Adult Health 1 Exam 2 – Vocabulary Practice Flashcards
Ulcerative Colitis (UC)
Definition and Pathophysiology
Ulcerative colitis is a chronic inflammatory bowel disease (IBD) characterized by the immune system mistakenly attacking the lining of the colon and rectum.
The inflammation starts in the rectum and spreads continuously through the colon.
Unlike other forms of IBD, UC affects only the inner lining of the bowel, resulting in extensive irritation and bleeding of the intestinal mucosa.
Clinical Manifestations
The hallmark symptom of ulcerative colitis is bloody diarrhea.
Patients often experience frequent bowel movements containing both blood and mucus due to the inflammation of the intestinal lining.
Pain is typically localized to the left lower quadrant (LLQ) of the abdomen because the descending and sigmoid colon are the areas most frequently involved.
During severe exacerbations, a patient may experience to liquid stools per day.
Laboratory Findings and Physiological Impact
Dehydration and Electrolytes: High frequency of liquid stools puts patients at risk for the loss of sodium (), potassium (), and chloride ().
Protein Levels: Inflamed bowel walls lead to protein loss, resulting in low serum albumin levels.
Hematology: Blood loss through diarrhea can result in anemia, indicated by low hemoglobin () and hematocrit () values.
Inflammatory Markers: Because inflammation is systemic throughout the colon, tests often show elevated White Blood Cell (WBC) counts, elevated Erythrocyte Sedimentation Rate (ESR), and elevated C-reactive protein (CRP).
Medical Emergencies and Complications
GI Bleeding: Sudden development of large amounts of blood in the stool, dizziness, tachycardia, or signs of shock constitute a medical emergency.
Colorectal Cancer: Chronic inflammation damages colon cells over time, increasing the long-term risk of malignancy.
Pharmacological Interventions
Aminosalicylates: Medications such as sulfasalazine are used to reduce inflammation in the intestinal lining and maintain remission.
Corticosteroids: Drugs like prednisone are used for acute exacerbations to rapidly suppress inflammation and decrease bleeding.
Steroid Side Effects: Long-term use can lead to osteoporosis, hyperglycemia, increased infection risk, peptic ulcers, and adrenal suppression.
Nutritional Support
During flare-ups, a high-protein, low-fiber diet is required. Protein facilitates healing, while low fiber reduces bowel stimulation.
Avoidance of triggers: Spicy foods, alcohol, caffeine, and dairy products.
Severe cases may require the patient to be NPO (nothing by mouth) for bowel rest, utilizing Total Parenteral Nutrition (TPN).
Key NCLEX Point
If a question describes bloody diarrhea, mucus in the stool, and left lower quadrant pain, the diagnosis is usually ulcerative colitis.
Crohn’s Disease
Definition and Pathophysiology
Crohn’s disease is a form of IBD that can affect any part of the gastrointestinal tract from the mouth to the anus.
It most commonly affects the terminal ileum, located in the right lower quadrant (RLQ).
Unlike UC, the inflammation extends through the entire bowel wall (transmural).
Skip Lesions: Patches of diseased bowel are separated by healthy tissue, creating a "cobblestone" appearance upon diagnostic visualization.
Clinical Manifestations
Chronic diarrhea (not typically bloody).
Right lower quadrant (RLQ) abdominal pain.
Significant weight loss and fatigue.
Steatorrhea: Fatty stools resulting from malabsorption of fats.
Complications
Fistulas: Abnormal connections between two body structures.
Strictures: Narrowing of the intestinal lumen, which may lead to bowel obstruction.
Nutritional and Laboratory Impact
Vitamin B12: Because the terminal ileum is the site for absorption, patients often develop deficiency and megaloblastic anemia.
Malnutrition: Diseased bowel prevents proper nutrient absorption, resulting in decreased albumin levels and severe weight loss.
Management: High-calorie, high-protein diets are essential. TPN may be necessary if oral intake is insufficient.
Key NCLEX Point
If a question mentions cobblestone lesions, fistulas, skip lesions, RLQ pain, or steatorrhea, think Crohn’s disease.
Appendicitis
Pathophysiology
Caused by an obstruction of the appendix, often by fecal material (fecalith), leading to bacterial invasion and inflammation.
It is a surgical emergency because delay can result in rupture.
Clinical Presentation
Classic pain pattern: Begins as vague periumbilical pain and then migrates to the right lower quadrant (RLQ).
McBurney’s Point: Tenderness at this specific RLQ location is a classic finding.
Associated symptoms: Nausea, vomiting, anorexia, fever, and rebound tenderness.
Diagnosis and Nursing Care
Labs: Leukocytosis ($↑ WBC$) is typical.
Imaging: CT scans and ultrasounds are used for confirmation.
Priorities: Keep the patient NPO, administer IV fluids, and monitor for rupture signs while preparing for surgery.
Contraindications: Never use heating pads or laxatives, as these increase the internal pressure and the risk of the appendix rupturing.
Key NCLEX Point
Periumbilical pain that migrates to the RLQ is the hallmark sign of appendicitis.
Peritonitis
Definition and Etiology
Life-threatening inflammation of the peritoneum (the membrane lining the abdominal cavity).
Common causes include a ruptured appendix, perforated peptic ulcer, or perforated diverticulum, allowing bacteria to enter the abdominal cavity.
Clinical Manifestations
The patient usually appears acutely ill and remains very still, as movement exacerbates pain.
Rigid, board-like abdomen: Caused by intense muscle guarding.
Other signs: Fever, abdominal distention, rebound tenderness, and absent bowel sounds.
Complications and Treatment
Complications include sepsis, hypovolemic shock, acute kidney injury (AKI), and electrolyte imbalances.
Management: NPO status, IV fluids, broad-spectrum antibiotics, and NG tube insertion for gastric decompression.
Surgery is frequently indicated to repair the source of the contamination.
Key NCLEX Point
A rigid, board-like abdomen is strongly associated with peritonitis.
Diverticulosis and Diverticulitis
Diverticulosis
Small pouches (diverticula) form in weakened areas of the intestinal wall, often due to chronic constipation and low-fiber diets.
Common in older adults and often discovered incidentally during colonoscopy.
Prevention: High-fiber diet, adequate fluid intake, and exercise to reduce colonic pressure.
Diverticulitis
Occurs when diverticula become inflamed or infected.
Symptoms: Left lower quadrant (LLQ) pain, fever, nausea, vomiting, and elevated WBC counts.
Management: Bowel rest, IV fluids, and antibiotics. A low-fiber or clear liquid diet is used only during the acute flare-up.
Contraindications: Rectal procedures and enemas are avoided during the acute phase due to perforation risk.
Key NCLEX Point
Left lower quadrant pain combined with fever usually suggests diverticulitis.
Pyelonephritis
Definition
A bacterial kidney infection that typically ascends from the bladder. Escherichia coli (E. coli) is the most frequent causative agent.
Clinical Presentation
Symptoms: Fever, chills, flank pain, and costovertebral angle (CVA) tenderness.
Urinary symptoms: Dysuria, frequency, and urgency.
Systemic signs: Nausea, vomiting, and confusion (especially in elderly patients).
Nursing Management
Priorities: Administer prescribed IV antibiotics and encourage hydration to flush the urinary tract.
Analgesia: Acetaminophen is preferred. Non-steroidal anti-inflammatory drugs (NSAIDs) should be avoided as they may worsen kidney injury.
Key NCLEX Point
Flank pain accompanied by costovertebral angle tenderness is highly suggestive of pyelonephritis.
Glomerulonephritis
Etiology and Pathophysiology
Commonly follows a streptococcal infection (e.g., strep throat).
Inflammation damages the glomerular membrane, leading to the leakage of blood and protein into the urine.
Clinical Presentation
Hematuria (blood in urine) and proteinuria (protein in urine).
Oliguria (low urine output).
Hypertension and facial or periorbital edema.
Diagnostic Findings and Care
Accumulation of waste results in elevated Blood Urea Nitrogen (BUN) and creatinine, and a reduced Glomerular Filtration Rate (GFR).
Nursing interventions: Strict intake and output (I&O) monitoring, daily weights, and blood pressure monitoring.
Restrictions: Fluid, sodium (), and protein restrictions as prescribed to reduce renal stress.
Key NCLEX Point
A history of strep throat followed by hematuria and periorbital edema identifies glomerulonephritis.
Nephrotic Syndrome
Pathophysiology
Damage to the glomeruli leads to massive proteinuria (leaking of large amounts of protein into the urine).
Low serum albumin results in a drop in plasma oncotic pressure, causing fluid to shift into the tissues (generalized edema/anasarca).
The liver increases lipid production to compensate for protein loss, causing hyperlipidemia.
Clinical Manifestations
Massive proteinuria and hypoalbuminemia.
Generalized edema and significant weight gain.
Fatigue and frothy urine (due to high protein content).
Management
Treatment: Diuretics for edema, ACE inhibitors or ARBs to reduce protein loss, and statins for lipid management.
Nursing focus: Daily weights, I&O, abdominal girth measurement, and monitoring skin integrity.
Key NCLEX Point
The classic triad for Nephrotic Syndrome is proteinuria + hypoalbuminemia + generalized edema.