Preparations • Groups insulin according to onset (O), peak (P), and duration (D) • Rapid- acting, Short- acting, Intermediateacting, Very Long-acting Rapid- Acting Insulin • Diagnostic Criteria • Symptoms of DM plus casual plasma glucose concentration greater than or equal to 200 mg/dL; OR • Fasting plasma glucose greater than or equal to 126 mg/dL; OR • Two- hour post load glucose greater than or equal to 200mg/dL during an oral glucose tolerance test; OR • HbA1-C greater than or equal to 6.5% • Glycosylated hemoglobin • Measures the percentage of hemoglobin that carries glucose • Reflects glucose control for the past 3 months Short- Acting Insulin Intermediate- Acting Insulin Very Long- Acting Insulin Combination Insulin Therapy • A short- or rapid-acting insulin is mixed with intermediate-acting insulin in the same syringe. • This allows the patient to have both mealtime and basal coverage without having to administer two separate injections. Combining Insulins in One Syringe 1. Wash hands. 2. Gently rotate NPH insulin bottle. 3. Wipe off tops of insulin vials with alcohol sponge. 4. Draw back amount of air into the syringe that equals total dose. (Ex. 48 units of air for 36 units NPH and 12 units regular insulin) Insulin Regimen Storage of Insulin • Heat and freezing alter insulin molecule • In use insulin vials and pens • ROOM temperature for up to 4 weeks • Unopened insulin vials and pens • Stored in the REFRIGERATOR • Pre-filled insulin syringe • Prefilled syringes with two different insulins • Store in refrigerator for up to 1 week ONLY • Prefilled syringes with only one type of insulin • Store in refrigerator for up to 30 days ONLY • Store in a vertical position with needle pointed up (to avoid clumping of suspended insulin in the needle) • Before injection, gently roll prefilled syringes between the palms 10 to 20 times (to warm the insulin and resuspend the particles) Insulin Administration • Route: • Subcutaneous • Regular insulin can be given IV • PO is contraindicated because insulin is inactivated by gastric acid • Golden rule: Never assume that because the patient already uses insulin, he or she knows and practices the correct insulin injection technique Systemic allergic reaction • Rare • Begins immediately after injection and becomes generalized urticaria • Treatment is desensitization • Small doses of insulin are given in increasing amounts Lipodystrophy • Lipoatrophy- loss of subcutaneous fat and appears as a slight dimpling or more serious pitting of SQ • Cause: repeated use of an injection site • Management: rotate injection sites • Lipohypertrophy - development of fibrofatty masses at the injection site Morning Hyperglycemia • An elevated blood glucose level on arising in the morning • Causes: Dawn Phenomenon or Somogyi Effect Complications of Insulin Therapy Dawn Phenomenon • Normal glucose level until approximately 3AM when blood glucose begins to rise • The elevation is associated with the release of growth hormone which decreases tissue sensitivity to insulin Dawn = DOWN insulin Local allergic reaction • Appears at the injection site 1 to 2 hours after administration • S/Sx: redness, swelling, tenderness, and induration • Usually resolves spontaneously, otherwise insulin type is changed Somogyi Effect • High dose evening/bedtime insulin produces a decline in blood glucose during the night • Hypoglycemia triggers release of counterregulatory hormones (i.e., glucagon, epinephrine, growth hormone, cortisol) Teach patients to rotate the injection within one anatomic site, such as the abdomen, for at least 1 week before using a different site, such as the right thigh. (This allows for better insulin absorption) which produces rebound hyperglycemia in the AM SoMogyi = So MOch insulin Morning Hyperglycemia Diagnostics • Check CBG Morning Hyperglycemia Management Oral Hypoglycemic Agents (OHA) ✓Biguanides ✓Sulfonylureas ✓Meglitinides ✓Alpha Glucosidase inhibitor ✓Thiazolidinediones ✓DDP-4 Inhibitor Biguanides • Metformin (Glucophage) • MOA: reduces glucose production by the liver and enhances tissue sensitivity at the tissue level • S/E: lactic acidosis, diarrhea • NRSG RESP: Needs to be held 1-2 days before IV contrast media given and for 48 hr after Sulfonylureas • Glipizide (Glucotrol), Glyburide (Glynase), Glimepiride (Amaryl) • MOA: • Stimulate beta cells to secrete insulin • Decrease glycogenolysis and gluconeogenesis. • Enhance cellular sensitivity to insulin. • S/E: weight gain, hypoglycaemia Meglitinides • Nateglinide (Starlix), Repaglinide (Prandin) • MOA: stimulates a rapid but short- lived release of insulin from the pancreas • S/E: Weight gain, hypoglycemia Alpha Glucosidase Inhibitor • “Starch blocker” • Acarbose (Precose), Miglitol (Glyset) • MOA: slows down the absorption of CHO in the small intestine • S/E: Gas, abdominal pain, diarrhea • NRSG RESP: Taken with the first bite of each main meal Thiazolidinediones • “Insulin sensitizers” • Pioglitazone (Actos), Rosiglitazone (Avandia) • MOA: increases insulin sensitivity, transport, and utilization at target tissues • S/E: • Pioglitazone: increases risk for bladder cancer and exacerbates heart failure • Rosiglitazone: increases risk for cardiovascular events Dipeptidyl Peptidase-4 (DPP-4) Inhibitors • Linagliptin (Trajenta), Sitagliptin (Januvia) • MOA: stimulate release of insulin from beta cells, decrease hepatic glucose production • S/E: pancreatitis, allergic reactions Sodium- Glucose CoTransporter 2 (SGLT2) Inhibitor • Canagliflozin (Invokana); Empagliflozin (Glyxambi) • MOA: blocks the reabsorption of glucose by the kidney, increasing glucose excretion, and lowering blood glucose levels Dietary Modifications Diabetes Meal Planning - A non-specific guide for when, what, and how much food to consume to receive adequate nutrition while maintaining blood glucose at the target range - Must take into consideration a patient’s goals, preferences, and lifestyle Characteristics of Diabetes Diet • Includes more non-starchy vegetables • High- fiber, fewer added sugars and refined grains • Whole foods are preferred over highly processed foods • Total calories will be prescribed by physician • Caloric distribution: • CHO: 50% to 60% • Fats: 20% to 30% • CHON: 10-15% to 20% • The plate method is a simple, visual way to make sure the patient gets enough nonstarchy vegetables and lean protein while limiting the amount of higher-carb foods eaten that have the highest impact on blood sugar levels. • The appropriate plate size is a 9-inch dinner plate • Fill half with nonstarchy vegetables • Nonstarchy vegetables are lower in carbohydrate, so they do not raise blood sugar very much. • Examples: asparagus, cabbage, carrots, cauliflower, cucumber, eggplant, okra, green beans, tomatoes • Fill one quarter with a lean protein • Animal- based: • Chicken, eggs • Fish • Shellfish • Lean beef, pork • Cheese • Plant- based: • Beans • Nuts • Tofu • Fill one quarter with carb foods. • Whole grains • Starchy vegetables (squash, potato, kamote) • Dairy products (milk, yogurt, soy milk) • Water is the best choice because it contains no calories or carbohydrates and has no effect on blood sugar. Other zero- or low-calorie drink options include: • Unsweetened tea (hot or iced) • Unsweetened coffee (hot or iced) • Sparkling water/club soda • Flavored water or sparkling water without added sugar • Diet soda or other diet drinks Exercise • Lowers blood glucose levels by increasing the uptake of glucose by body muscles and by improving insulin utilization • Guidelines: • Exercise 3x per week with no more than 2 consecutive days without exercise • Perform resistance training 2x a week if with type 2 DM • Exercise at the same time of the day and for the same duration each session • Use proper footwear and, if appropriate, other protective equipment • Avoid trauma to lower extremities • Inspect feet daily after exercise • Avoid exercise in extreme heat or cold • Avoid exercise during periods of poor metabolic control • Stretch for 10 to 15 minutes before exercising • Precaution: • Patients with blood glucose greater than 250 mg/dL and who have ketones in the urine should not exercise until urine test results are negative for ketones and the blood glucose level is closer to normal. • Exercising with elevated blood glucose increases secretion of glucagon, growth hormone, and catecholamines. • Patients who are on insulin therapy should be taught to eat a 15- g CHO snack (a fruit exchange) or a snack of complex carbohydrate with a protein to prevent hypoglycemia. Self- monitoring of Blood Glucose (SMBG) • Enables the patient to make decisions regarding food intake, activity patterns, and medication dosages. • Produces accurate records of daily glucose fluctuations and trends, and it alerts the patient to acute episodes of hyperglycemia and hypoglycemia. • Provides patients with a tool for achieving and maintaining specific glycemic goals. • Recommended for all insulin- treated patients with DM • HbA1-c (Glycosylated Hgb) is also monitored to review glucose control over the past 3 months. • Target parameters: • Pre- prandial CBG: 80-130 mg/dL • Post- prandial CBG (1-2 hours PC): < • 180mg/dL • HbA1c: < 7% • Non-diabetics: 4%- 5.6% Acute Complications of DM Hypoglycemia • Means low blood sugar • Occurs when blood glucose falls to less than 80 mg/dL • Severe hypoglycemia is when glucose levels are less than 40mg/dL • Causes: • Too much medication • Too little food • Excessive physical activity Management of Hypoglycemia • “Rule of 15” • Give 15 grams of fast- acting carbohydrate by mouth (e.g., 4-6 oz of soda, 8-10 lifesavers, 4-6 oz orange juice, or 1tbsp honey) • Wait 15 minutes then recheck blood glucose. • If blood glucose is still < 70mg/dL, give another 15-g fast acting carbohydrate • Once blood sugar is stable and next meal is more than 1 hour away, give additional food of longer- acting combination plus protein or fat once symptoms subside. • Crackers with peanut butter • 2 slices of white bread plus skimmed milk • Notify physician if symptoms do not subside after two to three administrations of fast- acting carbohydrates Severe Hypoglycemia • CBG <40mg/dL • Clinical Manifestations: • Unconsciousness or difficulty arousing from sleep • Seizures • Disoriented behaviour Management: • Glucagon 1mg SQ/IM • Return of consciousness may take up to 20 minutes after administration • Provide snack on awakening to prevent recurrence of hypoglycemia, except if with nausea • If nauseous, position to side lying • D50W (50% dextrose in water) • 25 to 50 mL of D50W IV Push • Used in hospital settings • Ensure IV-line patency Diabetic Ketoacidosis (DKA) • A life- threatening complication of type 1 DM • Causes: • Decreased or missed dose of insulin • Illness or infection • Undiagnosed or untreated DM • Clinical Manifestations Management: • Fluid Replacement • PNSS (0.9% NaCl) at 0.5 to 1L per hour for 2 to 3 hours • Half-strength NSS (0.45% NaCl) if hypertensive or hypernatremic • WOF: fluid overload (bounding pulse, crackles, headache) • Restoring Electrolytes • Important: rehydration and insulin cause a drop in potassium level • Rehydration increases potassium excretion via urine • Insulin transports potassium from the extracellular into the intracellular compartment • Potassium chloride IV infusion • INCORPORATE KCl into IV bottle. DO NOT GIVE KClVIA IV PUSH SINCE IT CAUSES CARDIAC ARREST • Use infusion pump for accurate delivery • Apply cold compress on IV site • Hold if patient is not urinating • Reversing acidosis and hyperglycemia • Regular insulin • Given via intravenous route at a slow, continuous rate • Infuse D5NSS or D5 0.45%NSS when blood glucose levels reach 250 to 300 mg/dL to avoid rapid drop in the blood glucose level during treatment Hyperglycemic Hyperosmolar NonKetotic Syndrome (HHNKS) • A metabolic disorder of type 2 DM • Characterized by severe hyperglycemia and hyperosmolarity • Occurs most often in older adults (50 to 70 years old) • Causes: • Infection • Illness (e.g., stroke, MI) • Medications that exacerbate hyperglycemia (thiazides) • Treatment/Procedures (dialysis or surgery) • Clinical Manifestations: • Blood glucose levels from 600 to • 2000mg/dL • Hypotension • Profound dehydration (dry mucous membranes, poor skin turgor) • Tachycardia • Variable neurologic signs (ALOC, seizures, hemiparesis) Management: • Same as DKA • Monitor closely for fluid overload Chronic Complications of DM Angiopathy • Damage to blood vessels secondary to chronic hyperglycemia • Etiology: • Accumulation of damaging byproducts of glucose metabolism, such as sorbitol, which is associated with damage to nerve cells; • Formation of abnormal glucose molecules in the basement membrane of small blood vessels such as those that circulate to the eye and kidney; • A derangement in red blood cell function that leads to a decrease in oxygenation to the tissues. Macrovascular Complications • Diseases of the large and medium-size blood vessels that occur with greater frequency and with an earlier onset in people with diabetes • Preventive Management: • Risk reduction: • Weight reduction • Smoking cessation • Control of BP • Dietary modification (Low salt, low fat) • Exercise Microvascular Complications • Result from thickening of the vessel membranes in the capillaries and arterioles in response to conditions of chronic hyperglycemia. • Specific to diabetes Proliferative Diabetic Retinopathy • Most severe form • Occurs in late stage of diabetic retinopathy • Neovascularization sec. to complete occlusion of retinal vessel • Patient sees black or red spots or lines; blindness if left untreated Management: • Laser photocoagulation therapy • Reduces risk of vision loss • Destroys the ischemic areas of the retina that produce growth factors that encourage neovascularization. Diabetic Retinopathy • Process of microvascular damage to the retina as a result of chronic hyperglycemia, nephropathy, and hypertension in patients with diabetes. Non- proliferative Diabetic Retinopathy • Most common form • Occurs in early stage of diabetic retinopathy • Microaneurysm sec. to partial occlusion of retinal vessel • Asymptomatic, but vision may be affected if macula is involved • Preventive Management: • Dilated eye exam within 5 years after onset of DM type 1 and annually thereafter • Maintain good glycemic control • Manage BP Diabetic Nephropathy • A microvascular complication associated with damage to the small blood vessels that supply the glomeruli of the kidney. • Results to end-stage kidney disease • Hypertension accelerates its progression