Medsurg 2: Gastro-Endo NUR149 PDF

MEDSURG 2: GASTRO-ENDO NUR149 Health history: TOPIC OUTLINE →Information about abdominal pain, dyspepsia, gas, nausea and...

MEDSURG 2: GASTRO-ENDO NUR149 Health history: TOPIC OUTLINE →Information about abdominal pain, dyspepsia, gas, nausea and vomiting, diarrhea, constipation, fecal incontinence, jaundice, and previous GI disease is obtained. A. GASTRO Common Symptoms: I. CH 38: ASSESSMENT OF DIGESTIVE AND GI → Pain FUNCTION ↪The character, duration, pattern, frequency, location, distribution of II. CH 39: MANAGEMENT OF PATIENTS WITH ORAL AND referred abdominal pain, and time of the pain can vary greatly depending ESOPHAGEAL DISORDERS on the underlying cause III. CH 40: Management of Gastric & Duodenal ↪ OLD CART: Onset, Location, Duration, Characteristic, Alleviating & Aggravating Factors, Radiation or Relieving Factors, Timing, Severity Disorders ↪ PQRST: Palliative factors/Provocative factors, Quality, IV. CH 41: MANAGEMENT OF PATIENT’S w/ INTESTINAL Radiation/Region, Severity, Timing/Treatment & RECTAL DISORDERS → Common sites of referred abdominal pain: V. CH 42: ASSESSMENT AND MANAGEMENT OF Assessment of the GI System PATIENTS WITH OBESITY Dyspepsia VI. CH 43: PATIENTS W/ HEPATIC DISORDERS ↪ Epigastric pain, also called indigestion. Most common symptom of VII. CH 44: B I L I A R Y D I S O R D E R S patients with GI dysfunction. B. ENDO Intestinal gas I. CH. 45 ASSESSMENT & MGMT OF PT WITH ↪ Bloating, distention, or feeling “full of gas” with excessive flatulence as a symptom of food intolerance or gallbladder disease. ENDOCRINE D/O Nausea & vomiting II. SESSION 13: D/O OF THE PITUITARY AND ↪ Nausea is a vague, uncomfortable sensation of sickness or THYROID GLANDS “queasiness” that may or may not be followed by vomiting. →Changes in bowel habits & stool characteristics ↪ May signal colonic dysfunction or disease. ↪ Constipation, diarrhea → Past health, family, & social history CH 38: ASSESSMENT OF DIGESTIVE & GI ↪ Oral care & dental visits FUNCTION ↪ Lesions in mouth ↪ Discomfort with certain foods Functions of the Digestive Tract ↪ Use of alcohol & tobacco - Breakdown of food for digestion ↪ Dentures - Absorption into the bloodstream of small nutrient molecules produced by digestion DIVISION OF THE ABDOMEN INTO FOUR QUADRANTS - Elimination of undigested unabsorbed foodstuffs & other OR NINE REGIONS waste products TERMS Diagnostic Tests Digestion: begins with the act of chewing, in which food is Serum Laboratory Studies broken down into small particles that can be swallowed Stool Tests (Fecalysis) and mixed with digestive enzymes. Breath Tests Abdominal Ultrasonography Absorption is the major function of the small intestine. Vitamins and minerals absorbed are essentially unchanged. PHYSICAL ASSESSMENT Absorption begins in the jejunum and is accomplished by active transport and diffusion across the intestinal wall into Oral cavity the circulation. → Lips → Gums (phenytoin & dilantin causes gingivitis) Elimination is the phase of the digestive process that → Tongue occurs after digestion and absorption when waste Abdominal assessment; four quadrant method products are eliminated from the body. → Inspection → Auscultation → Percussion Major Enzymes and Secretions: → Palpation Chewing and swallowing: saliva, salivary amylase Rectal inspection (break down carbs) Genetic Testing Gastric function: hydrochloric acid, (breakdown Imaging Studies: food and destroy ingested bacteria, pepsin, → CT, PET, MRI, Scintigraphy, Virtual Colonoscopy (protein digestion) intrinsic factor. Upper GI Tract Study Small intestine: amylase, lipase and trypsin from the pancreas, bile (secreted by liver stored in gallbladder) Lower GI Tract Study Chyme, emulsification, peristalsis GI Motility Studies  MEDSURG 2: GASTRO-ENDO NUR149 Endoscopic Procedures → Management: proper oral hygiene → EGD (Esophagogastroduodenoscopy) Individuals at risk: → Colonoscopy → Older adult, current smokers, low income, less educated → Anoscopy, Proctoscopy, & Sigmoidoscopy Connected to systemic disease: → Small-bowel Enteroscopy → CV, DM, rheumatoid → Endoscopy through an Ostomy Manometry & Electrophysiologic Studies Dental Plaque & Caries NURSING INTERVENTIONS - Dental plaque causes tooth decay, caries and treatment usually Inform the primary provider of known medical involves fillings, dental implants, and extractions. conditions or abnormal laboratory values that may - Prevention is fluoride varnish/gel toothpaste, routine dental care, affect the procedure community water fluoridation, refrain from smoking and alcohol, Assess for adequate hydration before, during, and less sugars, starch. More healthier snacks and brushing after immediately after the procedure, and provide each meal. Manage systemic diseases. education about maintenance of hydration - Periapical is tooth abscess – presence of puss in periosteum. Provide health information and procedural - Clinical manifestations: pain, cellulitis, facial edema, fever, and education to patients and significant others malaise. Provide instructions about postprocedure care and - Nursing management: needle aspiration is a drill opening to activity restrictions relieve pressure, pain, drain, extract. Help the patient cope with discomfort and alleviate - Assess for bleeding and instruct to use warm saline/water rice anxiety and take antibiotic and analgesic. Periapical Abscess GERONTOLOGIC CONSIDERATIONS: Xerostomia is decreased saliva production. Abscessed tooth Decreased appetite: decrease in taste buds and Presence of pus in the apical dental periosteum and tissue surrounding the apex salivary gland secretion, diminished sense of smell, Clinical Manifestations: and dental problems. Delayed emptying of the esophagus, decreased → Pain HCI acid secretion with subsequent reduction in → Cellulitis → Facial edema amount of intrinsic factor secreted. -Liver size will → Fever also decrease after age 50, gallbladder disease, → Malaise and risk for decreased food intake due to Medical & Nursing Management: economic constraints and immobility. → Needle aspiration; drill opening to relieve pressure, pain, and promote drainage; extraction → Assess for bleeding; instruct to use warm CH 39: MANAGEMENT OF PATIENTS WITH saline/water rinse; take antibiotic & analgesic ORAL AND ESOPHAGEAL DISORDERS Role of the Mouth in General Health DISORDER IN THE JAW Digestion begins in the mouth Temporomandibular disorders Changes in the oral cavity: (Table 39-1) o → Myofascial pain o Influence the type and amount of food ingested → Internal derangement of joint o Degree to which food particles mix with salivary enzymes → Degenerative joint disease Fractures (of bone) Disorders of the Jaw Mandibular structural abnormalities Temporomandibular disorders DISORDER IN THE SALIVARY GLANDS o Myofascial pain o Internal derangement of joint o Degenerative joint disease Fractures (of bone) Mandibular structural abnormalities Disorders of the Salivary Glands Diseases of the mouth interferes with communication Esophageal problems: o Affect food and fluid intake o Jeopardize general health Periodontal Disease Most common cause of tooth loss in adults → Gingivitis: inflammation of the gums → Periodontitis: involves soft tissue & bone supporting the teeth  MEDSURG 2: GASTRO-ENDO NUR149 → May bleed easily and present with red or white patch Late Manifestations: → Complaints of tenderness → Difficulty in chewing, swallowing, or speaking → Coughing up blood-tinged sputum → Enlarged cervical lymph nodes ASSESSMENT & MANAGEMENT Assessment Health history: include symptoms related to oral problems, oral hygiene and dental care, use of tobacco, alcohol, and eating and nutrition Inspect and palpate the structures of the mouth and neck Medical Management → Surgical resection → Radiation Therapy → Chemotherapy Nursing Management of Disorders of the Oral Cavity Promoting mouth care → Preventive oral care → Dental care before surgery or radiation therapy ORAL CANCER → Frequent gentle brushing and flossing or if pt cannot tolerate brushing, use of mouthwashes and other methods of cleaning and rinsing. Risk Factors → Patient education related to oral hygiene → Tobacco use, including smokeless tobacco → Encourage fluid intake to reduce dry mouth → Alcohol → Use of synthetic saliva such as oral balance or a saliva → Infection with HPV production stimulant such as Salagen → History of head and neck cancer → Ensure adequate food & fluid intake Increased incidence in men twice as often as → Assess nutritional requirements & dietary patterns women → Assess pt preferences & take into account social and May occur in any area, but lips, lateral tongue, and cultural factors when encouraging and floor of the mouth are most frequently affected. recommending dietary intake → Dietary consult → Support a positive self-image → Encourage patient to verbalize → Listen and offer acceptance and support → Referral to support group, psychiatric liaison, or spiritual advisor → Minimize pain → Avoid hot, spicy, or hard foods → Oral care → Viscous lidocaine or other pain meds → Prevent infection → Assess for signs & symptoms of infections → Appropriate wound & skin care → Patient education MOTILITY DISORDERS OF THE ESOPHAGUS MOTILITY DISORDERS: o Dilated tortuous narrowed end of the esophagus Manifestations of Oral Cancer o Achalasia: ineffective peristalsis of the esophagus Early Stage: and the failure of the esophageal sphincter to relax → Few or no symptoms in early stage in response to swallowing → Painless sore or mass that does not heal; o Diffuse Esophageal Spasm (DES): non - indurated ulcer with raised edges peristaltic contraction of esophageal smooth muscle  MEDSURG 2: GASTRO-ENDO NUR149 Assessment & Diagnostic Findings symptoms → X-rays → Teaching plan for client & family → Manometry Surgical Management → Barium swallow, CT chest, & endoscopy → Nissen Fundoplication Medical Management → Open surgery → Slow food/liquid intake → Endoluminal Fundoplication (Transoral) → Pharmacological approach: DIVERTICULA ↪H2 antagonist Medical term used to describe the small bulges that stick ↪ Antacids out of the side of the large intestine (colon). ↪Botox injection: Clostridium botulinum Most common in the sigmoid colon ↪ Balloon dilatation Is common & associated with aging. Surgical Management Diverticulosis: multiple diverticula without → Esophagomyotomy inflammation Diverticulitis: inflammation ESOPHAGEAL SPASM: o Jackhammer esophagus: hypercontractile Causes & Risk Factors: esophagus, occuring on more than 20% of → Aging, 4 wks, comes and goes; serious d. Medications condition that warrants a visit to the doctor e. Underlying diseases that may contribute (dehydration sx) 2. Patient Edu and Health Promotion 3. Restore or maintain a regular pattern of elimination a. Ensure adequate intake of fluids & high-fiber foods CAUSES b. Learn methods to avoid constipation o Infx c. Relieve anxiety about bowel elimination patterns o Meds d. Avoid complications o Tube feeding formulas o Metabolic & endocrine d/o o Various dx processes PREVENTION 1. Emphasize importance of responding to the urge to T Y P E S defecate SECRETORY DIARRHEA – HIGH-vol diarrhea. 2. Teach how to establish a bowel routine, & explain that Caused by ↑ production and secretion of water & having a regular time for defecation may aid in electrolytes by intestinal mucosa into the intestinal initiating the reflex (best time usually is after meal or lumen. = H2O build-up whenever they have the urge to defecate) Often assoc. w/ bacterial toxins & neoplasms 3. Provide dietary info OSMOTIC DIARRHEA – occurs when water is pulled into a. Suggest high-residue, high-fiber foods (fruits the intestines by the osmotic pressure of unabsorbed & veges), adding bran daily (introduce particles, slowing the reabsorption of water. gradually) Caused by lactase deficiency, pancreatic dysfunction, b. ↑ fluid intake (unless ci, heart dx) or intestinal hemorrhage. 4. Explain how an exercise regimen, increased unabsorbed substance draws water from plasma into ambulation, & abdominal muscle toning will ↑ muscle the intestinal lumen along osmotic agents strength and help propel colon contents MALABSORPTIVE DIARRHEA – combines mechanical & biochemical actions, inhibiting effective absorption of 5. Describe abdominal toning exercises nutrients a. Exercises that contracts abdominal muscles, Manifestations: malnutrition markers (ex. 4x daily (ex. Leg-to-chest exercises) Hypoalbuminemia 6. Explain that the N position (semi-squatting) Low-serum albumin levels = intestinal mucosa maximizes use of abdominal muscles & force of swelling & liquid stool gravity. – if px is pooping Infections & surgical procedures could cause 7. Avoid overuse or long-term use of stimulant laxatives malabsorption = causes wt. loss, diarrhea because they can weaken colonic function. INFECTIOUS DIARRHEA – results from infectious agents invading the intestinal mucosa. Q1: Which is ex. of laxative osmotic agent? CLOSTRIDIUM DIFFICILE most commonly identified a. Bisacodyl – stimulant laxative agent in abx-assoc. diarrhea in hospi (presence of b. Ducosate – emollient stool softener pathogen in body) c. Magnesium hydroxide – saline agent EXUDATIVE DIARRHEA – assoc. w/ damage to intestinal d. Polyethylene glycol & electrolytes mucosa, leading to oozing of mucus, blood, & plasma proteins from cells as a result of inflammation/injury. Caused by changes in mucosal integrity, epithelial loss, or tissue destruction by rad/chemo DIARRHEA Possible ulcerative colitis, crohn’s, rad. enteritis - ↑ frequency of bowel movements (more that 3 per day) w/ RISK FACTORS altered consistency (i.e., increased liquidity) of stool.  NUR 149: MEDSURG 2 GASTRO - Irritable Bowel Syndrome (IBS) – stomach cramps, bloating, o If baby: sunken fontanelle & eyes, few/no tears, diarrhea, constipation, comes and goes; LIFELONG problem infrequent diaper changes, drowsy/irritable - Inflammatory Bowel Dx (IBD) – c/b chronic inflammation of o SEVERE: lethargic, confused, dizziness when the GI tract (CROHN’S, ULCERATIVE COLITIS) standing up that does not go away, not passing urine - Lactose Intolerance – no dairy for more than 8 hrs, rapid but weak pulse, possible - Medications – thyroid replacements, laxatives, stool softeners, seizures/low LOC abx (kills N flora), chemotherapeutic drugs, antacids can cause - Cardiac Dysrhythmias diarrhea - CHRONIC DIARRHEA - Skin Care Issues r/t irritant - Tube Feeding Formulas dermatitis - Metabolic & Endocrine d/o o Diabetes o Addison’s Dx – Adrenal Insufficiency (too little PATIENT LEARNING NEEDS FOR DIARRHEA cortisol – used for metabolism & immune response, o Recognition of need for med. tx stress; too little aldosterone – regulates Na & K = BP) o Rest o Thyrotoxicosis – inappropriate high levels of thyroid o Diet & fluid Intake hormone (T3 & T4) ▪ BRAT diet (Bananas Rice, Applesauce, - Viral / Bacterial infx dx Toast) – rest the gut & reduce amt. of stool o Dysentery – blood / mucus in stool; caused by produced contaminated food/water, poor hand hygiene, o Avoid irritating foods (caffeine, carbonated swimming in contaminated water beverages, very hot & cold foods) o Shigellosis – CA: shigella bacteria o Perianal skin care o Food poisoning o Meds - Nutritional & Malabsorptive d/o o May need to avoid milk, fat, whole grains, fresh o Celiac dx – gluten sensitivity fruits, & veges o Lactose intolerance M A N I F E S T A T I O N S of D I A R R H E A - ↑ frequency & fluid content of stools FECAL INCONTINENCE - Abdominal cramps CAUSES - Distention o Anal Sphincter weakness – not able to control bowel - Borborygmus – intestinal rumbling caused by moving gas movements, poop leaking to the rectum w/out warning - Anorexia & thirst o Traumatic (ex. After surgical procedures involving - Painful spasmodic contractions of the anus rectum) & non-traumatic (ex. Scleroderma – - Tenesmus – feeling the need to pass stool even tho the autoimmune dx, inflammation & thickening in the skin bowels are empty (involves straining, pain, and cramping) & other areas of body) o Neuropathies: both peripheral (ex. Pudendal – ASSESSMENT & DIAGNOSTIC FINDINGS major nerve in the pelvic region, sends movements & o CBC sensation to genital area) & Generalized (ex. o Serum Chemistries Diabetes) o Urinalysis o Disorders of the pelvic floor (ex. Rectal prolapse) o Stool examination o Inflammation o Endoscopy / Barium Enema ▪ Radiation proctitis – inflammation of the rectum that occurs as a result of acute damage to the rectum sustained from pelvic rad. COMPLICATIONS ▪ IBD - Fluid & Electrolyte Imbalances o CNS Disorders (dementia, stroke, spinal cord injury, - Dehydration MS) o Dark, yellow, strong smelling urine o Diarrhea, Fecal Impaction w/ Overflow o Thirst o Behavioral Disorders o Peeing less than usual, 35 in women and >40 in men → Self-monitoring and strategizing ongoing lifestyle = greater risk for obesity changes aimed at a healthy weight → Hip-to-waist ratio – Women with waist-to-hip → Health sleep habits ratios greater than 0.80 and men with waist-to- → Intensive Behavioral Therapy; consisting of 12 to 24 hip ratios greater than 0.90 are presumed to sessions annually, which may include individual counseling have proportionally more visceral (i.e., sessions between the primary provider and patient, group abdominal) fat stores nutrition education sessions, and physical activity sessions Android Obesity – “apple-shaped” appearance → modest weight loss of 5% total body weight can be o greater risk for developing hypertension, associated with significant clinical improvements and benefits coronary artery disease, stroke, and type to patients with obesity 2 diabetes → 500 and 1000 calories daily from baseline, in order to Gynoid Obesity – “pear-shaped” body achieve a 5% to 10% reduction in weight within about 6 months can be achieved through increasing physical activity and decreasing caloric dietary intake → 150 minutes of moderate-intensity aerobic exercise weekly or 75 minutes of vigorous-intensity aerobic exercise weekly – physical activity recommendations for all adults (those with and without obesity) → The Dietary Approaches to Stop Hypertension (DASH) diet is an example of a superior healthy noncommercial diet, provides a solid foundation for achieving and maintaining weight loss due to its focus on low intake of fat and carbohydrates. → Mediterranean Diet – healthy diet plan that may form a basis for weight loss, though not specifically designed for this purpose MEDICATIONS FOR OBESITY (refer to table 42-2) →Antiobesity medication meant to supplement not → Lab studies: cholesterol, triglycerides, fasting supplant diet modification and exercise blood glucose, HbA1c, liver function tests  NUR 149: MEDSURG 2 GASTRO → Indications: BMI >30, BMI >27 with related concominant → Bariatric is derived from two Greek words meaning morbidity “weight” and “treatment.” Bariatric surgery is surgery → Action: inhibit gastrointestinal absorption of fats, indicated to treat obesity. altering central brain receptors to enhance satiety or → Bariatric surgical procedures work by restricting a reduce cravings patient’s ability to eat (restrictive procedure), interfering → The patient is monitored while taking the selected with ingested nutrient absorption (malabsorptive medication; if the patient does not lose at least 5% body procedures), or both. weight after 12 weeks, the prescription may need to be → Results in a weight loss of 10% to 35% of total body changed, or the patient may be referred for other weight- weight within 2 years postoperatively, with the majority of reduction therapy (e.g., bariatric surgery) weight loss occurring within the first year → Antiobesity medications are believed to be teratogenic. → type 2 diabetes, hypertension, and OSA may Women with obesity who are of childbearing years should be resolve; and dyslipidemia improves screened carefully and advised to avoid pregnancy if they seek → BMIs as low as 30 kg/m2 now considered a prescription for an antiobesity medication. candidates for surgical intervention if they have →Class of antiobesity medications known as comorbid conditions that may demonstrably the improve post weight loss (e.g., type 2 diabetes) sympathomimetic amines are only supposed to be → procedures may be performed by laparoscopy or by an prescribed for short-term use (i.e., no longer than 12 weeks). open surgical technique. They have many side effects, and patients do tend to regain weight once they are no longer taking these medications. NONSURGICAL INTERVENTIONS → ROUX-EN-Y GASTRIC BYPASS (RYGB) (combined → Minimally invasive interventions restrictive and malabsorptive procedure) – A → Vagal blocking – also known as “gastric stimulation” horizontal row of staples across the fundus of the Blocking of vagus nerve via implanted device stomach creates a pouch with a capacity of 20 to 30 Few side effects mL. The jejunum is divided distal to the ligament of A pre-programmed, pulsating signal is delivered Treitz, and the distal end is anastomosed to the new for 12 hours daily. pouch. The proximal segment is anastomosed to the → Intragastric balloon therapy jejunum. Endoscopic placement of saline-filled balloon → GASTRIC BANDING (restrictive procedure) – adjustable Remains in place for 3 to 6 months and reversible, done less commonly. Adverse effects: N/V, balloon rupture causing → A prosthetic device is used to restrict oral obstruction intake by creating a small pouch of 10 to 15 mL Pancreatitis and gastric or esophageal that empties through the narrow outlet into the perforation may also occur although these are remainder of the stomach. rare adverse events → SLEEVE GASTRECTOMY (restrictive procedure) – most → Bariatric embolization → ghrelin commonly performed procedure → The stomach is incised vertically and up to Obesity hypoventilation syndrome is characterized 85% of the stomach is surgically removed, by daytime hypoventilation with hypercapnea (i.e., leaving a “sleeve”- shaped tube that retains PaCO2 greater than 45 mm Hg) and hypoxemia intact nervous innervation and does not (i.e., PaO2 less than 80 mm Hg), and sleep- obstruct or decrease the size of the gastric disordered breathing. outlet. Potential adverse effects can be mitigated by → BILIOPANCREATIC DIVERSION WITH DUODENAL maintaining the patient in the low Fowler SWITCH (gastric restriction with intestinal malabsorption) – position, which maximizes diaphragmatic chest result in the most postoperative weight loss, and is therefore expansion, pulse oximetry monitoring may be more commonly indicated for patients with very high BMIs advisable, as well as supplemental oxygen - (also called sleeve gastrectomy with therapy duodenal switch) Half of the stomach is removed, leaving a small area SURGICAL INTERVENTIONS/BARIATRIC PROCEDURES that holds about 60 mL. The entire jejunum is excluded  NUR 149: MEDSURG 2 GASTRO from the rest of the gastrointestinal tract. The duodenum is disconnected and sealed off. The ileum is divided above the ileocecal junction, and the distal end of the jejunum is anastomosed to the first portion of the duodenum. The distal Ch. 43: PATIENTS W/ HEPATIC DISORDERS LIVER - largest gland o largest organ: skin - Upper R abdomen - a very vascular organ that receives blood from GI tract via the portal vein and from the hepatic artery 2 MAJOR BLOOD SUPPLY SOURCES OF LIVER: o PORTAL VEIN: poor O2 but rich in nutrients (from GIT) o HEPATIC ARTERY: rich in O2, supplies METABOLIC FUNCTIONS OF THE LIVER: blood to liver, duodenum, and pancreas - Glucose metabolism - Ammonia conversion FUNCTIONS: o NH3 – byproduct of protein breakdown o filter, protect, break down certain o liver produces enzymes that changes it to substances, store, clotting, produces bile UREA o UREA: check BUN and is filtered by kidney o ↑ NH3 = confusion, deterioration, lethargic (↓LOC) - Protein metabolism - Fat metabolism - Vitamin & iron storage - Bile Formation o liver produces bile - Bilirubin excretion o bilirubin – yellowish substance in the blood that forms after RBC breakdown; gives the brownish color of stool o JAUNDICE – yellow discoloration of skin & sclera (white, outer portion of eyes) o ↑ bilirubin is caused by: gallstones, liver issues, & other conditions o if not excreted: clay, gray colored stool - Drug metabolism LIVER FUNCTION STUDIES Serum Aminotransferases – indicators of injury to the liver cells; useful in detecting HEPATITIS 1. ASPARTATE AMINOTRANSFERASE (AST) – not specific to liver dse ↑ AST = cirrhosis, hepatitis, liver cancer used to be called SERUM GLUTAMIC- OXALOACETIC TRANSAMINASE  NUR 149: MEDSURG 2 GASTRO ▪liver problem that affects people 2. ALANINE AMINOTRANFERASE (ALT) – enzyme who drink little to no alcohol that breaks down protein in liver & bones; measured ▪ there is too much fat accumulation via blood levels in the liver (usually seen in overweight / obese) used to be called SERUM GLUTAMATE-PYRUVATE ▪ MASLD – Metabolic dysfunction- TRANSAMINASE Associated Steatotic Liver ↑ ALT = liver d/o Disease monitor the course of hepatitis, cirrhosis, the effects of tx that may be toxic to liver o nonalcoholic steatohepatitis (NASH) 3. GAMMA-GLUTAMYL TRANSFERASE (GGT) – ↑ ▪ serious form of fatty liver dse, levels are assoc. w/ cholestasis, alcoholic liver dse causing the liver to swell enzyme found in the liver that can indicate liver dse or ▪ liver is damaged due to fat deposits bile duct issues ▪ can get worse = scarring / cirrhosis 4. GAMMA-GLUTAMYL TRANSPEPTIDASE (GGTP) or liver cancer 5. LACTATE DEHYDROGENASE (LDH) ▪ MASH – Metabolic dysfunction- Associated Steatohepatitis Serum Alkaline phosphatase - ↑ AP = liver dse / bone abnormalities MANIFESTATIONS Serum Protein Studies - Jaundice Direct & indirect serum bilirubin, urine bilirubin, & urine - Portal Hypertension – increase in BP w/in portal bilirubin and urobilinogen venous system (veins form stomach, intestines, Clotting factors spleen, pancreas merge into the portal vein and will Serum Ammonia branch into smaller branc) Lipids o if vessels are blocked due to liver damage, ADDITIONAL DIAGNOSTIC STUDIES the bld cannot flow properly thru the liver - Liver Biopsy - Ascites & Varices o needle aspiration of liver tissue (6th ICS, mid- o Varices: ↑ pressure in portal veins leads to axillary line) to examine liver cells dev’t of large swollen veins w/in esophagus, - Ultrasonography stomach, rectum, umbilical area) - CT ▪ varices can rupture and cause - MRI bleeding o Ascites: accumulation of lfuid in peritoneal ASSESSMENT cavity HEALTH HX - Hepatic encephalopathy / coma - PREVIOUS exposure to hepatotoxic substances - Nutritional Deficiencies (meds, drug abuse) or infxs agent (schistosomiasis – parasitic dse caused by blood flukes/ flatworm Schistosoma) JAUNDICE - Travel, alcohol, drug use yellow / greenish-yellow sclera & skin caused by ↑ bilirubin - Lifestyle levels Bilirubin level: exceeds 2 mg/dL PHYSICAL ASSESSMENT TYPES: Hemolytic, Hepatocellular, Obstructive - skin (if there is yellow discoloration) - Hereditary Hyperbilirubinemia - cognitive status (due to ammonia) - hepatocellular & obstructive jaundice are most - palpation, percussion (if inflamed) assoc. w/ liver dse HEPATIC DYSFUNCTION HEMOLYTIC JAUNDICE - Acute / chronic, cirrhosis of the liver o cirrhosis – SCARrhosis; severe scarring of -results in abnormally high RBC destruction the liver due to many dse/conditions (hepatitis, alcoholism, schistosomiasis, - liver failure assoc. w/ alcohol use HEPATOCELLULAR JAUNDICE - infx -defective uptake or transport of bilirubin by hepatic cells o schistosomiasis -inability of the liver to transport bilirubin into bile - fatty liver dse o nonalcoholic fatty liver disease (NAFLD)  NUR 149: MEDSURG 2 GASTRO OBSTRUCTIVE JAUNDICE - blockage in bile duct system SIGNS AND SYMPTOMS ASSOCIATED WITH HEPATOCELLULAR AND OBSTRUCTIVE JAUNDICE HEPATOCELLULAR OBSTRUCTIVE ⚫ Mild or Severely ill ⚫ Dark orange-brown urine, ⚫ Lacks of appetite, nausea or clay-colored stools vomiting, weight loss ⚫ Dyspepsia and intolerance of ⚫ Malaise, fatigue, weakness fats, impaired digestion ⚫ Headache, chills, fever, ⚫ Pruritus infection PORTAL HYPERTENSION -obstructed blood flow through the liver results in increased pressure throughout the portal venous system -results in ▪Ascites ▪Esophageal varices ALBUMIN ASCITES - protein made by LIVER *PORTAL HYPERTENSION resulting in increased capillary -enters bloodstream & helps keep fluid from leaking out of the pressure and obstruction of venous blood flow blood vessels into other tissues *Vasodilation of SPLANCHNIC CIRCULATION (blood flow to ASSESSMENT OF ASCITES the major abdominal organs) ⚫ Record abdominal girth and weight daily *Changes in the ability to metabolize ALDOSTERONE, ⚫ Patient may have striae (stretch marks), distended veins, and increasing FLUID RETENTION umbilical hernia *Decreased synthesis of ALBUMIN, decreasing serum ⚫ Assess for fluid in abdominal cavity by PERCUSSION for osmotic pressure shifting DULLNESS or by fluid wave *Movement of albumin into the peritoneal cavity ⚫ Monitor for potential fluid and electrolyte imbalances TREATMENT OF ASCITES ⚫ Low-sodium diet ⚫ Diuretics ⚫ Bed rest ⚫ Paracentesis- needle is inserted into peritoneal cavity to obtain fluid ⚫ Administration of salt-poor albumin ⚫ Transjugular Intrahepatic Portosystemic Shunt (TIPS)- procedure that involves inserting a stent (tube) to connect the  NUR 149: MEDSURG 2 GASTRO portal veins to adjacent blood vessels that have a lower EARLY SIGNS: pressure. This relieves the pressure of blood flowing through the ⚫ Mental changes and motor disturbances diseased liver and can help stop bleeding and fluid back up It affects.. ⚫ Other methods: Peritoneovenous- ⚫ Mood and personality connection between the peritoneal cavity and the ⚫ Behavior and impulse control. systemic venous circulation via a shunting tube placed ⚫ Memory, concentration and thinking. subcutaneously connected with a one-way pressure ⚫ Consciousness, lucidity and sleep patterns. valve ⚫ Coordination and motor functions. ⚫ Autonomy and ability to care for yourself SPIRONOLACTONE -most often FIRST-LINE therapy in patients with ASCITES ASSESSMENT AND STAGES OF HEPATIC from CIRRHOSIS ENCEPHALOPATHY AMMONIUM CHLORIDE & ACETAZOLAMIDE ASSESSMENT - CONTRAINDICATED dt possiblity of PRECIPITATING ⚫ EEG- advise client not to sleep night before procedure; NO HEPATIC COMA CAFFEINE; need to shampoo hair before procedure ⚫ Changes in LOC ⚫ Potential seizures PATHOPHYSIOLOGY OF HEPATIC ENCEPHALOPATHY ⚫ Fetor Hepaticus- aka “Breath of the Dead” AND COMA -condition in which the breath of the patient is sweetish, musty, and occasionally fecal in nature. It is HEPATIC ENCEPHALOPATHY (aka PORTOSYSTEMIC associated with portal hypertension with portosystemic ENCEPHALOPATHY) shunts. -there is brain dysfunction caused by liver ⚫ Monitor fluid, electrolyte, and ammonia levels dysfunction; happens when your liver isn’t filtering toxins as it should. These toxins build up in your blood and affect your STAGES brain, causing confusion, disorientation and other changes. Possible symptoms by grade include: Hepatic encephalopathy can get better with treatment, but it Grade 0 can be life-threatening without. ⚫ Subtle changes in short-term memory, concentration and Life threatening complications: reaction time, only recognizable perhaps to you or those closest ⚫ Accumulation of ammonia and other toxic metabolites in the to you. They might show up on standard neuropsychological blood tests. *2 major alterations underlie its development in ACUTE and Grade 1 CHRONIC LIVER DSE ⚫ Mild confusion or forgetfulness. ⚫ HEPATIC INSUFFICIENCY: inability of the liver to detoxify toxic ⚫ Mood swings, like euphoria or anxiety. by-products of metabolism ⚫ Difficulties adding and subtracting. ⚫ PORTOSYSTEMIC SHUNTING: collateral vessels develop ⚫ Difficulties with fine motor skills, like writing. allowing elements of the portal blood (laden with potentially toxic ⚫ Sleeping during the day and waking at night. substances usually extracted by the liver) to enter the systemic Grade 2 circulation ⚫ Clear personality changes.  NUR 149: MEDSURG 2 GASTRO ⚫ Inappropriate or out-of-character behaviors. ENCEPHALOPATHY ⚫ Lethargy and apathy. Eliminate precipitating cause ⚫ Disorientation in time (what day or year is it?). -treating underlying condition causing it; managing any ⚫ Slurred speech (dysarthria). urgent condition that may have trigger it Grade 3 * Lactulose to reduce serum ammonia levels ⚫ Slow thinking and sluggish movements. -reducing toxins circulating in blood ⚫ Disorientation in space (Where am I?). -Ex. LAXATIVES ⚫ Drowsiness and loss of general awareness. * IV glucose to minimize protein catabolism ⚫ Severe confusion, delirium or amnesia. * Protein restriction ⚫ Involuntary twitching, tremors or asterixis. *Reduction of ammonia from GI tract by gastric suction, Grade 4 enemas, oral antibiotics (GEO) Total loss of consciousness (coma). -RIFAXIMIN- antibiotic non-absorbable by intestine; prevent TYPES OF HEPATIC ENCEPHALOPATHY hepatic encephalopathy TYPE A -NEOMYCIN- alternative caused by acute liver failure. *Discontinue sedatives, analgesics, and tranquilizers ⚫ This is a sudden loss of liver function (SAT) due to a sudden, severe liver injury. *Monitor or treat complications and infections ⚫ Viral infections, autoimmune liver Supplemental meds: disease and acetaminophen poisoning are common Branched chain amino acids- supplemental that helps build causes. Cerebral edema, swelling in your brain, is a frequent muscle and clear ammonia from blood through muscle tissue side effect that may contribute to the effects of hepatic Probiotics- encourage more helpful type of gut bacteria; at encephalopathy. Acute liver failure is an emergency and least compete with the less helpful types from the produced some cases may require a liver transplant. neurotoxins Other Tx: ACETYLCYSTEINE- antidote for acetaminophen poisoning Hemodialysis- eliminate toxins in blood of patient ESOPHAGEAL VARICES Type B -may be caused by complication of portal hypertension caused by a portosystemic shunt. ⚫ Occurs in 30% of patient with compensated cirrhosis and 60% ⚫ A shunt is when blood flow bypasses of patients with decompensated cirrhosis its normal route through a new, abnormal passageway. A ⚫ First bleeding episode has a mortality rate of 10% to 30% portosystemic shunt is when your portal circulation depending on severity bypasses your liver on its way to your systemic circulation. ⚫ Manifestations include hematemesis, melena, general TYPE C deterioration, and shock (GSMH) caused by chronic liver failure Patients with cirrhosis should undergo screening Chronic liver failure is the gradual decline of liver function endoscopy every 2 to 3 years from chronic liver disease. It’s not reversible. Chronic hepatitis C, chronic alcohol use *manage any variceal bleeding disorder and metabolic dysfunction-associated steatotic liver disease (MASLD) are common causes. SPLENOMEGALY- another complication of portal MEDICAL MANAGEMENT OF HEPATIC hypertension  NUR 149: MEDSURG 2 GASTRO TREATMENT OF BLEEDING VARICES #1 ⚫ Bleeding esophageal varices DO NOT result in an increase in ⚫ Treat for shock; administer oxygen renal perfusion; it is a result in a decrease in renal perfusion ⚫ IV fluids, electrolytes, volume dt loss of blood expanders, blood and blood products ⚫ Vasopressin (antidiuretic hormone/ HEPATITIS ADH), somatostatin, octreotide (VOS) to decrease bleeding ⚫ VIRAL HEPATITIS: a systemic viral ⚫ Nitroglycerin in combination with infection that causes necrosis and inflammation of liver vasopressin to reduce coronary vasoconstriction cells with characteristic symptoms and cellular and ⚫ Propranolol and nadolol to decrease biochemical changes portal pressure; used in combination with other treatment A and E: fecal-oral route ⚫ Balloon tamponade- inserted B and C: bloodborne (&body fluids) @esophagus or stomach D: only people with hepatitis B are at risk (bloodborne & body fluids) TREATMENT OF BLEEDING VARICES #2 ▪Hepatitis G and GB virus-C/ GBV-C (formerly known as ⚫ Endoscopic sclerotherapy- procedure HEPATITIS G) aka Human PEGIVIRUS (HPgV) - known to used to treat blood vessel malformation infect human but is not known to cause human disease -medication is injected into the vessel w/c makes them shrink ⚫ NONVIRAL HEPATITIS: toxic and drug (same w/ varicose veins) induced ⚫ Endoscopic variceal ligation- esophageal banding therapy -procedure that uses elastic bands to treat enlarged veins or HEPATITIS A - usually ACUTE STAGE esophageal varices - common in developing countries ⚫ Transjugular intrahepatic CA: Hepatitis A Virus (HAV) Portosystemic shunt (TIPS) MOT: ⚫ Additional therapies - fecal-oral route o spread by poor hand hygiene ⚫ Surgical management o person to person; ▪Surgical bypass procedures o contaminated food & water ▪Devascularization and transection- aims to control o oral-anal sex bleeding from varices in esophagogastric region Incubation period: - bet. 2 - 6 weeks - illness may last 4 - 8 weeks NURSING MANAGEMENT OF ESOPHAGEAL VARICES - contagious within 2 weeks before & 1-3 weeks after ⚫ Maintain safe environment; prevent exposure injury, bleeding and infection Mortality rate: ⚫ Administer prescribed treatments and - 0.5% ( 40 y/o) monitor for potential complications ⚫ Encourage deep breathing and Manifestations: - mild-flu like sx position changes (for drainage) o low-grade fever ⚫ Education and support of patient and o joint pain o GI disturbances (loss of appetite, N&V) family o fatigue  NUR 149: MEDSURG 2 GASTRO - anorexia Diagnostics: - later: jaundice & dark urine - Hepatitis B Surface Antigen (HBsAg) - indigestion & epigastric distress o detects whether the px is infectious or not w/ - enlargement of liver & spleen B virus o N: nonreactive (no infx) - Antibody Hepatitis B surface (Anti-HBs / HBsAb) Diagnostics: o detects for immune recover; 1. AntiHAV / Antibody Hepatitis A Virus o degree of immunity from HepB & cannot be 2. IgM & IgG infected a. (+) IgM = existing / present HepA virus o N: reactive b. (+) IgG = gone, but had an exposure Treatment: Treatments / Management - antivirals - Supportive tx (alleviating sx) o interferon Preventive measurements: ▪ SC; fatty layers of skin o vaccine ▪ given at 45 degrees angle (90 o hand washing, safe water, proper sewage degrees if small) disposal o immune globulin (should be given 2 weeks Preventions: prior to exposure to HAV) – for contacts to - sharp precautions provide passive immunity - abstinence - Bed rest - meticulous handwashing - Nutritional Support - immunoglobulin – given w/in 24 hrs prior to exposure HEPATITIS B Management of HepB - worldwide cause of cirrhosis & liver cancer - Medications: - bld is not screened in early times, therefore HBV is o chronic HepB = interferon rampant o antiviral agents - outcomes may be severe ▪ Entecavir (ETV) - HepB carrier - ↑ risk for chronic hepatitis & hepatic ▪ Tenofovir (TDF) cancer - Bed Rest & nutritional support - Vaccine: for persons at high risk, routine vaccinations CA: Hepatitis B Virus (HBV) for infants MOT: o exposed = passive immunization - blood, saliva, semen & vaginal secretions (immunoglobulins) o sexually transmitted o standard precautions & infection control o transmitted to infant @ at time of birth; measures prenatal o Screening of blood & blood products o sharing of needles, sharps ▪ 1980s, blood is not screened before o tattoo, blood transfusion bloodletting; causing HepB & HIV - percutaneous & permucosal cases to become rampant Incubation period: - 1 – 6 mos Manifestations: insidious & variable HEPATITIS C - similar to HAV (flu-like sx, GI sx) - most common bloodborne infx - loss of appetite - causes 1/3 of liver cancer cases - dyspepsia - most common reason for liver transplant - abdominal pain - chronic carrier state frequently occurs - generalized itching CA: Hepatitis C Virus (HCV) - malaise MOT: - weakness - blood & sexual contact - jaundice may / may not be evident o sharing of needles o needle sticks  NUR 149: MEDSURG 2 GASTRO Incubation period: - enlargement of liver & spleen - 15 – 160 days Diagnostics: Manifestations: mild - Antibody HEV Diagnostics: - Antibody Hepatitis C surface (Anti-HCV) Prevention: no vaccine - hand hygiene Treatment: - proper water supply; bottled waters when traveling - antivirals - cook meats well o Direct Acting Antivirals (DAA) Preventions: Other Liver disorders - Screening of blood supply Non-viral hepatitis - safety needles for HC workers - Toxic hepatitis - measures to reduce spread of infx as w/ HepB - Drug-induced hepatitis - Avoid alcohol & medications that affects liver o alcohol encourages progression of the dse Fulminant hepatic failure - Hand hygiene TOXIC HEPATITIS - Public health programs to ↓ needle sharing among - inflammation of the liver in reaction to certain drug users substances to which a person is exposed - can be caused by alcohol, chemical, drugs, nutritional supplements HEPATITIS D - in some cases, toxic hepatitis develops w/in hours or - only persons w/ HepB are at risk days of exposure to a toxin - likely to develop fulminant liver failure / chronic active hepatitis & cirrhosis Clinical Manifestations: - anorexia, nausea, & vomiting – usual sx CA: Hepatitis D Virus (HDV) - Jaundice & hepatomegaly – noted on PA MOT: - blood & sexual contact Severe cases: o IV / injection drugs - fever rise o patients undergoing hemodialysis - persistent vomiting w/ blood o recipients of multiple blood transfusions - severe clotting abnormalities & hemorrhages - Severe GI sx Incubation period: - delirium, coma, seizures - 30 – 150 days - death – due to fulminant hepatic failure Diagnostics: Medical MGT: - Anti-delta Antibodies w/ HBsAg 1. Early identification & removal of hepatotoxin 2. Maintain fluid & electrolyte imbalance Treatment: a. ready blood replacement if ever - antivirals 3. Liver Transplant if needed o Interferon Alfa – only licensed drug available to treat HDV infection DRUG-INDUCED HEPATITIS Drug-induced liver dse is the most common cause of acute HEPATITIS E liver failure. - resembles HepA, self-limiting, abrupt onset, not - acetaminophen (OTC medications used to treat fever chronic & pain) = leading cause of acute liver failure CA: Hepatitis E Virus (HEV) MOT: Clinical Manifestations: - fecal-oral route Onset is abrupt o contaminated water - chills, fever, rash, pruritus o undercooked meat o if occurred due to meds, STOP it - arthralgia, anorexia, & nausea Incubation period: - 15 – 65 days Late:  NUR 149: MEDSURG 2 GASTRO - Jaundice - Bilirubin level - Dark urine - Prolongation of Prothrombin time (PT) - Enlarged tender liver Treatment: FULMINANT HEPATIC FAILURE - N-acetylcysteine (NAC) – for acetaminophen aka ACUTE LIVER FAILURE poisoning Life threatening condition that happens when liver function - antivirals – for acute HepB rapidly deteriorates - steroids – for autoimmune flare-ups - may affect people w/ no preexisting liver dse. - penicillin – mushroom poisoning defined by the appearance of severe liver injury w/ hepatic encephalopathy into a previously healthy person HEPATIC CIRRHOSIS Possible causes: Types: - viral hepatitis & drug induced hepatitis – two most ALCOHOLIC: scar tissue characteristically surrounds the common portal areas - viral infections POSTNECROTIC: broad bands of scar tissue - toxic reactions BILIARY: scarring occurs in the liver around the bile ducts - autoimmune dse PATHOPHYSIOLOGY: Risk Factors: - living w/ alcohol disorder - living w/ hepatitis - having low nutritional status MANIFESTATIONS: - female - liver enlargement - older than 40 yrs - portal obstruction - ascites - infection & peritonitis Liver Cirrhosis – results from the inflammation - varices of liver cells → scars; nodules of the scar tissue - GI varices form w/in liver - edema causes: alcohol related dse, non- - Vitamin deficiency - anemia alcoholic fatty liver dse, HepB, HepC - mental deterioration Signs for Liver Cirrhosis: - Cachexia – wasting of body and muscles - Splenomegaly – due to portal HPN, causing spleen to enlarge - Bruising – due to abnormal clotting Non-invasive liver screening: o UTZ o HepB & HepC serology Clinical Manifestations: - Jaundice – yellowing of skin & eyes - Ascites – accumulation of fluid in the abdomen - Abdominal pain – liver capsule becomes stretched - Nausea & Vomiting - Malaise – feeling generally unwell - Dehydration Diagnosis: CH. 44: B I L I A R Y D I S O R - Blood Tests – to check for liver enzymes (AST, ALT) DERS  NUR 149: MEDSURG 2 GASTRO 3. BILIARY COLIC – intermittent RUQ pain caused by ANATOMY & PHYSIOLOGY gallstones irritating the bile duct GALLBLADDER: 4. CHOLANGITIS – bile duct inflammation - located on the R part of the abdomen, beneath the liver 5. GALLBLADDER EMPYEMA – pus in the gallbladder - stores BILE: (complication of cholecystitis) o aids in digestion of fats including fat-soluble 6. CHOLECYSTECTOMY – surgical removal of vitamins (ADEK) gallbladder; typical procedure o excretion of bilirubin thru stool (making it 7. CHOLECYSTOSTOMY – insertion of drain in brownish in color) gallbladder using C-tube or T-tube PANCREAS: - located behind the stomach TYPES OF STONES - produces pancreatic juices (enzymes) that help break 1. PIGMENT STONES down sugar, fats, & starches a. Black Stones – formed in sterile bile Exocrine: amylase (carbs), trypsin/protease (protein), b. Brown Stones – formed in infected lipase (fats), secretin (stimulates the secretion of bicarbonate- intrahepatic / extrahepatic ducts rich pancreatic fluid; regulates gastric acid) - 10% - 25% of cases Endocrine: insulin & glucagon (stabilizes glucose - Formed when ↑ levels of unconjugated bilirubin balance), somatostatin (inhibits pancreatic hormones: insulin & binds w/ calcium glucagon; gastrin, pancreatic enzymes) - ↑ risk in px w/ cirrhosis, hemolysis, & infx of biliary tract - CANNOT BE DISSOLVED & must be removed SURGICALLY 2. CHOLESTEROL STONES - stones made of fat o cholesterol (N constituent of bile) – insoluble in water. It’s solubility depends on bile acids & lecithin (phospholipids) in bile. - 75% of cases of gallbladder dse - In gallstone-prone px, there is: o ↓ bile acid synthesis + ↑ cholesterol synthesis in the liver, resulting in bile supersaturated w/ cholesterol. o Cholesterol precipitates out of bile to form stones - The cholesterol-saturated bile predisposes to the formation of gallstones & acts as an irritant that Common Bile Duct: usual site of obstruction due to produces inflammatory changes in the gallbladder. gallstones 3. MIXED (Pigment + Cholesterol) CHOLECYSTITIS CHOLE – BILE CYST – MEMBRANEOUS SAC ITIS – INFLAMMATION - inflammation of the Gallbladder - cause: CHOLELITHIASIS CAUSES CHOLELITHIASIS - GALLSTONES - calculi / gallstones, usually formed in the gallbladder - ACALCULOUS CHOLECYSTITIS from the constituents of bile o w/out stones - common & prevalent w/ increasing age (>40) o acute inflammation of the gallbladder in the KEY DEFINITIONS: absence of gallstones 1. CHOLESTASIS – Blockage to the flow of bile o possible due to: prolong use of TPN, fasting, 2. CHOLEDOCHOLITHIASIS – gallstone/s in the mechanical ventilators = (px in ICU), burn & common bile duct trauma px  NUR 149: MEDSURG 2 GASTRO RISK FACTORS - ↑ age (above 40 yrs of age) - Obesity, Frequent changes in wt, Rapid wt loss o due to ↑ cholesterol - Women (esp. those who have had multiple pregnancies) o cholesterol gallstones are commonly formed in women o ↑ progesterone during pregnancy reduces the gallbladder contractility = stasis & greater concentration of bile in gallbladder - Tx w/ high-dose estrogen o these medications are known to ↑ biliary cholesterol saturation o Low-estrogen therapy could also cause gallstones acc. to a study - Ileal resection / dse o px w/ ileal dse or resection develop pigment stones as a consequence of ↑ spillage of malabsorbed bile acids into the colon where they solubilize unconjugated bilirubin & promote its absorption, thereby increasing the rate of bilirubin secretion into the bile. Mixed (Pigment + Cholesterol): - Cystic fibrosis o due to ↑ mucus production/secretion o cells in the gallbladder have reduced ability to regulate fluid & chloride transport, which leads to problems w/ the secretion & fx of bile the bile becomes sticky, causing irritation & inflammation in the ducts & potentially obstructing bile ducts by formation of gallstones - Diabetes Mellitus o due to high cholesterol & triglycerides - 4 F’s o FAT (obese) o FAIR (ethnicity) o FEMALE; in her (multiparity) o FORTY PATHOPHYSIOLOGY Pigment Stones: CLINICAL MANIFESTATIONS - None or minimal sx - Acute / Chronic Pain o usually caused by epigastric distress: fullness, abdominal distention, vague pain in RUQ after eating fried/fatty foods (due to intolerance to fatty foods) - Biliary colic  NUR 149: MEDSURG 2 GASTRO o excruciating RUQ abdominal pain that give glucagon radiates to the R shoulder w/ nausea and During Procedure: vomiting o Monitor IV fluids ▪ causes R shoulder guarding o Administer necessary meds ▪ constant N&V may cause dehydration later on After: place NGT or conduct GI o Monitor VS decompression o Check for complications - Jaundice o Observe for the return of px gag reflex o due to unable to secrete bilirubin o areateus – prickly bilious particles in the skin 3. HIDA SCAN (Hepatobiliary iminodiacetic acid ▪ note itchiness scacn) - Changes in urine / stool color o test for diagnosing issues in liver, bile ducts, o dark urine & gallbladder. o clay-colored stool o we inject a radioactive tracer into the px veins - Vitamin Deficiency (A, D, E, K) and use a camera for imaging/visualization o bile digests fat-soluble vitamins - (+) Murphy sign MEDICAL MANAGEMENT o Let the px lie & palpate the mid-clavicular NUTRITIONAL & SUPPORTIVE THERAPY: 1. Rest RUQ of the abdomen then ask the px to inhale 2. IV Fluids o Once the px inhaled, the gallbladder will be 3. NG suction – for decompression exposed and makes contact w/ the palpating 4. Diet hand a. LOW-FAT liquids; HIGH-PROTEIN & ▪ px will suddenly stop deep breathing CARB; cooked fruits, rice or tapioca, lean due to pain meats, mashed potatoes, non-gas-forming - Fever vegetables, coffee, or tea (as tolerated) o due to inflammation b. AVOID eggs, cream, pork, fried foods (fatty foods), cheese, rich dressings, gas- C O M P L I C A T I O N S w/ obstruction forming vegetables, & alcohol - Abscess formation i. GAS-FORMING VEGETABLES: - Necrosis asparagus, cabbage, broccoli, - Perforation brussels sprouts, beans & lentils; - Peritonitis artichoke, onion, pears, wheat (fructose), milk (lactose) DIAGNOSTIC TESTS 1. ULTRASONOGRAPHY – dx procedure of choice; PHARMACOLOGIC THERAPY: o detects calculi in the gallbladder or a dilated 1. Antibiotic Agents common bile duct w/ 95% accuracy. 2. Analgesics o visualization of the gallbladder; see if it there o Morphine sulfate is contraindicated (causes are gallstones in gallbladder or common bile respi. depression) duct; if the wall thickens, or is inflamed, if 3. Gallstone-dissolving agents: there is a possible fluid around the Ursodeoxycholic Acid: UDCA (URSO, Actigall) gallbladder; & if pancreas has stones or is Chenodeoxycholic Acid: Chenodiol or CDCA also inflamed (Chenix) o 6 – 12 mos of therapy are required in many px 2. ENDOSCOPIC RETROGADE to dissolve CHOLANGIOPANCREATOGRAPHY (ERCP) o this tx is generally indicated for px who refuse Pre-procedure: surgery or for whom surgery is too risky o Px on NPO several hours before the (immunocompromised px, cons are severe) procedure; o contains bile acids that can break down o Px on moderate sedation due to endoscope gallstones (esp. small cholesterol stones) passing thru the mouth; reduces gag reflex o acts by inhibiting the synthesis and ▪ doctors may give anticholinergics secretion of cholesterol thereby leading to o Monitor for respiratory & CNS depression desaturated bile ▪ Hypotension – due to oversedation & vomiting  NUR 149: MEDSURG 2 GASTRO M E D I C A L M A N A G E M E N T of CHOLELITHIASIS ERCP DIETATY MGT MEDS: - Ursodeoxycholic acid - Chenodeoxycholic acid LAPAROSCOPIC CHOLECYSTECTOMY NONSURGICAL REMOVAL: - By instrumentation (may be referred as surgical removal) - Intracorporeal / extracorporeal lithotripsy (by the use of laser & shock wave) NONSURGICAL MANAGEMENT 1. DISSOLVING GALLSTONES - solvents are infused in diff. routes - tube, catheter, percutaneous, directly into the gallbladder (ex. inserted t-tube is shaped as a T,