Peptic Ulcers and Gastric Cancer: Pathophysiology, Clinical Manifestations, and Management, Lecture notes of Health sciences

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PRELIM/ SECOND SEMESTER/ JUSTINEDERECHO

OVERVIEW OF THE GASTROINTESTINAL SYSTEM

• GI tract- 7 - 7.9 m length
• Mouth
• Esophagus
• Stomach
• Small intestine
• Large intestine
• 20% of the total cardiac output- blood flow to the GI, increase significantly after eating
• Blood circulation- arteries along the entire length of the thoracic and abdominal aorta; portal venous system
• innervation: sympathetic and parasympathetic ANS
• sympathetic - generally inhibitory effect on the GI: o decreasing gastric secretion and motility o constriction of the sphincters and blood vessels
• parasympathetic - peristalsis and increased secretory activities
• subject to circulatory disturbances, faulty nervous system control, and aging
• many organic diseases
• many extrinsic factors can interfere with its normal function and produce symptoms
• Stress and anxiety FUNCTIONS & PROCESSES OF THE GASTROINTESTINAL SYSTEM Chewing and Swallowing
• chewing - breaking down of food into small particles that can be swallowed and mixed with digestive enzymes.
• saliva - enzymes
• ptyalin (salivary amylase) – starches
• swallowing - voluntary, regulated by the swallowing center in the medulla oblongata
• epiglottis
• esophagus - esophageal peristalsis Gastric Function
• stomach - stores and mixes food with secretions
• gastric acid - highly acidic fluid in response to the presence or anticipated ingestion of food; can total 2.4 L/day; a pH as low as 1; derives its acidity from hydrochloric acid (HCl)
• gastric secretion - o 1) to break down food into more absorbable components, o 2) to aid in the destruction of most ingested bacteria
• Pepsin - an important enzyme for protein digestion to polypetides
• Intrinsic Factor- combines with dietary vitamin B12 so that the vitamin can be absorbed in the ileum
• Peristaltic contractions - propel the stomach’s contents toward the pylorus
• Food remains in the stomach for a variable length of time, from 30 minutes to several hours
• Chyme - partially digested food mixed with gastric secretions
• Hormones, neuroregulators, and local
• regulators found in the gastric secretions control the rate of gastric secretions and influence gastric motility Small Intestine Function
• Duodenal secretions - from the accessory digestive organs (the pancreas, liver, and gallbladder) and the glands in the wall of the intestine itself.
• Contain digestive enzymes : amylase, lipase, and bile
• Pancreatic secretions - have an alkaline pH due to their high concentration of bicarbonate; neutralizes the acid entering the duodenum
• Trypsin - protein
• Amylase - starch
• Lipase – fats
• Pancreatic secretions - drain into the pancreatic duct, which empties into the common bile duct at the ampulla of Vater
• Bile - emulsifying ingested fats
• The sphincter of Oddi - controls the flow of bile
• Hormones, neuroregulators, and local regulators - control the rate of intestinal secretions and also influence GI motility.
• Intestinal secretions - total approximately 1 L/day of pancreatic juice, 0.5 L/day of bile, and 3 L/day of secretions from the glands of the small intestine
• Two types of contractions in the small intestine: 1) segmentation contractions and 2) intestinal peristalsis.
• Stimulated by the presence of chyme
• Carbohydrates - disaccharides (e.g., sucrose, maltose, and galactose) and monosaccharides (e.g., glucose, fructose)
• Glucose - the major carbohydrate that tissue cells use as fuel.
• Proteins - a source of energy after they are broken down into amino acids and peptides.
• Fats become monoglycerides and fatty acid through emulsification
• Chyme stays in the small intestine for 3 to 6 hours
• Villi - produce digestive enzymes as well as to absorb nutrients
• Absorption - the major function of the small intestine; begins in the jejunum and is accomplished by active transport and diffusion across the intestinal wall
• Nutrients - absorbed at specific locations in the small intestine and duodenum,

PRELIM/ SECOND SEMESTER/ JUSTINEDERECHO

• Fats, proteins, carbohydrates, sodium, and chloride - jejunum
• Vitamin B12 and bile salts - ileum
• Mg, phosphate, and K - throughout the small intestine Colonic Function
• Within 4 hours after eating, residual waste material passes into the terminal ileum and slowly into the proximal portion of the right colon through the ileocecal valve
• Bacteria - assist in completing the breakdown of waste material, especially of undigested or unabsorbed proteins and bile salts
• Two types of colonic secretions – o 1) an electrolyte solution and o 2) mucus
• Electrolyte solution - chiefly a bicarbonate solution; acts to neutralize the end products formed by the colonic bacterial action
• Mucus protects the colonic mucosa from the interluminal contents and provides adherence for the fecal mass
• Slow, weak peristalsis moves the colonic contents along the tract - for efficient reabsorption of water and electrolytes
• The waste materials from a meal eventually reach and distend the rectum - about 12 hours Waste Products of Digestion
• Feces - undigested foodstuffs, inorganic materials, water, and bacteria
• About 75% fluid and 25% solid material
• Brown color - from the breakdown of bile by the intestinal bacteria
• Chemicals formed by intestinal bacteria - responsible in large part for the fecal odor
• Gases formed contain methane, hydrogen sulfide, and ammonia, among others.
• Gases - absorbed into the portal circulation and detoxified by the liver or expelled from the rectum as flatus
• Elimination of stool – o a) distention of the rectum, o b) reflex contractions of the rectal musculature, o c) relaxation of the normally closed internal anal sphincter
• the internal sphincter is controlled by the ANS
• the external sphincter is under the conscious control of the cerebral cortex
• defecation - the external anal sphincter voluntarily relaxes to allow colonic contents to be expelled
• the external anal sphincter is maintained in a state of tonic contraction
• defecation is seen to be a spinal reflex (involving the parasympathetic nerve fibers) that can be inhibited voluntarily by keeping the external anal sphincter closed
• Contracting the abdominal muscles (straining) facilitates emptying of the colon
• The average frequency of defecation in humans is once daily, but this varies among people ASSESSMENT OF THE GASTROINTESTINAL SYSMTEM- HEALTH HISTORY Health History
• A focused GI assessment begins with a complete history
• Information - abdominal pain, dyspepsia, gas, nausea and vomiting, diarrhea, constipation, fecal incontinence, jaundice, and previous GI disease is obtained (Weber & Kelley, 2014). Common Symptoms
• Pain
• Dyspepsia
• Intestinal Gas
• N & V
• Change - bowel habits and stool characteristics Pain

1. character
2. duration
3. pattern
4. Frequency
5. location
6. distribution of referred abdominal pain
7. time of the pain
8. other factors - meals, rest, activity, and defecation patterns DYSPEPSIA

• Upper abdominal discomfort associated with eating
• Commonly called indigestion— is the most common symptom of patients with GI dysfunction.
• Affects 25% to 40% of the population over a lifetime
• Fatty foods cause the most discomfort because they remain in the stomach for digestion longer than proteins or carbohydrates
• Salads, coarse vegetables, and highly seasoned foods may also cause considerable GI distress. INTESTINAL GAS
• The accumulation of gas in the GI tract may result in o 1) belching (expulsion of gas from the stomach through the mouth) or o 2) flatulence (expulsion of gas from the rectum) o Complaints of bloating, distention, or feeling “full of gas” with excessive

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flatulence - a symptom of food intolerance or gallbladder disease. NAUSEA AND VOMITING

• Nausea - a vague, uncomfortable sensation of sickness or “queasiness”; that may or may not be followed by vomiting
• Can be triggered by odors, activity, medications, or food intake.
• The emesis (vomitus) - may vary in color and content and may contain undigested food particles, blood (hematemesis), or bilious material mixed with gastric juices.
• (1) visceral afferent stimulation (i.e., dysmotility, peritoneal irritation, infections, hepatobiliary or pancreatic disorders, mechanical obstruction)
• (2) CNS disorders (i.e., vestibular disorders, increased intracranial pressure, infections, psychogenic disorder)
• (3) irritation of the chemoreceptor trigger zone from radiation therapy, systemic disorders, and endogenous and exogenous toxins, which may include specific classes of drugs (e.g., oncologic chemotherapy medications)
• Distention of the duodenum or upper intestinal tract is a common cause of nausea
• Vomiting is a physiologic protective response that limits the effects of noxious agents by emptying the stomach contents and sections of the small intestine Change in Bowel Habits & Stool Characteristics
• may signal colonic dysfunction or disease.
• Diarrhea - typically associated with abdominal pain or cramping and nausea or vomiting
• Constipation - may be associated with anal discomfort and rectal bleeding
• Stool characteristics - normally light to dark brown
• specific disease processes and ingestion of certain foods and medications may change the appearance of stool
• Blood in the stool: melena - tarry-black color; bright or dark red.
• Bulky, greasy, foamy stools that are foul in odor and may or may not float
• Light-gray or clay-colored stool, caused by a decrease or absence of conjugated bilirubin
• Stool with mucus threads or pus that may be visible on gross inspection of the stool
• Stool Characteristics Small, dry, rock-hard masses occasionally streaked with blood Loose, watery stool that may or may not be streaked with blood PHYSICAL ASSESSMENT- ORAL CAVITY Oral Cavity
• Inspection and palpation
  • Dentures should be removed to allow good visualization of the entire oral cavity LIPS
  • inspect for moisture, hydration, color, texture, symmetry, and the presence of ulcerations or fissures
  • should be moist, pink, smooth, and symmetric MOUTH
  • Instruct to open the mouth wide
  • Insert a tongue blade to expose the buccal mucosa for an assessment of color and lesions.
  • Stensen duct GUMS
  • inflammation, bleeding, retraction, and discoloration.
  • odor of the breath
  • hard palate - color and shape. TONGUE
  • dorsum (back) - texture, color, and lesions.
  • movement - protrude and move laterally - to estimate the tongue’s size and symmetry and strength (CN 12)
  • touch the roof of the mouth with the tip of the tongue
  • lesions of the mucosa or any abnormalities involving the frenulum or superficial veins on the undersurface of the tongue - location, size, color, and pain
  • depress to visualize pharynx
  • tonsils, uvula, posterior pharynx
  • color, symmetry, and evidence of exudate, ulceration, or enlargement
  • the ovula and soft palate rise symmetrically with a deep inspiration upon saying “ah”= CN 10 PHYSICAL ASSESSMENT- ABDOMEN ABDOMEN
  • Inspection, Auscultation, Percussion, and Palpation
  • Supine with knees flexed slightly
  • divided into four quadrants or nine regions
  • mapping methods - for a thorough evaluation and appropriate documentation
  • imaginary line drawn vertically from the sternum to the pubis through the umbilicus and a horizontal line drawn across the abdomen through the umbilicus

PRELIM/ SECOND SEMESTER/ JUSTINEDERECHO

INSPECTION

• skin changes, nodules, lesions, scarring, discolorations, inflammation, bruising, or striae
• contour and symmetry of the abdomen
• any localized bulging, distention, or peristaltic waves are identified AUSCULTATION
• Always precedes percussion and palpation
• To determine the character, location, and frequency of bowel sounds and to identify vascular sounds
• Bowel sounds - using the diaphragm of the stethoscope
• The frequency and character of the sounds - heard as clicks and gurgles that occur irregularly and range from 5 to 30 per minute
• normal
• hypoactive
• hyperactive
• absent
• Bell of the stethoscope - any bruits in the aortic, renal, iliac, and femoral arteries
• Friction rubs are high pitched and can be heard over the liver and spleen during respiration
• Borborygmi (“stomach growling”) PERCUSSION
• To assess the size and density of the abdominal organs
• To detect the presence of airfilled, fluid-filled, or solid masses
• Used either independently or concurrently with palpation
• All quadrants are percussed for overall tympani and dullness
• Tympani
• Dullness PALPATION
• Light palpation - for identifying areas of tenderness or muscular resistance
• Deep palpation - to identify masses
• Testing for rebound tenderness is not performed by many examiners

PHYSICAL ASSESSMENT- RECTUM, PERIANAL REGION, AND

ANUS

RECTUM

• Inspection and Palpation
• evaluation of the terminal portions of the GI tract,
• anal canal - approximately 2.5 to 4 cm (1 to 1.6 inches) in length and opens into the perineum
• internal and external sphincters - normally keep the anal canal closed
• Gloves, water-soluble lubrication, a penlight, and drapes
• generally uncomfortable and often embarrassing for the patient, it is a mandatory part of every thorough examination
• Positions - knee-chest, left lateral with hips and knees flexed, or standing with hips flexed and upper body supported by the examination table
• External examination - inspection for lumps, rashes, inflammation, excoriation, tears, scars, pilonidal dimpling, and tufts of hair at the pilonidal area
• tenderness, inflammation, or both - pilonidal cyst, perianal abscess, or anorectal fistula or fissure
• Patient is asked to bear down - appearance of fistulas, fissures, rectal prolapse, polyps, and internal hemorrhoids
• Internal examination - performed with a gloved lubricated index finger inserted into the anal canal while the patient bears down
• tone of the sphincter, any nodules or irregularities of the anal ring DIAGNOSTIC EVALUATION GI Diagnostic Studies
• Can confirm, rule out, stage, or diagnose various disease states,
• majority of these tests and procedures are performed on an outpatient basis in special settings designed for this purpose (e.g., endoscopy suite or GI laboratory)
• Preparations includes clear liquid diet, fasting, ingestion of a liquid bowel preparation, the use of laxatives or enemas, and ingestion or injection of a contrast agent or a radiopaque dye
• These measures are poorly tolerated by some patients and are especially problematic in older adults or patients with comorbidities because bowel preparations can significantly alter the internal fluid and electrolyte balance Serum Laboratory Studies
• CBC
• complete metabolic panel
• prothrombin time/partial thromboplastin time
• triglycerides
• liver function tests
• amylase, and lipase

PRELIM/ SECOND SEMESTER/ JUSTINEDERECHO

• more specific studies may be indicated, such as
• carcinoembryonic antigen (CEA), cancer antigen (CA) 19–9, and alpha-3272 fetoprotein - sensitive and specific for colorectal and hepatocellular carcinomas, respectively
• CEA is a protein that is normally not detected in the blood of a healthy person; therefore, when detected it indicates that cancer is present, although not what type of cancer is present
• CA 19-9 is also a protein that exists on the surface of certain cells and is shed by tumor cells, making it useful as a tumor marker to follow the course of the cancer
• elevated in most patients with advanced pancreatic cancer, colorectal, stomach, and bile duct cancers Stool Test
• Basic examination - consistency, color, and occult (not visible) blood
• Additional studies - fecal urobilinogen, fecal fat, nitrogen, Clostridium difficile, fecal leukocytes, calculation of stool osmolar gap, parasites, pathogens, food residues, and other substances
• Stool samples - usually collected on a random basis unless a quantitative study (e.g., fecal fat, urobilinogen) is to be performed.
• Random specimens should be sent promptly to the laboratory for analysis
• Quantitative 24- to 72-hour collections must be kept refrigerated until transported to the laboratory
• Some stool collections require the patient to follow a specific diet or refrain from taking certain medications before the collection; patient education is important
• Fecal occult blood testing (FOBT) - one of the most commonly performed stool tests
• can be useful in initial screening for several disorders
• used most frequently in early cancer detection programs
• Fecal immunologic tests (FIT) use monoclonal or polyclonal antibodies to detect the globin protein in human hemoglobin
• Dietary restrictions are not required prior to submission of the stool specimen
• Hematoporphyrin assays detect the broadest range of blood derivatives, but a strict dietary protocol is essential
• Stool DNA testing Breath Tests
• The hydrogen breath test - to evaluate carbohydrate absorption, to aid in the diagnosis of bacterial overgrowth in the intestine and short bowel syndrome.
• determines the amount of hydrogen expelled in the breath after it has been produced in the colon
• Urea breath tests - to detect the presence of Helicobacter pylori - Because H. pylori metabolizes urea rapidly, the labeled carbon is absorbed quickly; it can then be measured as carbon dioxide in the expired breath to determine whether H. pylori is present - Prior to urea breath testing, the patient is instructed to avoid antibiotics or bismuth subsalicylate (Pepto- Bismol) for 1 month before the test; - sucralfate (Carafate) and omeprazole (Prilosec) for 1 week before the test; and cimetidine (Tagamet), famotidine (Pepcid), and ranitidine (Zantac) for 24 hours before the test Abdominal Ultrasonography - A noninvasive diagnostic technique in which highfrequency sound waves are passed into internal body structures, and the ultrasonic echoes are recorded on an oscilloscope as they strike tissues of different densities - Detection of an enlarged gallbladder or pancreas, the presence of gallstones, an enlarged ovary, an ectopic pregnancy, or appendicitis. Ultrasonography is an operator-dependent diagnostic technique - Advantages : o absence of ionizing radiation o no noticeable side effects o relatively low cost o almost immediate results - It cannot be used to examine structures that lie behind bony tissue, - Gas and fluid in the abdomen or air in the lungs also prevent transmission of ultrasound - produces no ill effects - pregnant women have concerns regarding the energy emitted by the probe. - Endoscopic ultrasonography (EUS) - a specialize enteroscopic procedure that aids in the diagnosis of GI disorders - By providing direct imaging of a target area NURSING INTERVENTION: - The patient is instructed to fast for 8 to 12 hours before ultrasound testing to decrease the amount of gas in the bowel. - If gallbladder studies are being performed, the patient should eat a fat-free meal the evening before the test. - If barium studies are to be performed, they should be scheduled after ultrasonography - Patients who receive moderate sedation are observed for about 1 hour to assess for level of consciousness, orientation, and ability to ambulate. - Patients treated on an outpatient basis are given instructions regarding diet, activity, and how to monitor for complications Imaging Studies - x-ray - Upper Gastrointestinal Tract - Study Lower Gastrointestinal Tract Study

PRELIM/ SECOND SEMESTER/ JUSTINEDERECHO

• contrast studies
• computed tomography (CT) scan
• magnetic resonance imaging (MRI) scan
• positron emission tomography (PET) scan
• scintigraphy (radionuclide imaging)
• virtual colonoscopy Endoscopic Procedures
• Upper Gastrointestinal Fibroscopy/ Esophagogastroduodenoscopy Fibroscopy of the upper GI tract allows direct visualization of the esophageal, gastric, and duodenal mucosa through a lighted endoscope (gastroscope)
• EGD - the gastroenterologist views the GI tract through a viewing lens and can obtain images through the scope to document findings
• Electronic video endoscopes also are available that attach directly to a video processor, converting the electronic signals into pictures that are projected on a screen
• Fiberoptic Colonoscopy - provides a computer- simulated view of the air-filled distended colon using conventional CT scanning
• Direct visual inspection of the large intestine (anus, rectum, sigmoid, transcending and ascending colon) is possible by means of a flexible fiberoptic colonoscope MANAGEMENT OF PATIENTS WITH DISORDERS OF THE ESOPHAGUS ACHALASIA
• absent or ineffective peristalsis of the distal esophagus accompanied by failure of the esophageal sphincter to relax in response to swallowing
• narrowing of the esophagus just above the stomach results in a gradually increasing dilation of the esophagus in the upper chest
• may progress slowly and occurs most often in people 40 years or older
• The main symptom is dysphagia
• sensation of food sticking in the lower portion of the esophagus
• food commonly regurgitated either spontaneously or intentionally by the patient to relieve the discomfort produced by prolonged distention of the esophagus by food that will not pass into the stomach
• report non-cardiac chest or epigastric pain and pyrosis (heartburn) that may or may not be associated with eating.
• secondary pulmonary complications may result from aspiration of gastric contents
• X-ray studies - esophageal dilation above the narrowing at the gastroesophageal junction Barium swallow, computed tomography (CT) scan of the chest, and endoscopy
• manometry confirms the diagnosis
  • Instruct to eat slowly and to drink fluids with meals
  • Oral calcium channel blockers and nitrates have been used to decrease esophageal pressure and improve swallowing.
  • Botox injection into quadrants of the esophagus via endoscopy
  • pneumatic dilation ESOPHAGEAL SPASM
  • diffuse esophageal spasm (DES) and hypertensive peristalsis aka nutcracker esophagus (NE)
  • DES - spasms are normal in amplitude, but are uncoordinated, move quickly, or occur at various places in the esophagus at once
  • NE - peristalsis is coordinated but the amplitude is very high
  • Hypercontractile esophagus aka jackhammer esophagus - is an extreme form of NE in which the contractions involve the entire esophagus and occur over a prolonged period
  • NE - more common in women and usually manifests in middle age; cause is unknown, but stress may be a factor
  • a relationship between NE and psychiatric disorders or psychotropic medications
  • characterized by dysphagia, odynophagia, and chest pain similar to that of coronary artery spasm
  • Dysphagia - more common in DES from the noncoordinated peristalsis.
  • Esophageal manometry
  • first-line therapy includes calcium channel blockers (nifedipine [Procardia], verapamil [Calan]) and nitrates (nitroglycerin).
  • Smooth muscle relaxants (sildenafil [Viagra]), anticholinergics (botulinum toxin), antianxiety medications (tricyclic antidepressants), and PPIs
  • small, frequent feedings and a soft diet
  • dilation or myotomy procedures may be performed
  • surgical procedures that also address GERD may be beneficial HIATAL HERNIA
  • the opening in the diaphragm through which the esophagus passes becomes enlarged, and part of the upper stomach moves up into the lower portion of the thorax.
  • occurs more often in women than in men.
  • two main types: sliding and paraesophageal
  • Sliding (Type I) hiatal hernia - the upper stomach and the gastroesophageal junction are displaced upward and slide in and out of the thorax
  • About 95% of patients with esophageal hiatal hernia have a sliding hernia.

PRELIM/ SECOND SEMESTER/ JUSTINEDERECHO

• A paraesophageal hernia occurs when all or part of the stomach pushes through the diaphragm beside the esophagus
• Paraesophageal hernias are further classified as types II, III, or IV, depending on the extent of herniation
• Type IV has the greatest herniation
• Sliding hernia - pyrosis, regurgitation, and dysphagia, but many patients are asymptomatic; vague symptoms of intermittent epigastric pain or fullness after eating
• Large hiatal hernias - intolerance to food, nausea, and vomiting.
• Sliding hiatal hernias are commonly associated with GERD.
• Hemorrhage, obstruction, and strangulation can occur with any type of hernia
• confirmed by x-ray studies; barium swallow;
• esophagogastroduodenoscopy (EGD) - the passage of a fiberoptic tube through the mouth and throat into the digestive tract for visualization
• chest CT scan
• frequent, small feedings that can pass easily through the esophagus
• advise not to recline for 1 hour after eating, to prevent reflux or movement of the hernia
• elevate the head of the bed on 4- to 8-inch (10- to 20- cm) to prevent the hernia from sliding upward
• surgical hernia repair DIVERTICULUM
• esophageal diverticulum
• out-pouching of mucosa and submucosa that protrudes through a weak portion of the musculature of the esophagus
• may occur in one of the three areas of the esophagus— pharyngoesophageal (upper), midesophageal (middle), or epiphrenic (lower)
• most common type of diverticulum is Zenker diverticulum - in the pharyngoesophageal area
• Zenker diverticula - caused by a dysfunctional sphincter that fails to open, which leads to increased pressure that forces the mucosa and submucosa to herniate
• dysphagia, fullness in the neck, belching, regurgitation of undigested food, and gurgling noises after eating
• on a recumbent position - regurgitation of undigested food; coughing
• halitosis and a sour taste in the mouth
• A barium swallow - nature and location of a diverticulum
• manometric studies may be performed for patients with epiphrenic diverticula to rule out a motor disorder
• Esophagoscopy - is contraindicated because of the danger of perforation of the diverticulum
• s - surgical removal of the diverticulum.
• Diverticulotomy

GERD

• gastroesophageal reflux disease (GERD)
• a fairly common disorder
• backflow of gastric or duodenal contents into the esophagus
• causes troublesome symptoms and/or mucosal injury to the esophagus
• an incompetent lower esophageal sphincter, pyloric stenosis, hiatal hernia, or a motility disorder
• incidence seems to increase with aging and is seen in patients IBS and obstructive airway disorders (asthma, COPD, cystic fibrosis), peptic ulcer disease, and angina
• associated with tobacco use, coffee drinking, alcohol consumption, and gastric infection with Helicobacter pylori.
• pyrosis (heartburn, commonly described as a burning sensation in the esophagus)
• dyspepsia (indigestion), regurgitation
• dysphagia or odynophagia
• hypersalivation
• esophagitis
• symptoms may mimic those of a heart attack
• GERD can result in dental erosion, ulcerations in the pharynx and esophagus, laryngeal damage, esophageal strictures, adenocarcinoma, and pulmonary complications
• the patient’s history
• diagnostic testing - an endoscopy or barium swallow to evaluate damage to the esophageal mucosa
• ambulatory 12- to 36-hour esophageal pH monitoring is used to evaluate the degree of acid reflux
• Educate the patient to avoid situations that decrease lower esophageal sphincter pressure or cause esophageal irritation
• Instruct to eat a low-fat diet; avoid caffeine, tobacco, beer, milk, foods containing peppermint or spearmint, and carbonated beverages
• Avoid eating or drinking 2 hours before bedtime
• Maintain normal body weight
• Avoid tight-fitting clothes
• Elevate the head of the bed by at least 30 degrees
• Antacids/Acid neutralizing agents
• H2 receptor antagonists
• Prokinetic agents
• PPIs
• Reflux inhibitors
• Surface agents/ALginatebased barriers BARRETT ESOPHAGUS
• a condition in which the lining of the esophageal mucosa is altered
• It affects 5.6% of the population in the US
• occurs in association with GERD
• eventually causes changes in the cells lining the lower esophagus

PRELIM/ SECOND SEMESTER/ JUSTINEDERECHO

• cells that are to cover the exposed area no longer form the normal, squamous mucosa, instead form columnar-lined epithelium that resembles the intestines.
• BE is the only known precursor to esophageal adenocarcinoma (EAC)
• symptoms of GERD, notably frequent heartburn
• symptoms related to peptic ulcers or esophageal stricture, or both
• EGD (esophagogastroduodenosco py) is performed
• usually reveals an esophageal lining that is red rather than pink
• Biopsies - high-grade dysplasia (HGD) is evidenced by the squamous mucosa of the esophagus replaced by columnar epithelium
• Monitoring varies depending on the extent of cell changes.
• Follow-up biopsies are recommended no sooner than 3 to 5 years after a biopsy shows no evidence of dysplasia
• Individualized treatment
• surveillance with biopsies
• use of proton pump inhibitors (PPIs)
• endoscopic resection
• radiofrequency ablation (high-frequency heat energy that kills surrounding cells and tissues)
• consideration of metal stents for severe dysphagia palliation BENIGN TUMORS
• rare, but can arise anywhere along the esophagus
• leiomyoma (tumor of the smooth muscle)- can occlude the lumen of the esophagus and cause dysphagia, pain, and pyrosis
• are asymptomatic or present with multiple symptoms that have been present for a long period of time
• diagnosis may be made incidentally
• confirmed by endoscopy and needle biopsy
• due to the slow growth of most of these tumors, monitoring and minimally invasive techniques (endoscopic, thoracic, or laparoscopic resections) tend to be indicated rather than surgical resection MANAGEMENT OF PATIENT WITH GASTRIC AND DOUDENAL DISORDERS GASTRITIS
• inflammation of the gastric or stomach mucosa
• a common GI problem
• affects women and men about equally and is more common in older adults
• may be acute - lasting several hours to a few days
• may be chronic - resulting from repeated exposure to irritating agents or recurring episodes of acute gastritis Acute Gastritis - classified as erosive or nonerosive - based upon pathologic manifestations present in the gastric mucosa - erosive form of acute gastritis - most often caused by local irritants such as aspirin and other NSAIDs , alcohol consumption, and gastric radiation therapy - nonerosive form of acute gastritis - most often caused by an infection with Helicobacter pylori - a more severe form of acute gastritis is caused by the ingestion of strong acid or alkali, which may cause the mucosa to become gangrenous or to perforate - scarring can occur and result in pyloric stenosis (narrowing or tightening) or obstruction. - acute gastritis also may develop in acute illnesses, especially when the patient has had major traumatic injuries; burns; severe infection; hepatic, kidney, or respiratory failure; or major surgery - acute gastritis from acute illnesses, burns, severe infection, etc is often referred to as stress-related gastritis Chronic Gastritis - classified according to the underlying causative mechanism - infection with H. pylori - chronic H. pylori gastritis, implicated in the development of peptic ulcers, gastric adenocarcinoma (cancer), and gastric mucosa-associated lymphoid tissue lymphoma - Chronic gastritis caused by a chemical gastric injury (gastropathy) - result of long-term drug therapy (e.g., aspirin and other NSAIDs) - reflux of duodenal contents into the stomach most often occurs after gastric surgery (e.g., gastrojejunostomy and gastroduodenostomy) - Autoimmune disorders such as Hashimoto thyroiditis, Addison disease, and Graves’ disease are also associated with the development of chronic gastritis Pathophysiology - disruption of the mucosal barrier that normally protects the stomach tissue from digestive juices (e.g. HCl and pepsin) - impaired mucosal barrier allows corrosive HCL, pepsin, and other irritating agents (e.g., NSAIDs and H. pylori) to come in contact with the gastric mucosa - result in inflammation (acute gastritis - inflammation is usually transient and self-limiting in nature - inflammation causes the gastric mucosa to become edematous and hyperemic (congested with fluid and blood) and to undergo superficial erosion - superficial ulceration may occur as a result of erosive disease and may lead to hemorrhage - chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes, and eventually atrophy (or thinning) of the gastric tissue

PRELIM/ SECOND SEMESTER/ JUSTINEDERECHO

Clinical Manifestation (Acute Gastritis)

• a rapid onset of symptoms
• epigastric pain or discomfort,
• dyspepsia (indigestion),
• anorexia,
• hiccups
• nausea and vomiting can last from a few hours to a few days Clinical Manifestation (Erosive Gastritis)
• may cause bleeding - hematemesis, melena or hematochezia Clinical Manifestation (Chronic Gastritis)
• complain of fatigue
• pyrosis (a burning sensation in the stomach and esophagus that moves up to the mouth; heartburn) after eating
• belching
• a sour taste in the mouth
• early satiety
• anorexia
• nausea and vomiting
• some patients may have only mild epigastric discomfort or report intolerance to spicy or fatty foods or slight pain that is relieved by eating
• may not be able to absorb vitamin B12 due to diminished production of intrinsic factor by the stomach’s parietal cells due to atrophy
• asymptomatic Assessment & Diagnosis
• definitive diagnosis - by an endoscopy and histologic examination of a tissue specimen obtained by biopsy
• complete blood count (CBC) - to assess for anemia as a result of hemorrhage or pernicious anemia.
• detecting H. pylori infection Medical Management (Acute Gastritis)
• management of bleeding if present
• supportive therapy is supportive - nasogastric (NG) intubation, antacids, H2 blockers, PPIs and IV fluids
• Fiberoptic endoscopy may be necessary
• emergency surgery to remove gangrenous or perforated tissue
• gastric resection or a gastrojejunostomy (anastomosis of jejunum to stomach to detour around the pylorus) to treat pyloric obstruction Medical Management (Chronic Gastritis)
• diet modification
  • promote rest
  • reduce stress
  • recommend avoidance of alcohol and NSAIDs, and initiating medications that may include antacids, H blockers, or proton pump inhibitors
  • H. pylori may be treated with selected drug combinations Nursing Management
  • Reducing anxiety
  • Promoting Optimal Nutrition
  • Promoting Fluid Balance
  • Relieving Pain CONSTIPATION Fecal Elimination
  • Changes in patterns of fecal elimination - symptoms of functional disorders or diseases of the GI tract
  • constipation, diarrhea, and fecal incontinence
  • fewer than three bowel movements weekly
  • bowel movements that are hard, dry, small, or difficult to pass
  • a very common GI disorder
  • women, particularly pregnant women
  • who recently had surgery older adults, non- Caucasians, and those of lower socioeconomic status
  • a symptom and not a disease
  • can indicate an underlying disease or motility disorder of the GI tract
  • can be caused by certain medications - anticholinergic agents, antidepressants, anticonvulsants, antispasmodics (muscle relaxants), calcium channel antagonists, diuretic agents, opioids, aluminum- and calcium-based antacids, and iron preparations
  • other causes - weakness, immobility, debility, fatigue, and an inability to increase intra-abdominal pressure to facilitate the passage of stools,
  • many develop constipation because they do not take the time to defecate or ignore the urge to defecate
  • a result of dietary habits (i.e., low consumption of fiber and inadequate fluid intake)
  • lack of regular exercise
  • a stress-filled life chronic enema, laxative, and suppository abuse Pathophysiology
  • interference with one of three major functions of the colon: 1) mucosal transport (i.e., mucosal secretions facilitate the movement of colon contents), 2) myoelectric activity (i.e., mixing of the rectal mass and
    3. propulsive actions) or the processes of defecation (e.g., pelvic floor dysfunction) 3 Classes of Constipation

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1. Functional Constipation o involves normal transit mechanisms of mucosal transport; most common; can be successfully treated by increasing intake of fiber and fluids 2. Slow-transit Constipation o caused by inherent disorders of the motor function of the colon (e.g., Hirschsprung disease); infrequent bowel movements 3. Defecatory disorders o caused by dysfunctional motor coordination between the pelvic floor and anal sphincter; can cause not only constipation but also fecal incontinence Clinical Manifestations

• fewer than three bm per week
• abdominal distention
• pain and bloating
• a sensation of incomplete evacuation
• straining at stool
• the elimination of small volume, lumpy, hard, dry stools
• Rome IV Diagnostic Criteria for Functional Constipation Assessment & Diagnosis
• secondary causes of constipation should be excluded
• severe, intractable constipation needs further diagnostic testing
• diagnosis is based on the patient’s history, physical examination, possibly the results of a barium enema or sigmoidoscopy, and stool testing for occult blood
• anorectal manometry (i.e., pressure studies such as a balloon expulsion test) may be performed to assess malfunction of the sphincter
• Defecography and colonic transit studies
• Tests s- pelvic floor magnetic resonance imaging (MRI) may identify occult pelvic floor defects Complications
• Increased arterial pressure
• straining at stool
• fecal impaction
• fecal incontinence
• hemorrhoids (dilated portions of anal veins) develop as a result of perianal vascular congestion caused by straining
• fissures (normal or abnormal folds, grooves, or cracks in body tissue) may result from the passage of the hard stool through the anus, tearing the lining of the anal canal.
• rectal prolapse
• megacolon - a dilated and atonic colon caused by a fecal mass that obstructs the passage of colon contents
• Fecal impaction occurs when an accumulated mass of dry feces cannot be expelled.
• may be palpable on digital examination, may produce pressure on the colonic mucosa that results in ulcer formation, and may cause fecal incontinence Medical Management
• Treatment targets the underlying cause and prevention of recurrence
• education, exercise, bowel habit training, increased fiber and fluid intake, and judicious use of laxatives
• discontinuing laxative use or replacing medications that could cause or exacerbate constipation with other nonconstipating medications
• Routine exercise to strengthen abdominal muscles is encouraged
• Biofeedback to help learn to relax the sphincter mechanism to expel stool
• Daily dietary intake of 25 to 30 g/day of fiber (soluble and bulk forming) is recommended, especially for the treatment of constipation in the older adult
• bulk-forming agents (fiber laxatives), saline and osmotic agents, lubricants, stimulants, or fecal softeners Nursing Management
• HPI
• Past medical and surgical history
• Provide patient education DIARRHEA
• an increased frequency of bowel movements (more than 3 per day)
• with altered consistency (i.e., increased liquidity) of stool
• associated with urgency, perianal discomfort, incontinence, nausea, or a combination of these factors
• any condition that causes increased intestinal secretions, decreased mucosal absorption, or altered motility can produce diarrhea.
• classified as acute, persistent, or chronic
• acute diarrhea - self-limiting, lasting 1 or 2 days
• persistent diarrhea - lasts between 2 and 4 weeks
• chronic diarrhea - persists for more than 4 weeks and may return sporadically
• acute and persistent diarrheas - frequently caused by viral infections and some drugs (antibiotics e.g., erythromycin) and magnesium-containing antacids (e.g., magnesium hydroxide [Milk of Magnesia])
• chronic diarrhea - caused by adverse effects of chemotherapy, antiarrhythmic agents, antihypertensive agents, metabolic and endocrine disorders

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Pathophysiology

• Acute and persistent diarrheas - classified as either noninflammatory (large-volume) or inflammatory (small-volume).
• Enteric pathogens that are noninvasive (e.g., S. aureus, Giardia) - cause noninflammatory diarrhea, which is characterized by a large volume of loose, watery stools
• dysentery pathogens - invade the intestinal mucosa and cause inflammatory changes typically result in smaller volumes of stool that is bloody; Shigella, Salmonella, and Yersinia species
• chronic diarrhea - secretory, osmotic, malabsorptive, infectious, and exudative.
• Secretory diarrhea - usually high-volume diarrhea associated with bacterial toxins and chemotherapeutic agents used to treat neoplasms, caused by increased production and secretion of water and electrolytes by the intestinal mucosa into the intestinal lumen
• Osmotic diarrhea - water is pulled into the intestines by the osmotic pressure of unabsorbed particles, slowing the reabsorption of water
• can be caused by lactase deficiency, pancreatic dysfunction, or intestinal hemorrhage
• Malabsorptive diarrhea - combines mechanical and biochemical actions, inhibiting effective absorption of nutrients
• Low serum albumin levels lead to intestinal mucosa swelling and liquid stool
• Infectious diarrhea results from infectious agents invading the intestinal mucosa
• Exudative diarrhea is caused by changes in mucosal integrity, epithelial loss, or tissue destruction by radiation or chemotherapy.
• Diarrhea may also be caused by laxative misuse Clinical Manifestation
• increased frequency and fluid content of stools
• abdominal cramps
• distention
• borborygmus
• anorexia
• thirst
• painful spasmodic contractions of the anus
• tenesmus (ineffective, sometimes painful straining with a strong urge)
• related to dehydration and to fluid and electrolyte imbalances
• voluminous, greasy stools - intestinal malabsorption
• presence of blood, mucus, and pus in the stools - inflammatory enteritis or colitis
• oil droplets - may be suggestive of pancreatic insufficiency
• nocturnal diarrhea may be a manifestation of diabetic neuropathy - C. difficile infection Assessment & Diagnosis - CBC - serum chemistries - urinalysis - routine stool examination and stool examinations for infectious or parasitic organisms, bacterial toxins, blood, fat, electrolytes, and white blood cells - endoscopy or barium enema Complications - Dehydration - Loss of potassium) may cause cardiac dysrhythmias - Loss of bicarbonate with diarrhea can also lead to metabolic acidosis - Urinary output less than 0.5 mL/kg/h for 2 to 3 consecutive hours, muscle weakness, paresthesia, hypotension, anorexia, and drowsiness with a potassium level less than 3.5 mEq/L (3.5 mmol/L) - Chronic diarrhea can also result in skin care issues related to irritant dermatitis Medical Management - controlling symptoms, - preventing complications - eliminating or treating the underlying disease Nursing Management - Assess and monitor the characteristics and pattern of diarrhea - Health history - medication therapy, medical and surgical history, and dietary patterns and intake; recent acute illness or recent travel to another geographic area - abdominal auscultation and palpation for tenderness - Inspection of the abdomen, mucous membranes, and skin - to determine hydration status - Stool samples are obtained for testing - Assess the perianal area for skin excoriation - Encourage to increase intake of liquids and foods low in bulk until the symptoms subside - Avoid caffeine, alcoholic beverages, dairy products, and fatty foods for several days - Antidiarrheal medications as prescribed - IVF may be necessary - Monitor serum electrolyte levels closely and immediately reports evidence of dysrhythmias or a change in LOC - Teach perianal skin care PEPTIC ULCER DISORDER (PUD) - location - gastric, duodenal, or esophageal ulcer - an excavation (hollowed-out area) that forms in the mucosa of the stomach, in the pylorus (the opening

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between the stomach and duodenum), in the duodenum or in the esophagus

• erosion of a circumscribed area of mucosa is the cause
• erosion may extend as deeply as the muscle layers or through the muscle to the peritoneum (thin membrane that lines the inside of the wall of the abdomen)
• more likely to occur in the duodenum than in the stomach
• occur alone, but they may occur in multiples
• Chronic gastric ulcers tend to occur in the lesser curvature of the stomach, near the pylorus
• Esophageal ulcers occur as a result of the backward flow of HCl from the stomach into the esophagus (GERD)
• Women and men have about equivalent lifetime risk of developing peptic ulcers
• The rates among middle-aged adults have diminished over the past several decades, whereas the rates among older adults have increased
• In the past, stress and anxiety were thought to be causes of peptic ulcers, but research has documented that most peptic ulcers result from infection with H. pylori
• may be acquired through ingestion of food and water
• person-to-person transmission through close contact and exposure to emesis
• Although H. pylori infection is common in the United States, most infected people do not develop ulcers
• not known why H. pylori infection does not cause ulcers in all people
• most likely the predisposition to ulcer formation
• depends on certain factors - type of H. pylori and other as yet unknown factors
• The use of NSAIDs such as ibuprofen and aspirin is also a major risk factor for peptic ulcers
• infection with H. pylori and concomitant use of NSAIDs are synergistic risks
• smoking and alcohol consumption may be risks, although the evidence is inconclusive
• no evidence that the ingestion of milk, caffeinated beverages, and spicy foods are associated with the development of PUDs
• Familial tendency also may be a significant predisposing factor
• People with blood type O are more susceptible
• association between PUD and COPD, cirrhosis of the liver, and chronic kidney disease
• PUD is also associated with Zollinger–Ellison syndrome (ZES) Pathophysiology
• occur mainly in the gastroduodenal mucosa
  • erosion is caused by the increased concentration or activity of acid–pepsin or by decreased resistance of the normally protective mucosal barrier
  • damaged mucosa cannot secrete enough mucus to act as a barrier against normal digestive juices
  • exposure of the mucosa to gastric acid (HCl), pepsin, and other irritating agents (e.g., NSAIDs or H. pylori) leads to inflammation, injury, and subsequent erosion of the mucosa
  • duodenal ulcers secrete more acid than normal
  • gastric ulcers tend to secrete normal or decreased levels of acid
  • impaired mucosal barrier may result in the formation of peptic ulcers
  • use of NSAIDs inhibits prostaglandin synthesis, which is associated with a disruption of the normally protective mucosal barrier
  • damage to the mucosal barrier also results in decreased resistance to bacteria
  • thus infection from H. pylori bacteria may occur
  • ZES is suspected when a patient has several peptic ulcers or an ulcer that is resistant to standard medical therapy
  • Clinical manifestations: hypersecretion of gastrin, duodenal ulcers, and gastrinomas (islet cell tumors) in the pancreas or duodenum
  • epigastric pain, pyrosis diarrhea, and steatorrhea (fatty stools)
  • ZES associated with MEN-1 syndrome Pathophysiology (Stress Ulcer)
  • acute mucosal ulceration of the duodenal or gastric area that occurs after physiologically stressful events (burns, shock, sepsis, and multiple organ dysfunction syndrome)
  • clinically different from peptic ulcers
  • most common in patients who are ventilator- dependent after trauma or surgery
  • within 24 hours of trauma or surgery reveals shallow erosions of the stomach wall;
  • by 72 hours, multiple gastric erosions are observed
  • as the stressful condition continues, the ulcers spread.
  • when the patient recovers, the lesions are reversed
  • typical of stress ulceration
  • Curling ulcer - frequently observed about 72 hours after extensive burn injuries and often involves the antrum of the stomach or the duodenum
  • Cushing ulcer - common in patients with a traumatic head injury, stroke, brain tumor, or following intracranial surgery
  • thought to be caused by increased ICP which results in overstimulation of the vagal nerve and an increased secretion of gastric acid (HCl)
  • Curling ulcers and Cushing ulcers may occur in the esophagus, stomach, or duodenum and are usually deeper and more penetrating than typical stress ulcers

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Clinical Manifestation

• may last for a few days, weeks, or months
• may disappear only to reappear, often without an identifiable cause
• have no signs or symptoms.
• commonly occur in older adults and those taking aspirin and other NSAIDs
• dull, gnawing pain or a burning sensation in the midepigastrium or the back
• gastric ulcers - the pain commonly occurs immediately after eating
• duodenal ulcers - pain most commonly occurs 2 to 3 hours after meals
• duodenal ulcers - relief of pain after eating or after taking an antacid
• nonspecific symptoms (gastric ulcers or duodenal ulcers) - pyrosis vomiting, constipation or diarrhea, and bleeding
• often accompanied by sour eructation (burping), which is common when the patient’s stomach is empty
• vomiting is rare - could be a result of gastric outlet obstruction
• vomiting may or may not be preceded by nausea; usually follows a bout of severe pain and bloating, which is relieved by vomiting
• constipation or diarrhea
• bleeding peptic ulcers - hematemesis, melena
• perforation - sudden onset of signs and symptoms
• severe, sharp upper abdominal pain, which may be referred to the shoulder
• extreme abdominal tenderness; and nausea or vomiting
• Hypotension and tachycardia may occur (shock) Assessment & Diagnosis
• pain, epigastric tenderness, or abdominal distention.
• Upper endoscopy - preferred diagnostic procedure
• a biopsy of the gastric mucosa and any suspicious lesions can be obtained.
• Endoscopy - lesions that, are not evident on x-ray studies; H. pylori infection
• H. pylori - serologic testing for antibodies against the H. pylori antigen, stool antigen test, and urea breath test
• periodic CBCs to determine the extent of blood loss and whether or not blood transfusions are advisable
• periodic stool testing - for occult blood
• gastric secretory studies - diagnosing ZES and achlorhydria (lack of hydrochloric acid HCl, hypochlorhydria (low levels of HCl), or hyperchlorhydria (high levels of HCl) Medical Management
• antibiotics to eradicate H. pylori
  • to eradicate H. pylori as indicated and to manage gastric acidity
  • medications, lifestyle changes, and surgical intervention
  • combination of antibiotics, PPIs, and bismuth salts to suppress or eradicate H. pylori
  • 10 to 14 days
  • two antibiotics (e.g., metronidazole or amoxicillin and clarithromycin plus a PPI (e.g., lansoprazole , omeprazole, or rabeprazole
  • Research is currently being conducted to develop a vaccine against H. pylori
  • H2 blockers and PPI - reduce gastric acid secretion
  • advise to adhere to and complete the medication regimen to ensure complete healing of the ulcer
  • avoid the use of aspirin and other NSAIDs
  • stress the importance of following the prescribed regimen so that the healing process can continue uninterrupted and the return of chronic ulcer symptoms can be prevented
  • high risk for stress ulcers (e.g., patients who are mechanically ventilated for more than 48 hours) may be treated prophylactically with either H2 blockers or PPIs and cytoprotective agents (e.g., misoprostol, sucralfate) because of the increased risk of upper GI tract hemorrhage
  • Smoking Cessation
  • Dietary Modification Medical Management (Surgical Management)
  • with intractable ulcers (those failing to heal after 12 to 16 weeks of medical treatment), life-threatening hemorrhage, perforation, or obstruction and for those with ZES that is unresponsive to medications
  • vagotomy, with or without pyloroplasty (transecting nerves that stimulate acid secretion and opening the pylorus)
  • antrectomy - removal of the pyloric (antrum) portion of the stomach with anastomosis (surgical connection) to either the duodenum (gastroduodenostomy or Billroth I) or jejunum (gastrojejunostomy or Billroth II) Nursing Management
  • Relieving pain
  • Reduce anxiety
  • Optimal nutritional status
  • Monitor and mange potential complications - hemorrhage, perforation and penetration Signs and Symptoms of Perforation
  • sudden, severe upper abdominal pain (persisting and increasing in intensity)
  • pain may be referred to the shoulders - the right shoulder, because of irritation of the phrenic nerve in the diaphragm

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• Vomiting
• Collapse (fainting)
• Extremely tender and rigid (boardlike) abdomen
• Hypotension and tachycardia, indicating shock GASTRIC CANCER
• a more common diagnosis among older adults,
• men have a higher incidence than women
• worldwide, is the fifth most common cancer diagnosis, with the highest incidence in Eastern Asia (e.g., Republic of Korea, Mongolia, and Japan)
• Diet appears to be a significant risk factor
• high in smoked, salted, or pickled foods and low in fruits and vegetables may increase the risk
• H. pylori infection - a major risk factor the development of gastric cancer
• other factors - chronic inflammation of the stomach (gastritis), pernicious anemia, smoking, obesity, achlorhydria, gastric ulcers, previous partial gastrectomy (more than 20 years ago), and genetics
• sporadic
• 5% to 10% gastric cancers have a familial component Pathophysiology
• 90 - 95% are adenocarcinomas (arise from the mucus- producing cells of the inner-most lining of the stomach
• up to 40% develop in the lower part, 40% in the middle part, and 15% in the upper part; 10% involve more than one of these parts of the stomach
• begins with a lesion involving cells on the top layer of the stomach mucosa
• the lesion then penetrates cells in the deeper layers of the mucosa, submucosa, and stomach wall
• the lesion infiltrates the stomach wall and extends to organs or structures adjacent to the stomach
• lymph node involvement and metastasis tend to occur early due to the abundant lymphatic and vascular networks of the stomach.
• common sites of metastasis include the liver, peritoneum, lungs, and brain Clinical Manifestations
• associated with few if any symptoms in the early stages
• early-stage disease may include pain that is relieved by antacids, resembling those of benign ulcers, and are seldom definitive
• advanced disease are similar to those of PUD - dyspepsia (indigestion), early satiety, weight loss, abdominal pain just above the umbilicus, loss or decrease in appetite, bloating after meals, and nausea or vomiting
• fatigue - result of the cancer itself or blood loss from the lesion infiltrating the stomach or surrounding tissue Assessment &Diagnosis
  • advanced gastric cancer may be palpable as a mass.
  • ascites and hepatomegaly (enlarged liver) may be apparent if the cancer cells have metastasized to the liver
  • Sister Mary Joseph’s nodules - palpable nodules around the umbilicus, are a sign of a GI malignancy, usually a gastric cancer
  • esophagogastroduodenoscopy for biopsy and cytologic washings - diagnostic study of choice
  • barium x-ray examination of the upper GI tract
  • endoscopic ultrasound to assess tumor depth and any lymph node involvement
  • CT scanning - to assess for surgical resectability of the tumor before surgery is scheduled.
  • CT scans of the chest, abdomen, and pelvis are valuable in staging gastric cancer
  • CBC to evaluate for the presence of anemia
  • tumor markers - carcinoembryonic antigen (CEA), carbohydrate antigen (CA 19 - 9), and CA 50 are monitored
  • t umor marker values - usually elevated in the presence of gastric ca before treatment and decrease if the tumor is responding to the treatment Medical Management
  • multimodal - surgery, chemotherapy, targeted therapy, and radiation therapy
  • resectable tumor undergoes a surgical procedure to remove the tumor and appropriate lymph nodes
  • tumor that is not surgically resectable or those with advanced disease, cure is less likely Surgical Management
  • total gastrectomy may be performed for a resectable cancer
  • reconstruction of the GI tract
  • esophagojejunostomy - anastomosing the end of the jejunum to the end of the esophagus
  • radical partial (subtotal) gastrectomy for a resectable tumor in the middle and distal portions of the stomach
  • Billroth I or a Billroth II operation
  • Billroth I - limited resection and offers a lower cure rate than the Billroth II
  • Billroth II procedure - wider resection removing approximately 75% of the stomach and decreases the possibility of lymph node spread or metastatic recurrence. Complication of Gastric Surgery
  • hemorrhage, dumping syndrome, bile reflux, and gastric outlet obstruction.
  • postop bleeding from the surgical site - a common complication of gastric surgery
  • may be severe (hemorrhage) and manifest as vomiting large amounts of bright red blood, which may result in hemorrhagic shock

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• Dumping syndrome –
• Bile reflux - prolonged exposure of bile acid from the duodenum results in irritation and damage to the gastric mucosa, which may lead to gastritis, esophagitis, and possibly peptic ulcer formation; burning epigastric pain that may increase after meals
• Gastric outlet obstruction
• Postoperative gastric outlet obstruction - caused by narrowing (stenosis) or scar tissue (stricture) formation at the surgical anastomosis site Medical Management
• Chemotherapy and Targeted Therapy
• Radiation Therapy Nursing Management
• Reduce Anxiety
• Optimal nutritional status
• Relieving pain
• Providing psychological support FECAL INCONTINENCE
• the recurrent involuntary passage of stool from the rectum for at least 3 months.
• influence factors:
  1. the ability of the rectum to sense and accommodate stool,
  2. the amount and consistency of stool,
  3. the integrity of the anal sphincters and musculature, and
  4. rectal motility Pathophysiology
• may be a symptom of an underlying condition
• results from conditions that interrupt or disrupt the structure or function of the anorectal unit
• anal sphincter weakness, both traumatic (e.g., after surgical procedures involving the rectum) and nontraumatic (e.g., scleroderma)
• neuropathies both peripheral (e.g., pudendal)
• generalized (e.g., diabetes); disorders of the pelvic floor (e.g., rectal prolapse); inflammation (radiation proctitis, IBD)
• CNS disorders (e.g., dementia, stroke, spinal cord injury, multiple sclerosis)
• Diarrhea
• fecal impaction with overflow
• behavioral disorders.
• more common with advancing age (i.e., weakness or loss of anal or rectal muscle tone) Clinical Manifestations
• minor soiling
• occasional urgency and loss of control
  • complete incontinence
  • poor control of flatus,
  • diarrhea or constipation.
  • passive incontinence occurs without warning
  • urge incontinence with the sensation of the urge to
  • defecate but cannot reach the toilet in time Assessment & Diagnosis
  • medical history
  • treatment depends on the cause
  • rectal examination
  • endoscopic examination (flexible sigmoidoscopy) to rule out tumors, inflammation, fissures, or impaction
  • anorectal manometry, anal endosonography, pelvic MRI scan, and transit studies Medical Management
  • correcting the underlying cause
  • psyllium (Metamucil) as a fiber supplement
  • loperamide 30 minutes prior to meals
  • Biofeedback therapy with pelvic floor muscle training
  • Bowel training programs can also be effective
  • Sacral nerve stimulation
  • surgical reconstruction or repair of anal sphincter, artificial sphincter implantation, anal sphincter bulking by injection of synthetic agents, sacral nerve stimulation, or fecal diversion Nursing Management
  • Obtains a thorough health history - previous surgical procedures, chronic illnesses, dietary patterns, bowel habits and problems, and current medication regimen.
  • Assist in identifying stool characteristics - frequency, volume, and consistency of the feces
  • rectal examination
  • Removal of impacted feces before instituting any preventive therapies
  • Initiate a bowel training program
  • Biofeedback in conjunction with pelvic floor exercises
  • Bowel regulation - therapeutic use of diet and fiber
  • Maintain skin integrity
  • When continence sometimes cannot be achieved - assist the patient and family to accept and cope with this chronic situation MANAGEMENT OF PATIENT WITH DISORDERS OF MALABSORPTION Irritable Bowel Syndrome
  • a chronic functional disorder
  • characterized by recurrent abdominal pain associated with disordered bowel movements, which may include diarrhea, constipation, or both
  • women are affected more often than men, with

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• typically diagnosed in adults younger than 45 years of age
• a complex interplay of genetic, environmental, and psychosocial factors are thought to be associated with the onset of IBS
• chronic stress, sleep deprivation, surgery, infections, diverticulitis, and some foods (e.g., milk, yeast products, eggs, wheat products, red meat) Pathophysiology
• results from a functional disorder of intestinal motility
• may be related to neuroendocrine dysregulation - changes in serotonin signaling, infection, irritation, or a vascular or metabolic disturbance
• peristaltic waves are affected at specific segments of the intestine and in the intensity with which they propel the fecal matter forward
• there is no evidence of inflammation or tissue changes in the intestinal mucosa Clinical Manifestation
• symptoms can vary widely, ranging in intensity and duration
• from mild and infrequent to severe and continuous
• main symptom - alteration in bowel patterns: constipation (classified as IBS-C), diarrhea (classified as IBSD), or a combination of both (classified as IBS-M for “mixed”)
• IBS-U (unknown) - with IBS who do not fit any of the three categories of IBS
• pain, bloating, and abdominal distention and changes in bowel pattern
• abdominal pain is sometimes precipitated by eating and is frequently relieved by defecation
• IBS occurs concomitant with other GI disorders Assessment & Diagnosis
• clinical manifestations of IBS must be present sometime during the last 3 months with onset for at least 6 months prior to diagnosis
• recurrent abdominal pain for at least one day weekly, associated with 2 or more of the following: abdominal pain related to defecation; abdominal pain associated with a change in frequency of stool; abdominal pain associated with a change in form/appearance of stool
• recording the quality and quantity of bowel movements in a stool diary
• CBC
• Creactive protein or fecal calprotectin
• serologic tests for celiac disease
• stool studies and colonoscopy Medical Management
• Relieve abdominal pain and control diarrhea or constipation - Lifestyle modification - stress reduction, ensuring adequate sleep, and instituting an exercise regimen, - Introduction of soluble fiber (e.g., psyllium) to the diet - Restriction and then gradual reintroduction of foods that are possibly irritating - IBS-D - to address diarrhea - IBS-C - to address constipation - smooth muscle antispasmodic agents (e.g., dicyclomine [Bentyl]). - antidepressants - probiotics Nursing Management - Provide patient and family education and encourage self-care activities - Provide education on the appropriate use of a bowel habit diary, - Emphasize and reinforce good sleep habits and good dietary habits - Keep a 1- to 2-week food diary - Encourage to eat at regular times and to avoid food triggers. - Not to take fluids with meals because this results in abdominal distention. - Discourage alcohol use and cigarette smoking - Stress management - relaxation techniques, CBT, yoga, and exercise CELIAC DISEASE - a disorder of malabsorption caused by an autoimmune response to consumption of products that contain the protein gluten - Gluten - wheat, barley, rye, and other grains, malt, dextrin, and brewer’s yeast - Celiac disease has become more common in the past decade - Celiac disease also has a familial risk component, particularly among first-degree relatives - Risk - those with type 1 diabetes, Down syndrome, and Turner syndrome - may manifest at any age in a person who is genetically predisposed Pathophysiology - genetic predisposition - exhibit an autoimmune response to gluten products that is both humoral and cell mediated - not known what trigger or triggers may incite this autoimmune response, although it cannot occur if gluten is not ingested - inflammation of the epithelial cells that line the small intestines - the mucosal villi of the small intestine become denuded and cannot function - loss of ability to absorb both micronutrients and macronutrients, causing systemic nutritional deficits

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Clinical Manifestations

• diarrhea, steatorrhea, abdominal pain, abdominal distention, flatulence, and weight loss
• fatigue, general malaise, depression, hypothyroidism, migraine headaches, osteopenia, anemia, seizures, paresthesias in the hands and feet, and a red, shiny tongue
• Dermatitis herpetiformis - a rash that is frequently associated with celiac disease in adults; clusters of erythematous macules that develop into itchy papules and vesicles on the forearms, elbows, knees, face, or buttocks Assessment & Diagnosis
• presenting signs and symptoms
• a family history and risk factor
• a series of serologic tests and endoscopic biopsy
• It is important that the patient continues to consume gluten products during testingto avoid a false negative serologic finding
• Immunoglobulin A (IgA) antitissue transglutaminase (tTG) - 90% sensitive and 95% specific to celiac disease
• biopsies of the proximal small intestine Medical Management
• chronic, noncurable, lifelong disease
• refrain from exposure to gluten in foods and other products
• specific, targeted treatment for specific symptoms - anemia (folate, cobalamin, or iron supplements), osteopenia (treatment for osteoporosis)
• Encourage to eat at regular times and to avoid food triggers.
• Not to take fluids with meals because this results in abdominal distention.
• Discourage alcohol use and cigarette smoking
• Stress management - relaxation techniques, CBT, yoga, and exercise PERITONITIS
• inflammation of the peritoneum,
• usually a result of bacterial infection but may occur secondary to a fungal or mycobacterial infection
• most common bacteria implicated are Escherichia coli and Klebsiella, Proteus, Pseudomonas, and Streptococcus species.
• 1) Primary peritonitis (spontaneous bacterial peritonitis or SBP) - a spontaneous bacterial infection of ascitic fluid.
• This occurs most commonly in adult patients with liver failure
• 2) Secondary peritonitis - secondary to perforation of abdominal organs with spillage that infects the serous peritoneum
• most common causes include a perforated appendix, perforated peptic ulcer, perforated sigmoid colon caused by severe diverticulitis, volvulus of the colon and strangulation of the small intestine
• 3) Tertiary peritonitis - a result of a suprainfection in a patient who is immunocompromised.
• Tuberculous peritonitis in a patient with AIDS is an example of tertiary peritonitis
• rare causes of peritonitis Pathophysiology
• Secondary peritonitis - abdominal contents leak into the abdominal cavity,
• Bacterial proliferation
• Edema of the tissues
• Exudation of fluid develops
• Peritoneal fluid becomes turbid
• Hypermotility of the intestinal tract, followed by paralytic ileus with an accumulation of air and fluid in the bowel Clinical Manifestations
• depend on the location and extent of the inflammation
• early clinical manifestations - signs and symptoms of the disorder causing the condition
• first, pain is diffuse but then becomes constant, localized, and more intense over the site of the pathologic process (site of maximal peritoneal irritation)
• pain aggravated by movement usually aggravates it
• abdomen becomes extremely tender and distended
• the muscles become rigid.
• Rebound tenderness may be present
• anorexia, nausea and vomiting
• paralytic ileus
• fever, increased pulse rate
• hypotension
• manifestations mirror those of sepsis and septic shock Assessment & Diagnosis
• Elevated WBC consistent with bacterial infection
• Low Hgb and Hct if blood loss has occurred
• Serum electrolyte studies - altered levels of K, Na, Cl
• abdominal x-ray - air and fluid levels and distended bowel loops
• abdominal ultrasound, CT scan, MRI - abscesses (localized collection of purulent material surrounded by inflamed tissues) and fluid collections
• Peritoneal aspiration and culture and sensitivity studies
• infection and identify the causative organisms Medical Management
• Fluid, colloid, and electrolyte replacement
• administration of several liters of an isotonic solution
• Analgesic medications for pain
• Antiemetic agents for nausea and vomiting

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• Intestinal intubation and suction to relieve abdominal distention and in promote intestinal function and promote lung expansion
• Oxygen therapy and airway intubation and ventilatory assistance occasionally are required.
• Antibiotic therapy initiated early in the treatment of peritonitis
• identify the source of infection and eradicate it Surgical Management
• excision (e.g., appendix), resection with or without anastomosis (e.g., intestine), repair (e.g., perforation), and drainage (e.g., abscess)
• fecal diversion may need to be created
• ultrasound-guided and CTguided peritoneal drainage of abdominal and extraperitoneal abscesses Nursing Management
• Intensive care is needed for the patient with septic shock
• Increase fluid and food intake gradually and reduce parenteral fluids as prescribed
• A worsening clinical condition may indicate a complication, and the nurse must prepare the patient for emergency surgery
• The nursing management of a patient treated for secondary peritonitis is based upon the patient’s primary diagnosis and treatment WK 3- ASSESSMENT AND MANAGEMENT OF PATIENTS WITH DIABETES Classification
• type 1 diabetes type
• 2 diabetes,
• gestational diabetes latent autoimmune diabetes of adults (LADA)
• diabetes associated with other conditions or syndromes Type 1 Diabetes
• affects approximately 5% of adults with the disease
• characterized by the destruction of the pancreatic beta cells
• genetic, immunologic, and possibly environmental (e.g., viral) factors
• a genetic predisposition, or tendency, toward the development of type 1 diabetes - found in people with certain human leukocyte antigen types
• evidence of an autoimmune response in type 1 diabetes
• Regardless of the specific cause, the destruction of the beta cells results in decreased insulin production, increased glucose production by the liver, and fasting hyperglycemia - glucose derived from food cannot be stored in the liver but instead remains in the bloodstream - contributes to postprandial (after meals) hyperglycemia - If the concentration of glucose in the blood exceeds the renal threshold for glucose (usually 180 to 200 mg/dL or 9.9 to 11.1 mmol/L) the kidneys may not reabsorb all of the filtered glucose - glucose appears in the urine (glycosuria) - glycosuria is accompanied by excessive loss of fluids and electrolytes - osmotic diuresis - Insulin normally inhibits glycogenolysis (breakdown of stored glucose) and gluconeogenesis (production of new glucose from amino acids and other substrates), contribute further to hyperglycemia - fat breakdown occurs - increased production of ketone bodies (highly acidic substance formed when the liver breaks down free fatty acids in the absence of insulin) – DKA Diabetic Ketoacidosis - Diabetic ketoacidosis (DKA) - a metabolic derangement that occurs most commonly in persons with type 1 diabetes and results from a deficiency of insulin - highly acidic ketone bodies are formed, and metabolic acidosis occurs - polyuria, polydipsia, nausea, vomiting, and fatigue with eventual stupor and coma if not treated fruity breath odor due to the presence of ketoacids Type 2 Diabetes - affects approximately 95% of adults with the disease - occurs more commonly among people who are older than 30 years and obese, although its incidence is rapidly increasing in younger people because of the growing epidemic of obesity in children, adolescents, and young adults - The two main problems - 1) insulin resistance and 2) impaired insulin secretion. - Insulin resistance - a decreased tissue sensitivity to insulin - Insulin binds to special receptors on cell surfaces and initiates a series of reactions - glucose metabolism - genetic factors - to overcome, increased amounts of insulin must be secreted to maintain the glucose level at a normal or slightly elevated level - beta cells cannot keep up with the increased demand for insulin, the glucose level rises and type 2 diabetes develops - metabolic syndrome - hypertension, hypercholesterolemia, abdominal obesity, and other abnormities - despite the impaired insulin secretion that is characteristic of type 2 diabetes, there is enough insulin present to prevent the breakdown of fat

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• DKA does not typically occur in type 2 diabetes
• uncontrolled type 2 diabetes may lead to another acute problem—hyperglycemic hyperosmolar syndrome (HHS)
• slow, progressive glucose intolerance
• onset may go undetected for many years
• symptoms are frequently mild - fatigue, irritability, polyuria, polydipsia, poorly healing skin wounds, vaginal infections, or blurred vision (if glucose levels are very high) Other Types
• Gestational Diabetes
• Latent Autoimmune Diabetes of Adults (LADA) Prevention
• Lifestyle modifications focused on weight reduction of greater than 7% of initial body weight and physical activity of moderate intensity
• Behavior modification strategies
• Exercise Clinical Manifestation
• depend on the patient’s level of hyperglycemia.
• Classic clinical - “three Ps”:
• polyuria, polydipsia, and polyphagia polyuria and polydipsia - a result of the excess loss of fluid associated with osmotic diuresis
• polyphagia - from the catabolic state induced by insulin deficiency and the breakdown of proteins and fats
• fatigue and weakness, sudden vision changes, tingling or numbness in hands or feet, dry skin, skin lesions or wounds that are slow to heal, and recurrent infections
• onset of type 1 diabetes - associated with sudden weight loss or nausea, vomiting, or abdominal pains, if DKA has developed. Assessment and Diagnostic
• abnormally high blood glucose level
• Fasting plasma glucose (FPG) - blood glucose determination obtained in the laboratory after fasting for at least 8 hours
• Random plasma glucose,
• 2 - hour postload - glucose level 2 hours after receiving glucose Medica Management
• main goal - normalize insulin activity and blood glucose levels to reduce the development of complications - patients with diabetes strive for glucose control (HgbA1c less than 7%) to reduce their risk of complications - careful screening of patients for capability and responsibility is a key step in initiating intensive therapy. - The therapeutic goal for diabetes management is to achieve normal blood glucose levels (euglycemia) without hypoglycemia while maintaining a high quality of life - 5 components: o 1) nutritional therapy, o 2) exercise, o 3) monitoring, o 4) pharmacologic therapy, and o 5) education. constant assessment and modification of the treatment plan by health professionals and daily adjustments in therapy by the patient. patient and family education Nursing Management - Glucose control- 140 - 180 mg/dL - Management of patients with DKA and HHS - Long-term management and avoidance of potential complications of diabetes - a solid educational foundation ACUTE COMPLICATIONS OF DIABETES HYPOGLYCEMIA - Insulin Reactions - low (hypo) sugar in the blood (glycemia) - less than 70 mg/dL (3.7 mmol/L) - severe hypoglycemia < 40 mg/dL (2.5 mmol/L) - too much insulin or oral hypoglycemic agents, too little food, or excessive physical activity - may occur at any time of the day or night - often before meals, - late afternoon - the peak of the morning NPH (Neutral Protamine Hagedorn) insulin - middle-of-the-night - peaking evening or predinner NPH insulins, especially when no bedtime snack - 1) adrenergic symptoms and 2) CNS symptoms. - mild hypoglycemia - SNS is stimulated - surge of epinephrine and norepinephrine: sweating, tremor, tachycardia, palpitation, nervousness, and hunger - moderate hypoglycemia - brain cells are deprived of glucose: impaired function of the CNS (inability to concentrate, headache, lightheadedness, confusion, memory lapses, numbness of the lips and tongue, slurred speech, impaired coordination, emotional changes, irrational or combative behavior, double vision, and drowsiness - blood glucose monitoring - avoid potentially dangerous activities - blood glucose monitoring - avoid potentially dangerous activities

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• treat with carbohydrates
• blood glucose monitoring
• avoid potentially dangerous activities
• treat with carbohydrates
• initiate emergency measures
• patient education DIABETIC KETOACIDOSIS
• caused by an absence or markedly inadequate amount of insulin.
• three main clinical features of DKA: o 1) Hyperglycemia, o 2) Dehydration and electrolyte loss, and o 3) Acidosis (Attached yt link: Week 3B page 12): Diabetic Ketoacidosis (DKA) explained with cartoons! (youtube.com)
• Rehydration
• Restoring electrolytes
• Reversing acidosis HYPEROSMOLOR HYPERGLYCEMIA STATE (HSS)
• resulting from a relative insulin deficiency initiated by an illness that raises the demand for insulin
• a serious condition in which hyperosmolarity and hyperglycemia predominate, with alterations of the sensorium (sense of awareness)
• ketosis is usually minimal or absent
• persistent hyperglycemia causes osmotic diuresis
• loss of water and electrolytes
• to maintain osmotic equilibrium, water shifts from the intracellular fluid space to the extracellular fluid space
• glycosuria + and dehydration = hypernatremia and increased osmolarity
• hypotension, profound dehydration (dry mucous membranes, poor skin turgor), tachycardia, and variable neurologic signs (e.g., alteration of consciousness, seizures, hemiparesis) (Attached yt link: Week 3B page 19-20): Hyperosmolar Hyperglycemic Nonketotic Syndrome | Panmedicad (youtube.com) & DKA diabetic ketoacidosis vs. HHS (HHNS) NCLEX (youtube.com) LONG-TERM COMPLICATIONS OF DIABETES (Attached yt link: Week 3C page 2) MACROVASCULAR
• Diabetic macrovascular complications - changes in the medium to large blood vessels - vessel walls thicken, sclerose, and become occluded by plaque that adheres to the vessel walls
• blood flow is blocked
  • occur more often and at an earlier age in patients with diabetes 3 main types - 1) coronary artery disease, 2) cerebrovascular disease, and 3) peripheral vascular disease
  • MI is common
  • typical ischemic symptoms may be absent in patients with diabetes - no early warning signs of decreased coronary blood flow and may have “silent” MIs
  • lack of ischemic symptoms may be secondary to autonomic neuropathy
  • occlusive changes or the formation of an embolus can lead to TIAs and strokes.
  • symptoms of a stroke may be similar to symptoms of acute diabetic complications (HHS or hypoglycemia)
  • occlusive peripheral arterial disease - diminished peripheral pulses and intermittent claudication (pain in the buttock, thigh, or calf during walking)
  • severe form - increased incidence of gangrene and subsequent amputation in patients with diabetes MICROVASCULAR
  • Diabetic retinopathy Nephropathy Diabetic Neuropathies - peripheral neuropathy, autonomic neuropathies ASSESSMENT OF THE ENDOCRINE SYSTEM (Attached yt link: Week 4A page 2): Overview of the Endocrine System (youtube.com) ENDOCRINE GLANDS
  • pituitary gland
  • thyroid gland
  • parathyroid glands
  • adrenal glands
  • pancreatic islets
  • ovaries, and testes HORMONES
  • help regulate organ function in concert with the nervous system
  • amount of circulating hormones depends on their unique function and the body’s needs
  • hormone concentration in the bloodstream is maintained at a relatively constant level
  • negative feedback system - when the hormone concentration increases, further production of that hormone is inhibited and vice versa
  • (1) amines and amino acids (e.g., epinephrine, norepinephrine, and thyroid hormones)
  • (2) peptides, polypeptides, proteins, and glycoproteins (e.g., thyrotropin-releasing hormone [TRH], folliclestimulating hormone [FSH], and growth hormone [GH])

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• (3) steroids (e.g., corticosteroids, which are hormones produced by the adrenal cortex or their synthetic equivalents)
• (4) fatty acid derivatives (e.g., eicosanoid, retinoids)
• paracrine action - act locally in the area where they are released; e.g., the effect of sex hormones on the ovaries
• autocrine action - act on the actual cells from which they were released; e.g., the effect of insulin from pancreatic beta cells on those cells Assessment
• Health History and ROS - changes (1) the severity of these changes, (2) the length of time the patient has experienced the changes, (3) how these changes have affected the patient’s ability to carry out ADLs, (4) the effect of the changes on the patient’s self- perception, and (5) family history
• Physical Assessment - vital signs; head-to-toe inspection; and palpation of skin, hair, and thyroid
• compare with previous findings, if available
• physical, psychological, and behavioral changes should be noted Diagnostic Evaluation
• Blood tests - to determine the levels of circulating hormones, the presence of autoantibodies, and the effect of a specific hormone on other substances (e.g., the effect of insulin on blood glucose levels).
• serum levels - hypofunction or hyperfunction
• Radioimmunoassays - radioisotope-labeled antigen tests to measure the levels of hormones or other substances
• Urine tests - to measure the amount of hormones or the end products of hormones excreted by the kidneys
• one-time specimens or 24-hour urine specimens
• Stimulation tests - to confirm hypofunction of an endocrine organ
• Suppression tests - to detect hyperfunction of an endocrine organ
• Imaging studies - radioactive scanning, MRI, CT, etc.
• Genetic screening