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Digestive System Disorders
NURS 202: Pathophysiology
Terms in this set (76)
Part of the stomach protrudes through the opening (hiatus) in the diaphragm into the thoracic cavity.
GERD (Gastroesophageal Reflux Disease)
* Results when LES is relaxed or ineffective.
* Permits reflux of gastric secretions (from stomach into lower portion of esophagus.
* S/S: Pain (burning, radiating up/down esophagus), Radiate to jaw, neck, back
* Prognosis: Depends on early identification and treatment
* Chronic Symptoms: No real progression of disease or alterations of distal esophageal mucosa
* Conservative Treatment: weight reduction, avoiding foods/drugs that increase acid secretion, and decrease LES pressure. High protein, low fat diet. Small frequent meals, avoid tobacco.
* Drugs: Proton pump inhibitors, Histamine 2 (H2) antagonists, antacids
* Nursing: provide education, maintain IV fluids, pain mgmt, NG tube latency and drainage, head elevated.
Respiratory status: facilitate deep breathing, coughing w/ splinting, monitor incision for redness/drainage, maintain closed-chest drainage system, discharge instructions regarding diet, meds and symptom management.
Peptic Ulcer Disease (PUD)
Acute or Chronic Inflammation (Altered gastric secretions - erosions in mucosal lining of the esophagus, stomach or duodenum).
* H. pylori: Breakdown of the mucosal lining
--> Cellular injury and inflammation
--> altered secretions and sustained inflammation
* Cause of Duodenal Ulcers: Vagus nerve
--> stimulates the antrum cells in pylorus --> release of gastrin.
* At Risk: H. Pylori, Alcohol Abuse, Smoking, Chronic NSAID use, Type O Blood, Chrohn's Disease
* S/S: Localized pain in epigastric area, Gastric Ulcer Pain (upper epigastrium, localized to left midline), Bleeding, Perforation of Ulcer
* Tx: Medications (PPI, H2 antagonists, mucosal protectants, antibiotics). Stress Modification Techniques, Surgery.
* Nursing: education, promote comfort, adequate hydration, nutrition. Checking for H. pylori.
* Post-Operative Complications:
--> Dumping Syndrome (after gastrectomy) - food rapidly enters jejunum and distention, fullness, cramping, nausea, rumbling, gurgling in bowel.
--> Anemia (loss of absorbing surface of intestine)
* Acute form of peptic ulcers
- Severe illness
- Systemic trauma
- Ulcers in the presence of burns are often called "Curling's Ulcers".
* S/S: painless upper GI tract bleeding (hemorrhage 2-3 days after initial injury).
* Tx: prevention, hemorrhaging stress ulcer (NG placement w/ suction, endoscopic procedure to treat bleeding).
* Nursing: identify pts at risk, assess for early s/s, assess stools for hidden/occult blood, assess for vital signs.
* Malignant neoplasm in the stomach
No single causative agent
* At Risk: Men twice as much as women, Chronic gastritis, H. pylori.
* S/S: vague, mild until cancer is advanced.
--> Initial signs include anorexia, feelings of indigestion
--> Epigastric discomfort, weight loss, fatigue, or feeling of fullness after eating.
--> Occult blood in stool, iron-deficiency anemia
* Tx: surgery (gastric resection), chemotherapy, radiation, Vitamin B12 injections
* Acute or chronic inflammation of the pancreas.
- auto digestion of the tissues...considered a medical emergency.
- follows premature activation of the pancreatic proenzymes within the pancreas itself.
* S/S: sudden onset may follow intake of a large meal or large amount of alcohol.
Severe epigastric or abdominal pain - radiating to the back is the primary symptom, pain increases when supine.
* Signs of shock - low BP, pallor, sweating, rapid weak pulse, low grade fever, and abdominal distention.
* Tests: serum amylase levels rise within 12-12 hours, fall after 48 hours. serum lipase are also elevated for around a week. Hypocalcemia is common.
* Tx: all oral intake stopped. bowel distention is relieved to reduce pancreatic stimulation. Analgesics given for pain relief (not morphine). IV fluids, Support nutrition (TPN, lipids), Medications (pancreatic enzymes, PPI, H2 antag, anticholinergics, antacids, antibiotics).
--> Peritoneal Lavage
--> Surgery (drain pancreatic duct, remove necrotic tissue)
* Nursing: NG patency, Vital signs, Monitor for evidence of hemorrhage, shock, infection, Restrictions (diet, alcohol).
* Mortality rate: 20% or higher in individuals with concomitant diseases or elderly persons,
1. Retching - begins with deep breath (lower esophageal)
2. Closing glottis, raising soft palate
3. Ceasing respiration
4. Relaxing gastro-esophageal sphincter
5. Contracting abdominal muscles
Characteristics of Vomitus
* Presence of blood - hematemesis
--> Coffee Grounds
* Yellow or green-stained vomitus
--> bile from the duodenum
* Deeper brown colour
--> May indicate content from lower intestine
*Recurrent vomiting of UNDIGESTED food
--> problem with gastric emptying or infection.
Excessive frequency of stools (loose or watery consistency)
--> Chronic (persists at least 2 weeks, May be occasional, brief or responsive
--> Nursing: environment, pt. concerns, assessment, skin, in/out, vitals, collection of stool samples, antidiarrheal medications
-- S/S: normal BMs (2-3 daily to one weekly), subjective
-- Pattern changes: less frequent, smaller stool volumes, difficulty moving stool through rectum
-- Can be occasional, or chronic (lifelong nuisance)
-- TX: goal is to return to normal bowel activity
-- Nursing: encourage reg. bowel fxn, diet/exercise, increase dietary fibre and fluid intake.
--> inflammation/ulceration of upper digestive tract
Dull Aching Pain
--> stretching of liver capsule
Cramping or diffuse pain
--> inflammation, distention, stretching of intestines
Colicky, often severe pain
--> smooth muscle spasms - severe inflammation/obstruction
Causes: vomiting, diarrhea, infection
At Risk: poverty, inadequate nutrient intake, substance abuse, over reliance of processed foods
S/S: weakness, lethargy, emaciate appearance, intolerance to cold, flaky skin
Labs: low Hgb
TX: high calorie/protein foods, fortified supplement, unable: TPN/enteral intake.
NURSING: identify pts at risk, dietary hx.
Child Onset Obesity
Related to a greater than normal number of fat cells, which are located over entire body.
Adult Onset Obesity
Related to greater than normal number of fat cells, which are centrally located.
Modifiable risk factors: diet high in sat. fats.
Biological mother obese: 75% chance of children becoming obese.
Disorders of the Oral Cavity
* Cleft lip or cleft palate (which arise in 6th or 7th week of gestation).
* Inflammatory lesions: Aphthous ulcers
--> Streptococcus sanguines may be involved
--> Small painful lesions
--> Usually heal spontaneously
* Candidiasis (Oral: Thrush):
--> Candidia albicans - causative agent
--> Risk: PTs on broad-spectrum antibiotics, cancer therapy, immunocompromised individuals or persons w/ disabilities
--> May appear red or swollen
--> White curd like patches
* Esophageal cancer is a fast-growing and metastasizing type of cancer.
* Most commonly in distal esophagus
* Significant dysphagia in later stages
* Poor prognosis due to late manifestations
* Treatment often involves several weeks of chemotherapy and radiation therapy followed by surgery.
* Nursing: Promote nutritional status, feeding tube patency, HOB 30 degrees, In/Outs, Daily Weights, Effective respiratory management.
* Gastric mucosa is inflamed
* May be ulcerated or bleeding
* May result from infection by microorganisms, allergies, spicy or irritating foods, excessive alcohol intake, ingestion of ASA or NSAIDS, corrosive or toxic substances, radiation/chemo.
* Basic Signs: anorexia, nausea, vomiting, hematemesis, epigastric pain, cramps, general discomfort, w/ infection, diarrhea may develop.
* Usually self-limiting
Characterized by atrophy of stomach mucosa.
--> Loss of secretory glands
--> Reduced production of intrinsic factor
--> H. pylori infection often present
--> Signs may be vague
--> Increased risk of peptic ulcers and gastric carcinoma
--> Certain autoimmune disorders are associated with one type of chronic gastric atrophy
Inflammation of the stomach and intestines
--> Usually caused by infection
--> May also be caused by allergic reactions to food or drugs
--> Microbes can be transmitted by fecal-contaminated water, soil or food.
--> Most infection safe self-limiting
--> May cause epidemic outbreaks in refugee or disaster settings
--> Safe sanitation essential for prevention
* A peptic ulcer, also known as PUD or peptic ulcer disease, is an ulcer (defined as mucosal erosions equal to or greater than 0.5 cm) of an area of the gastrointestinal tract that is usually acidic and thus extremely painful.
* As many as 70-90% of ulcers are associated with Helicobacter pylori, a spiral-shaped bacterium that lives in the acidic environment of the stomach; however, only 40% of those cases go to a doctor.
Ulcers can also be caused or worsened by drugs such as aspirin, Plavix (clopidogrel), ibuprofen, and other NSAIDs.
* Locations: most commonly found in the proximal duodenum (duodenal ulcers) or the the antrum of the stomach (gastric ulcers)
Development begins with the breakdown of mucosal barrier.
--> inadequate blood supply
--> excessive glucocorticoid secretion or medication
--> atrophy of gastric mucosa
--> increased acid-pepsin secretions
* Complications with the peptic ulcer
* Signs/Symptoms: epigastric burning, localized pain usually
* Diagnostic Tests: fiberoptic endoscopy, barium x-ray, endoscopic biopsy
* Treatment: combination of antimicrobial and proton pump inhibitor to eliminate H. pylori, reduction of exacerbating symptoms
Acute gastric mucosal lesions occuring after medical crisis or trauma
First indicator - hemorrhage and severe pain
*Malignant tumor of the stomach.
*Arises primarily in the mucous glands
*Mostly in the antrum or pyloric areas
*Early carcinoma: confined to mucosa and submucosa
*Later stages: involves muscularis, and eventually invades serosa and spreads to lymph.
*Asymptomatic in the early stages (often poor prognosis)
*Diet seems to be key factor (smoked foods, nitrates, nitrites)
*Genetic influences play role
*Symptoms are vague until cancer is advanced
*Surgery together with chemo, and radiation may relieve symptoms.
*Survival rate less than 20%
* Control of gastric emptying is lost or gastric contents are "dumped" without complete digestion
* May follow gastric digestion
* Hyperosmolar chyme draws fluid from vascular compartment into intestine - resulting in intestinal distention, increased intestinal motility, and decreased BP
* Occurs during or shortly after meals.
* Hypoglycemia 2-3 hours after meal.
* May be resolved by dietary changes (freq small meals, high in protein, low in simple carbs)
* Often resolves over time.
Narrowing of the pyloric sphincter that blocks the passage of food from the stomach into the duodenum
May be a developmental anomaly
Signs appear within several weeks after birth
--> Projectile vomiting immediately after feeding
--> Firm mass can be palpated at pylorus
--> Infant fails to gain weight
--> Surgery required to remove obstruction
--> May be acquired later in life
--> Persistant feeling of fullness
--> Increased incidence of vomiting
Abnormal condition of gallstones
Solid material (calculi) that form in bile
Acute or chronic inflammation of the gallbladder and cystic duct
Acute inflammation of the bile duct characterized by pain in the upper-right quadrant of the abdomen, fever, and jaundice.
Bile duct obstruction due to gallstones. This ranges from asymptomatic to common bile duct obstruction, which can lead to dilation of the common bile duct and bacterial overgrowth.
Systemic infection can result
A stone formed in the biliary tract, consisting of cholesterol or bile pigments and calcium salts.
Small - silent and excreted in bile
Large - obstruct flow of bile in cystic or common bile ducts - causing severe pain, which is often referred to sub scapular area
Risk Factors for Gallstones
--> Female gender, obesity, rapid weight loss (starvation diets-body depends on lipids for energy leading to breakdown of ketones), pregnancy (usually only symptomatic after pregnancy), medications (estrogens, thiazides, and some cholesterol medication like Questran).
Yellowing of the skin and whites of the eyes from a backup of bile metabolic by-products from the blood into body tissues. May result from blockage of the ducts draining bile from the liver into the intestines or excessive breakdown of red blood cells. Hemoglobin from destroyed RBC' s is broken down, and in part, ends up in bile secretions.
Excessive destruction of RBCs in which the liver is unable to handle the additional bilirubin
Described as hemolytic anemia.
Caused by cirrhosis or hepatitis and the necrosis of liver cells.
after liver and before intestines, occurs when bile flow is obstructed between the liver and the intestine
A widespread inflammation of liver cells, usually caused by a virus
Alcholic: fatty liver
Idiopathic: fatty liver
Viral: local infection
Infection elsewhere in body: infectious mononucleosis/amebiasis
Chemical or drug toxicity
A,B,C,D,E - System infection that primarily affects liver cells. Blood testing is needed to distinguish b/t different types of hepatitis.
--> Only body defense is formation of antibodies via vaccination
--> Supportive Measures: rest, diet (high in carbs, proteins, vitamins)
--> Chronic hepatitis can be treated with interferon
Hepatitis A (HAV)
Formerly called infectious hepatitis. It is caused by enterically transmitted (oral-fecal route)
Hepatitis B (HBV)
Serum hepatitis. Transmission: blood & body fluids. Yes-chronic carriers have increased risk for hepatocellular cancer. Spread & Source: contaminated needles, syringes & blood products
Hepatitis C (HCV)
Common cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma, contracted through sexual contact or blood transfusion
Hepatitis D (HDV)
Occurs with RNA virus and occurs ONLY concurrently with acute or chronic HBV.
Incomplete RNA virus, also called delta virus
Hepatitis E (HEV)
transmitted by fecal-oral route, usally through contaminated water
The first stage of hepatitis preceding the appearance of jaundice; includes flu-like symptoms
The second stage of hepatitis, which includes the appearance of jaundice & associated symptoms such as elevated bilirubin levels, dark or tar-colored urine & clay-colored stools
The convalescent stage of hepatitis in which the jaundice decreases and the color of the urine and stool return to normal.
Weakness persists for weeks.
Toxic or Nonviral Hepatitis
Chemicals or drugs cause inflammation and necrosis in the liver.
Drugs: acetaminophen, halothane, phenothiazines, tetracycline.
Chemicals: carbon tetrachloride, toluene, ethanol
Direct effect of toxins.
May result from sudden exposure to large amounts or lower dose over longterm.
Chronic disease of the liver with gradual/progressive destruction of cells and formation of scar tissue of the liver; commonly caused by alcoholism.
cirrhosis characterized by a prolonged state of jaundice because of retention of bile and bile duct inflammation
caused by viral hepatitis and certain drugs or chemicals
inflammation and scarring from metabolic disease
Initial: Fatty Liver
--> Enlargement of liver
--> Asymptomatic (reversible with reduced alcohol intake)
Secondary: Alcoholic hepatitis
--> Inflammation and cell necrosis
--> Fibrous scar tissue formation (irreversible change)
Tertiary Stage: End-stage cirrhosis
--> Fibrotic tissue replaces normal tissue
--> Little normal function remains
Functional Losses with Cirrhosis
- Decreased removal and conjugation of bilirubin
- Decreased production of bile
- Impaired digestion, absorption of nutrients
- Decreased production of blood-clotting factors
- Impaired glucose/glycogen metabolism
- Impaired conversion of ammonia to urea
- Decreased inactivation of hormones and drugs
--> Drug dosages must be carefully monitored to avoid toxicity
- Decreased remove of toxic substances
- Reduction of bile entering intestine (impaired digestion and absorption)
- Backup of bile in the liver (obstructive jaundice)
- Blockage of blood flow through the liver (portal hypertension)
- Congestion in the spleen (increasing hemolysis)
- Inadequate storage of iron, Vitamin B12
- Congestion in intestinal walls and stomach
- Development of esophageal varices (hemorrhage)
- Develops of ascites (accumulation of fluid in peritoneal cavity, which causes abdominal distention and pressure)
Initial Cirrhosis Manifestations
Fatigue, anorexia, weight loss, anemia, diarrhea, dull aching pain may be present in URQ.
Advanced Cirrhosis Manifestations
Ascites, peripheral edema, increased bruising, esophageal varices (may rupture, leading to hemorrhage, circulatory shock), jaundice, encephalopathy.
Treatment for Cirrhosis
* Avoidance of alcohol or specific cause
* Supportive or symptomatic treatment
* Dietary restrictions
* Balancing serum electrolytes
* Antibiotics to reduce intestinal flora
* Emergency treatment if esophageal varices rupture
* Liver transplant
-> Most commonly occurs as secondary tumor that has metastasized from breast, lung, or from other GI structures
-> Primary tumors are rare in US, but common worldwide,
-> Causes of primary tumours = chronic cirrhosis and hepatitis
-> Diagnosis usually occurs with advanced stages
-> Chemotherapy - possible lobectomy or radio frequency ablation (RFA) procedure
--> Inflammation of the pancreas
--> Results in auto digestion of the tissue
--> May be acute or chronic (acute is considered medical emergency)
--> Pancreas lacks a fibrous capsule, and destruction may progress into tissue surrounding the pancreas.
--> Substances released by necrotic tissue lead to widespread inflammation (hypervolemia and circulatory collapse may follow)
--> S/S: severe epigastric or abdominal pain, radiating to the back (primary symptoms), signs of shock (due to hypervolemia), low-grade fever until infection develops (then rises), abdominal distention and decreased bowel sounds.
--> Diagnostic Tests: serum amylase (first rise, then fall after 48 hours), serum lipid levels are elevated, hypcalcemia, leukocytosis.
--> Treatment: oral intake is stopped, treatment for shock and electrolyte imbalances, and analgesics for pain relief.
escape of bile, blood, or pancreatic secretions into peroneal cavity due to rupture
septicaemia may result
* Risk Factors: smoking, pancreatitis and dietary factors
* Weight loss and jaundice early manifestations
* Frequently asymptomatic until well advanced
* Metastases occur early (mortality rate is close to 95%)
A cancer originating in glandular tissue
* Malabsorption syndrome
* Intolerance to gluten (protein component of wheat, barley, and oats
* Appears to have genetic link
* Defect in intestinal enzyme
* Destruction of mucosal cells
* First signs appear when cereals are added (4-6mos)
-> Steatorrhea (presence of excess fat in feces), muscle wasting, failure to gain weight, irritability, and malaise.
-> Diagnosed by a series of blood tests
-> Gluten-free diet for treatment, and medications include: corticosteroids, antidiarrheal, anticholinergics. Infants: Vitamin D
Chronic Inflammatory Bowel Disease (IBDs)
* Chrohn's Disease and Ulcerative Colitis are chronic IBDs
* Causes unknown
* Genetic factor appears to be involved
* Chrohn's: often occurs during adolescence
* Ulcerative Colitis: Second or Third decade
* Many similarities between Chrohn's and UC.
Irritable bowel disease that produces inflammation & damage anywhere along the GI tract.
* "Skip lesions" - affected areas separated by areas of normal tissue.
* Progressive inflammation and fibrosis may cause obstructed area...the damaged walls impair processing and absorption of food. The inflammation stimulates intestinal motility.
* Interference with digestion and absorption.
--> Hypoproteinemia, Avitaminosis, Malnutrition, and possibly steatorrhea.
* S/S: nonbloody diarrhea
* Other complications: adhesions between loops may form and fistulas (an abnormal passage between a hollow or tubular organ and the body surface, or between two hollow or tubular organs) may develop.
* Children will suffer from delayed growth and sexual maturation.
* Glucocorticoid used in treatment
* Highest in females 15-25 years of age
* Inflammation inside of the rectum
* Cause unknown
* Start in rectum and move up the colon
* Edema and Hyperemia (increased blood flow to bowel mucosa)
* Multiple bowel abscesses (ulcerations --> bleeding, which leads to increased peristalsis, and diarrhea.
* Progresses through the colon
* Mucosa and submucosa are inflamed
--> Tissue destruction interferes with absorption of fluid and electrolytes in the colon
* Severe acute episodes (toxic megacolon) may develop
* Diarrhea marked with up to 12 stools per day.
--> Containing blood and mucus. Cramping pain.
* At risk - urban, upper middle class, higher educated populations. Women more than men, 20-40 years old.
* S/S: blood diarrhea, cramping abdominal pain
* Progressive (periods of exacerbation and remission)
Treatment for IBD
* Team Approach
* Anti-inflammatory medications
--> Sulfasalazine, or glucocorticoids
* Antimotility agents
* Nutritional supplements
* Immunotherapeutic agents
* Surgical resection (ileostomy, or colostomy) - only for complications of Chrohn's
* Health Teaching: medication, diet, stress-mgmt.
* Community resource groups
* Monitor drug therapy, ins/outs
Acute inflammation of the appendix obstruction of lumen by feces, parasites, foreign body
* Fluid buildup inside the appendix, microorganisms proliferate.
Most common cause of paediatric abdominal surgery and most common cause of surgical emergency in childhood- if rupture occurs.
If rupture occurs: release of contents into peritoneal cavity.
Result: Generalized peritonitis (may be life-threatening)
Treatment: surgical removal of appendix and application of antimicrobial drugs
Appendicitis Signs and Symptoms
General periumbilical pain
Nausea and vomiting
Pain (severe) and localized to LRQ (rebound tenderness develops)
After rupture: pain subsides temporarily.
Pain recurs (severe generalized abdominal pain and guarding).
Low-Grade fever and leukocytosis
"Boardlike" abdomen (peritonitis caused muscles to spasm)
Development of diverticula
- Forms gaps between majuscule layers
- Congenital weakness of wall may be a factor
- Weaker areas bulge when pressure increases
- S/S: Cramping, Tenderness, Nausea, Vomiting, Δ Bowel Habits, Distention, Slight Fever, Elevated White Blood Cell Count
Treatment: Antimicrobial drugs, dietary modifications. Colonoscopy, High-Fiber Diet, Antibiotics, Pain Control, NG Tube, IV Fluids, Surgery (Colon Resection)
Outpouching (herniation) of the mucosa through the muscular layer of the colon
Asymptomatic diverticular disease
Inflammation of the diverticula
Common problem in the Western world, affecting primarily older individuals.
*Adenocarcinoma of the colon or rectum, or both.
*Most malignancies develop from adenomatous (tumor is a benign tumor of epithelial tissue with glandular origin, glandular characteristics, or both) polyps.
*Early diagnosis is essential.
*Cancer occurs primarily in persons over 50 years of age.
*Risk Factors: Genetics, Long-term ulcerative colitis, Environmental Factors, including diet low in fiber.
*Initial Signs: depend largely on the location of the growth.
*General Signs: Change in bowel habits (alternating diarrhea and constipation), Bleeding, Fatigue, Stool is ribbon-lik, Weightloss, Anemia.
*Treatment: Surgical removal with radiation and/or chemotherapy. Ostomy and ostomy bag.
Lack of movement of intestinal contents through the intestine.
--> Mechanical obstructions (tumors, adhesions, hernias, etc)
--> Functional or dynamic obstructions (impairment of peristalsis -- spinal cord injury, paralytic ileus (disruption of the normal propulsive ability of the gastrointestinal tract) due to toxins or electrolyte imbalance
--> Gases or fluids accumulate proximal to blockage, distending the intestine.
--> Increasing strong contractions of proximal intestine (effort to move contents along)
--> Pressure increases in lumen
--> Compression of veins in wall
--> Intestinal wall becomes oedematous
--> Prevention of absorption
--> Intestinal distention leads to persistent vomiting
--> This leads to additional loss of fluid and electrolytes
--> Hypovolemia can result
--> Intestinal awl becomes ischemic and necrotic (if obstruction is not removed, gangrene ensues).
--> Ischemia and necrosis (decreased innervation, and cessation of peristalsis)
--> Paralytic ileus occurs if it is not a cause to begin with.
Usually temporary paralysis of intestinal wall that may occur after abdominal surgery or peritoneal injury and that causes cessation of peristalsis; leads to abdominal distention and symptoms of obstruction
Acute inflammation of the serous membrane lining the abdominal cavity and covering the abdominal viscera.
May result form chemical irritation or directly from bacterial invasion of the sterile peritoneal cavity.
- Sudden, severe, generalized abdominal pain
- Localized tenderness at site of underlying problem
- Vomiting is common
- Dehydration, hypovolemia, low BP, tachycardia, fever, leukocytosis
- Depends on primary cause
- Surgery might be required
- Massive antimicrobial drugs (specific to causative organism).
inflammation of the peritonium due to a ruptured appendix, direct trauma, or intestinal obstruction and gangrene
Pelvic Inflammatory Disease
Infection of the upper female genital tract-the cervix, uterus, fallopian tubes, and ovaries
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