Gastrointestinal and Elimination Disorders Flashcards

Gastroesophageal Reflux Disease (GERD)

Gastroesophageal reflux disease, or GERD, is defined as the backflow of gastric or duodenal contents, or both, into the esophagus. This condition is characterized by an incompetent Lower Esophageal Sphincter (LES) and is often viewed as a sign of poor digestion. Regionally or popularly, it is referred to as heartburn, particularly when it occurs in adults. It is essential to recognize that the primary pathophysiological driver is the presence of pressure differences between the esophagus and the stomach, where the LES becomes dysfunctional. Consequently, esophageal motility is slowed and gastric emptying is delayed.

Risk factors for GERD involve anything that effectively lowers LES pressure. This includes the consumption of acidic and fatty foods, alcohol, obesity, smoking, and the presence of a hiatal hernia or pregnancy. Other related conditions that may exacerbate or contribute to the risk include pyloric stenosis, irritable bowel syndrome (IBS), asthma, Chronic Obstructive Pulmonary Disease (COPD), and Cystic Fibrosis (CF). Interestingly, dietary choices like protein, carbohydrates, and non-fat milk have been noted to increase LES pressure, which helps keep the sphincter closed.

Diagnostics for GERD rely on several key tests. An Upper Endoscopy (EGD) serves as the first gold standard to detect scarring, esophageal damage, or cancer. An esophageal biopsy may also be performed to collect a sample of gastric acid or tissue. Other tests include $24\,hr$ ambulatory pH monitoring and the barium swallow test. In children, a barium swallow involves giving the patient dye or barium followed by an X-ray to determine if the fluid refluxes upward from the stomach. Priority assessment cues include assessing for heartburn, meal intake habits (especially how late one eats), smoking habits, difficulty swallowing, and a feeling of fullness in the throat. Clinical terms for these symptoms include pyrosis, which is pain in the epigastric region, and dyspepsia, referring to indigestion pain in the upper abdomen.

Priority interventions for GERD revolve around dietary and lifestyle management. Patients should have nothing to eat or drink within $2\,hours$ of bedtime and avoid lying down immediately after eating. It is recommended to elevate the head of the bed (HOB) by $4-6\,inches$ at night to prevent night-time reflux. Patients must avoid triggers such as spicy foods, acidic foods, mint, tomatoes, fatty foods, dairy, chocolate, citrus, and alcohol. Effective nursing implications include teaching cessation of smoking, weight loss, and avoiding late-night snacking. For infants, feeding should occur in an upright position. Special care must be taken with older adults as they may perceive GERD pain similarly to angina or chest pain.

Pharmacological therapy for GERD includes antacids such as Tums for mild to moderate symptoms, typically taken $1-3\,hours$ after meals and at bedtime to neutralize acid. Proton Pump Inhibitors (PPIs), often ending in the suffix "-zole" (e.g., omeprazole), reduce gastric secretions and promote healing and should be taken $30-60\,minutes$ before meals. Histamine Receptor Blockers (H2 blockers) like Pepcid also help decrease esophageal acid. Cholinergic agents may be used to increase LES pressure. Long-term use of PPIs carries a specific risk of osteoporosis because they can stop the absorption of calcium. Surgical options include hiatal hernia repair or a Nissen Fundoplication, which is performed when the condition is unresponsive to pharmacologic and lifestyle changes.

Peptic Ulcer Disease (PUD)

Peptic Ulcer Disease (PUD) involves a break in the mucous lining of the gastric mucosa, which can occur in several locations. These ulcers thrive in acidic environments. Duodenal ulcers are the most common type. Pathophysiologically, ulcers are categorized as acute or chronic. Acute ulcers have a short duration and heal quickly, whereas chronic ulcers involve deep erosion and long duration. A common cause of ulceration is infection with H. pylori or the use of NSAIDs like ibuprofen or naproxen. Gastric ulcers are less common, typically occurring in adults over $50\,years$. Duodenal ulcers are more frequent in the $35-45\,year$ age range and can erode through the entire stomach wall, leading to scarring.

Risk factors predisposing a patient to PUD include dietary factors, chronic H. pylori infection, use of NSAIDs and corticosteroids, caffeine, alcohol, smoking, certain diseases, and stress. Assessment cues vary by location. Gastric ulcers typically cause high epigastric pain that is gnawing and occurs $30-60\,minutes$ after eating; nausea and vomiting are common, and pain is often worse at night. In contrast, duodenal ulcers cause epigastric and back pain occurring $2-3\,hours$ after eating. Notably, eating food or taking antacids often relieves duodenal ulcer pain. If bleeding occurs, bright red blood indicates it has not transitioned far through the tract, while darker stools indicate older blood.

Diagnostics for PUD include endoscopy and tests for H. pylori via breath, blood, or stool samples. A biopsy may be performed during endoscopy to check for stomach cancer cells. A CBC may reveal an elevated WBC count indicating infection or low hemoglobin/hematocrit indicating anemia from bleeding. Priority interventions for acute care include making the patient NPO, providing IV fluids for dehydration, and administering blood transfusions if needed. Medications to heal the ulcer and antibiotics to eradicate H. pylori are essential. Chronic care involves stress reduction, smoking cessation, and diet control. Potential complications include hemorrhage, gastric outlet obstruction, and perforation, which is signaled by sudden, severe upper abdominal pain and a rigid, board-like abdomen. There is also a risk of gastric adenocarcinoma.

Pharmacologic therapy often uses combination treatments to eradicate H. pylori. Triple therapy consists of Clarithromycin + amoxicillin + a PPI. Quad therapy includes Bismuth subsalicylate + tetracycline + metronidazole + a PPI. Mucosal protectors like sucralfate (Carafate) are used to coat the stomach and should be taken on an empty stomach. Discharge planning should emphasize taking medication as prescribed (usually $4\,weeks$ for duodenal and $8\,weeks$ for gastric ulcers), avoiding NSAIDs/aspirin, and reporting symptoms like severe pain, fever, or blood in the emesis or stool.

Pyloric Stenosis

Pyloric stenosis is the narrowing of the pyloric canal between the stomach and the duodenum, which prevents food from passing into the small intestine. This occurs because the pylorus becomes enlarged and inflamed, creating a smaller opening. The definitive cause is unknown, but it develops after birth and is most common in young babies between $3-6\,weeks$ of age. Risk factors include Caucasian or Northern European ancestry, mothers treated with antibiotics late in pregnancy, babies treated with antibiotics in the first weeks of life, male gender, bottle feeding, premature birth, and smoking during pregnancy.

Cues for pyloric stenosis include projectile vomiting as the stenosis worsens and persistent hunger. A key clinical sign is an olive-shaped lump in the umbilicus region of the abdomen. Wavelike contractions may be seen across the abdomen. Due to the inability to pass food, babies may fail to gain weight or lose weight. Dehydration is a significant concern, monitored by the number of diapers, daily weights, and the status of fontanels (depressed fontanels indicate dehydration). Diagnostics involve an ultrasound to view the pylorus and serum electrolytes, specifically checking sodium and potassium levels.

Priority interventions include monitoring daily weights and intake and output (I&O). An NG tube is often used preoperatively to decompress the stomach. Surgery is the definitive treatment. Post-surgery, the infant remains NPO until feedings are ordered. Nurses must monitor for abdominal distention and initiate small feedings, often starting with clear liquids and advancing as tolerated. Complications include failure to thrive, jaundice, dehydration, electrolyte imbalances, and erosion or bleeding of the stomach. Parents should be instructed to report a fever greater than $101.3\,^{\circ}F$, vomiting after clear liquids, or redness, bleeding, or pus at the surgical site.

Cleft Lip and Palate

Cleft lip and palate are congenital abnormalities resulting from the incorrect closure or fusion of the lip and palate. This fusion may never occur or only occur partially, and it can be unilateral or bilateral. Pathophysiologically, this is often due to chromosomal or genetic abnormalities, exposure to teratogens (like smoking or diabetes during pregnancy), or environmental factors such as a lack of folic acid ($400\,mcg/day$) during the second month of pregnancy.

Assessment cues include feeding difficulties (as the baby cannot breastfeed normally), chronic ear infections, speech issues, hearing impairment, and airway obstruction risks. There is an extra opening where milk and bacteria can pass through, increasing the risk for aspiration. Cleft lip can often be detected on a prenatal ultrasound around $18-20\,weeks$. Surgery for a cleft lip is typically performed within the first $3-6\,months$, while a cleft palate is usually corrected within the first year of life.

Priority teaching for parents includes the use of special nipples for feeding and the necessity of feeding the baby in an upright position. Post-surgical care is critical: the baby should sleep on their side to protect the site, and pacifiers should be avoided after surgery. Nurses should teach the use of suction bulbs and the importance of rinsing the mouth with water using a syringe after feedings to maintain cleanliness at the surgical site. Daily weights and I&O monitoring are necessary to ensure adequate nutrition.

Benign Prostatic Hyperplasia (BPH)

Benign Prostatic Hyperplasia (BPH) is a noncancerous enlargement of the prostate that compresses the urethra, causing urinary obstruction. It is common in aging men and significantly affects the quality of life. The condition is influenced by androgens; as men age, testosterone decreases, making the prostate more sensitive to estrogen and less sensitive to dihydrotestosterone (DHT). Risk factors include age (90% of men by age $85$ have symptoms), smoking, heavy alcohol consumption, genetic predisposition, and a Western diet. Racial background also plays a role, with Black and Hispanic men developing symptoms earlier than White men, while Asian men develop them later.

Priority assessments for BPH focus on obstructive and irritative symptoms: urinary frequency, nocturia, hesitancy in starting urination, decreased force of the stream, abdominal straining, decreased volume, and post-void dribbling. Diagnostics include the PSA (Prostate-Specific Antigen) blood test, which should not be performed after a Digital Rectal Exam (DRE) as the exam will elevate PSA levels. Other tests include post-void residual urine tests to determine the volume of urine remaining in the bladder, urinalysis, uroflowmetry, and cystoscopy for visualization.

Pharmacologic therapy involves two main classes. Alpha-Adrenergic Blockers (e.g., Alfuzosin, Silodosin, Tamsulosin) relax smooth muscles in the bladder and prostate to improve urine flow; side effects include dizziness, orthostatic hypotension, and sexual dysfunction. 5-Alpha-Reductase Inhibitors (e.g., Finasteride, Dutasteride) serve to reduce the size of the prostate by interfering with testosterone production; side effects include decreased libido, erectile dysfunction, and gynecomastia (enlargement of breasts in men). Lifestyle changes include urinating at the first urge, avoiding alcohol and caffeine (which act as diuretics), and avoiding OTC cold/sinus medications that cause vasoconstriction. Surgery often involves a Transurethral Resection of the Prostate (TURP). For patients with continuous bladder irrigation (CBI) post-op, the calculation for true output is: $\text{Total drainage} - \text{Irrigant infused} = \text{Urine output}$. For example, if $200\,mL$ is infused and $500\,mL$ is collected, the actual urine output is $300\,mL$.

Encopresis and Enuresis

Encopresis is the voluntary or involuntary retention of stool, often leading to leakage. It usually results from a child being "too busy" and putting off defecation, leading to constipation, dilation of the lower bowel, and incompetence of the inner sphincter. This results in irregular, painful, hard stools and a potentially offensive body odor. Diagnostics include anorectal manometry and rectal motility tests. Treatment involves a high-fiber diet, ample fluids, and behavioral modification techniques like scheduled toilet-sitting. Medications like Miralax may be used to pull water into the GI tract.

Enuresis is bedwetting during sleep in children aged $7$ or older, and is more common in boys. Causes include maturational delay, uncompleted toilet training, or overproduction of urine at night. Treatment involves moisture alarms that alert the child to wake up when they sense fluid, bladder training, and occasionally medications like desmopressin. It is noted that "pull-ups" do not typically help train the child to use the potty.

Hypospadias and Epispadias

Hypospadias is a congenital condition where the urethral opening is located on the ventral surface (bottom) of the penis. Epispadias refers to an opening on the dorsal surface. Mild cases may not require treatment, but more severe cases require surgery to ensure normal sexual functioning and prevent psychological effects. Surgery is typically performed around $6\,months$ of age. Parents should be educated to delay circumcision, as the foreskin may be needed for the surgical repair.

Urinary Calculi (Kidney Stones)

Urinary calculi, or kidney stones, vary in size and can lodge anywhere in the urinary tract. Lithiasis refers to stone formation, while nephrolithiasis specifically refers to stones in the kidney. Risk factors include dehydration, UTIs, immobility, urinary stasis, and family history. Stones can be composed of calcium oxalate, calcium phosphate, uric acid, or struvite. Symptoms include renal colic (severe pain with sympathetic response), dull suprapubic pain (for bladder stones), and gross hematuria. If stones obstruct the ureter, it can lead to hydronephrosis, where pressure builds up behind the obstruction, potentially leading to renal failure.

Diagnostics include a $24-hour$ urine collection to measure calcium, phosphorus, and uric acid levels, as well as KUB (Kidney, Ureter, Bladder) X-rays, CT scans, and renal ultrasonography. Medical management focuses on pain control, hydration (PO and IV), and antiemetics for nausea. Lithotripsy (ESWL) uses shockwaves to break stones into smaller pieces that can be passed. Nurses should strain all urine to catch stones for chemical analysis and encourage a fluid intake of $2-3\,L$ of non-sugar-sweetened beverages.

Intestinal Bowel Obstruction

Intestinal obstructions can be mechanical (physical blockages like adhesions, hernias, or tumors) or non-mechanical (functional/paralytic ileus where motility stops). Small intestinal obstructions involve a proximal accumulation of contents, fluid, and gas, causing rapid onset of crampy pain, fecal vomiting, and dehydration. If a patient is vomiting acid, they may develop metabolic alkalosis. Laboratory tests may show slightly elevated WBCs and electrolyte imbalances (low sodium, chloride, and potassium).

Large bowel obstructions typically progress more slowly and are often caused by cancer, diverticular disease, or volvulus (twisting of the intestines). Cues include constipation, weight loss, anorexia, and ribbon-shaped stools. Management for both typically starts with NPO status, IV fluid replacement (isotonic solutions like LR or NS), and the insertion of an NG tube for bowel decompression. Absolute priority in small bowel obstruction is hydration and electrolyte monitoring. Surgery, such as a partial colectomy or colostomy, may be required if necrosis or absolute obstruction is present. Post-operative education includes following an ostomy care routine and avoiding heavy lifting.

Questions & Discussion

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