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Nursing Diagnosis 

Topic Genitourinary Male/Female & Gynecological Concerns

– Introduction

– Body 

– Conclusion

– References

Gastrointestinal Diseases

Group 5:

Leticia Bernal Leon

Daydig Rodriguez

Maria Rodriguez

Karina Silveira

Instructor:

Dr. Alain Llanes Rojas, DNP, APRN, FNP-BC

Miami Regional University

Diagnosis, Symptoms & Illness Management

MSN5600

Gastroesophageal Reflux

Gastroesophageal reflux that does not cause symptoms is known as physiologic reflux. In nonerosive reflux disease (NERD), individuals have symptoms of reflux disease but no visible or minimal esophageal mucosal injury

Gastroesophageal reflux disease (GERD) is the reflux of acid and pepsin or bile salts from the stomach to the esophagus that causes esophagitis. The severity of the esophagitis depends on the composition of the gastric contents and esophageal mucosa exposure time.

Definition & Classification

Gastroesophageal Reflux

Causes

GERD can be caused by abnormalities or alterations in

1. Lower esophageal sphincter function

2. Esophageal motility

3. Gastric motility or emptying

Esophageal function studies include the following:

Determination of the lower esophageal sphincter (LES) pressure (manometry)

Graphic recording of esophageal swallowing waves, or swallowing pattern (manometry)

Detection of reflux of gastric acid back into the esophagus (acid reflux)

Detection of the ability of the esophagus to clear acid (acid clearing)

An attempt to reproduce symptoms of heartburn (Bernstein test)

Gastroesophageal Reflux

Risk Factors

Obesity

Hiatal hernia

Use of drugs or chemicals that relax the LES (anticholinergics, nitrates, calcium channel blockers, nicotine)

Cigarette smoke.

Trigger Factors

Coughing

Vomiting

Straining at stool

Asthma

Chronic cough

Sinusitis.

Gastroesophageal Reflux

Common Symptoms

Heartburn that occurs 30 to 60 minutes after meals and when the patient bends over or lies down.

Regurgitation of sour or bitter gastric contents

Belching, and fullness of the stomach

Upper abdominal pain within 1 hour of eating.

Atypical Symptoms

chronic cough

asthma attacks

chronic laryngitis

sinusitis

discomfort during swallowing.

Noncardiac chest pain.

Dysphagia

Gastroesophageal Reflux

Clinical manifestations are related to mucosal injury from acid regurgitation and the frequency and duration of reflux events.

The symptoms worsen if the individual lies down or if intraabdominal pressure increases because of coughing, vomiting, or straining at stool.

Uncomplicated GERD that is responsive to first-line therapy does not require an endoscopy.

Patients who do not respond to therapy and those with suspected complications should undergo an endoscopic examination

Management & Evaluation

Differential diagnosis

Gastritis

Peptic ulcer

Gastric cancer

Cholelithiasis

Angina pectoris.

Gastroesophageal Reflux

Diagnosis of GERD is based on the history and clinical manifestations.

An upper endoscopy with biopsy is the standard diagnostic procedure for GERD. It confirms the diagnosis and documents the type and extent of tissue damage.

Esophageal endoscopy: shows hyperemia, edema, erosion, and strictures. Esophagitis is divided into four grades, which are determined endoscopically:

Grade 1 is defined by erythema of the distal esophagus.

Grade 2 consists of scattered erosions.

Grade 3 involves confluence of erosions involving less than 50% of the diameter of the esophagus.

Grade 4 involves confluence of erosions involving greater than 50% of the diameter.

Tissue biopsy: Dysplastic changes can be identified (Barrett esophagus)

Impedance/pH monitoring measures the movement of stomach contents upward into the esophagus and the acidity of the refluxate.

H. pylori Test: it is detected using the urea breath test, this is the most accurate method.

H. pylori–specific serum immunoglobulin G (IgG) and immunoglobulin A (IgA) antibodies.

Measurement of H. pylori stool antigen levels.

Diagnosis

Gastroesophageal Reflux

For most patients, empiric treatment is initiated based on the severity of symptoms, history, and physical examination.

If H. pylori bacterium is present

Combination of antibiotics to kill the bacterium will be ordered for two weeks

(amoxicillin, clarithromycin, metronidazole, tinidazole, tetracycline and levofloxacin)

The antibiotics used will be determined by patient characteristics and current antibiotic resistance rates.

Eliminating or reducing use of injurious drugs, alcohol consumption and smoke cessation

Help the ulcer to heal with medication.

Proton pump inhibitors are the agents of choice for controlling symptoms and healing esophagitis. These drugs require at least 30 minutes to take effect; they also can be taken before a meal

(omeprazole, lansoprazole, rabeprazole, esomeprazole and pantoprazole)

Histamine H2-receptor antagonist to reduce acid production

(famotidine, cimetidine and nizatidine)

Antacids to neutralize stomach acid it can provide symptom relief

Cytoprotective agents to protect the lining of GI Tract

(sucralfate and misoprostol)

Prokinetics to reduce reflux by increasing LES tone and promoting peristalsis and gastric emptying.

(metoclopramide or bethanechol)

Treatment

Laparoscopic fundoplication is the most common surgical intervention when medical treatment fails.

Gastroesophageal Reflux

Nonpharmacological Treatment (Lifestyle Modification Treatment)

Sit up for at least 1 hr after eating.

Elevate head of bed 6-8 in, using blocks.

Avoid straining, lifting, bending over, and wearing tight belts, especially on a full stomach.

Avoid drugs that decrease lower esophageal sphincter pressure such as theophylline, nitrates, calcium channel blockers, α-adrenergic antagonists, β-agonists, and benzodiazepines.

Avoid anticholinergics and other drugs that decrease salivation; avoid drugs that decrease peristalsis.

Avoid foods that decrease lower esophageal sphincter pressure such as onions, garlic, mint, and alcohol.

Avoid foods that are esophageal irritants such as citrus, vinegar, caffeine, chocolate, peppermint, red sauces, spicy and high-fat foods, and large meals, as well as excessive fluid intake with meals.

Cease smoking and alcohol use to reduce GI and esophageal irritation.

Strive for a gradual, sustained loss of 2 lb per month if overweight.

Gastroesophageal Reflux

Most patients have very mild disease, although it is possible for the patient to develop rare complications such as:

Active erosive esophagitis: Severe esophagitis causes mucosal injury and inflammation with hyperemia, increased capillary permeability, edema, tissue fragility, erosions, and ulcerations

Fibrosis and thickening may develop. Edema, fibrosis (strictures), esophageal spasm, or decreased esophageal motility may result in dysphagia with weight loss.

Esophageal adenocarcinoma: In all, 10% of patients with GERD develop Barrett’s esophagus, precancerous lesions (Barrett esophagus) with progression to adenocarcinoma can be a long-term consequence.

Complications

Gastritis

Definition

Gastritis is an inflammatory disorder of the gastric lining. This injury to the mucus lined barrier that protect the stomach wall allows digestive juices to damage the stomach. It can affect the corpus, fundus or antrum, or the entire mucosa (pangastritis).

The most common Causes are:

Drugs and chemicals like Nonsteroidal anti-inflammatory drugs (ibuprofen, naproxen, or indomethacin), aspirin, chemotherapeutic agents, alcohol, and cigarette smoke

Helicobacter pylori infection–Shock and hypotension can decrease mucosal blood flow contributing to acute gastritis.

Gastritis can be:

Acute: occur suddenly.

Chronic: appear slowly over the time and involves chronic inflammation, mucus atrophy, and epithelial metaplasia that progresses over years.

Classification

Gastritis

Gastritis

Chronic gastritis is usually classified as:

Type A, or immune (fundal) is the most rare and severe form of gastritis and is associated with loss of T-cell tolerance and development of autoantibodies against parietal cells or intrinsic factor, or both. Pernicious anemia can develop from decreased vitamin B12 absorption and is a risk factor for gastric carcinoma

Type B, nonimmune (antral) associated with H. pylori that may trigger the immune response. Chronic use of alcohol, tobacco, and nonsteroidal anti-inflammatory drugs are contributing factors. H. pylori can also progress to autoimmune atrophic gastritis and involve the fundus, thus becoming pangastritis

Type AB, or pangastritis (types of chronic gastritis occur and the antrum is more severely involved.

Type C, is associated with reflux of bile and pancreatic secretions into the stomach, causing chemical injury.

Gastritis

Symptoms can usually be managed with consumption of smaller meals, and including a soft, bland diet.

Burning ache in upper abdomen

Nausea

Vomiting

Anorexia

Feeling of fullness in upper stomach after eating

Epigastric tenderness

bleeding

Symptoms

Gastritis

Doctor may first take a medical history and perform a physical exam, then diagnostic tests will be ordered, such as:

Laboratory tests for H. pylori.

H. pylori is detected using the urea breath test, this is the most accurate method.

H. pylori–specific serum immunoglobulin G (IgG) and immunoglobulin A (IgA) antibodies.

Measurement of H. pylori stool antigen levels.

Endoscopy.  An endoscopy with biopsy is the standard diagnostic procedure. It confirms the diagnosis and documents the type and extent of tissue damage.

Upper gastrointestinal series (barium swallow): creates images of your esophagus, stomach, and small intestine. During the X-ray, you swallow a white liquid (containing barium) that coats your digestive tract and makes an ulcer more visible.

Diagnosis

Differential Diagnosis

GERD

PUD

Cholecystitis

Pancreatitis

Diverticulosis

IBS

Usually, treatment will involve killing the H. pylori bacterium if it is present:

Combination of antibiotics to kill the bacterium will be ordered for two weeks

(amoxicillin, clarithromycin, metronidazole, tinidazole, tetracycline and levofloxacin)

The antibiotics used will be determined by patient characteristics and current antibiotic resistance rates.

Eliminating or reducing use of injurious drugs, alcohol consumption and smoke cessation.

Help the ulcer to heal with medication.

Proton pump inhibitor to block acid production and promote healing.

(omeprazole, lansoprazole, rabeprazole, esomeprazole and pantoprazole)

Histamine H2-receptor antagonist to reduce acid production

(famotidine, cimetidine and nizatidine)

Antacids to neutralize stomach acid it can provide symptom relief

Cytoprotective agents to protect the lining of GI Tract

(sucralfate and misoprostol)

Gastritis

Treatment

In some cases, gastritis can lead to :

Peptic Ulcers Disease

GI bleedings inducing iron deficiency anemia

Pernicious anemia can develop because intrinsic factor is less available to facilitate vitamin B12 absorption. Gastric secretion analysis confirms achlorhydria and loss of intrinsic factor

Gastritis

Complications

Peptic Ulcer Disease

Definition

Your digestive tract is coated with a mucous layer that normally protects against acid. But if the amount of acid is increased or the amount of mucus is decreased, you could develop an ulcer. Peptic ulcers are open sores that develop on the inside lining of the lower esophagus, stomach, or upper portion of the small intestine.

The most common Causes are

infection with the Bacterium H. Pylori

habitual use of aspirin and NSAIDs

secondary to some diseases and certain lifestyles

Peptic Ulcer Disease

Excessive use of alcohol, smoking, obesity

Gastritis, acute pancreatitis, COPD, Cirrhosis

Genetic predisposition

Age greater than 65 years and socioeconomic status.

Psychologic stress but the exact mechanism of causation is not known

Risk factors include

Peptic Ulcer Disease

Peptic ulcers can be

Single or multiple,

Acute or chronic,

Superficial or deep.

Superficial ulcerations are called erosions because they erode the mucosa but do not penetrate the muscularis mucosae.

True ulcers extend through the muscularis mucosae and damage blood vessels, causing hemorrhage or perforating the gastrointestinal wall.

Gastric or duodenal

Gastric Ulcer: that occur on the inside of the stomach – typical “food-pain “pattern

Duodenal Ulcer: that occur on the inside of the upper portion of the small intestine (duodenum)– typical “pain-food-relief” pattern.

Classification

Burning stomach pain

Feeling of fullness, bloating, or belching

Intolerance to fatty foods

Heartburn

Anorexia, nausea and vomiting

Dark blood in stools, or stools that are black or tarry (melena)

Trouble breathing

Feeling faint

Unexplained weight loss

Symptoms

Peptic Ulcer Disease

CHARACTERISTICS GASTRIC ULCER DUODENAL ULCER
Incidence
Age at onset 50–70 years 20–50 years
Family history Usually negative Positive
Sex (prevalence) Equal in women and men Equal in women and men
Stress factors Increased Average
Ulcerogenic drugs Normal use Increased use
Cancer risk Increased Not increased
Pathophysiology
Helicobacter pylori infection Often present (60%–80%) Often present (95%–100%)
Abnormal mucus May be present May be present
Parietal cell mass Normal or decreased Increased
Acid production Normal or decreased Increased
Serum gastrin Increased Normal
Serum pepsinogen Normal Increased
Associated gastritis More common Usually not present
Clinical Manifestations
Pain Located in upper abdomen Located in upper abdomen
Intermittent Intermittent
Pain-antacid-relief pattern Pain-antacid or food-relief pattern
Food-pain pattern Nocturnal pain common
Clinical course Chronic ulcer without pattern of remission and exacerbation Pattern of remissions and exacerbations for years

Table 1. Characteristics of Gastric and Duodenal Ulcers

To detect an ulcer, doctor may first take a medical history and perform a physical exam. Then diagnostic tests will be ordered, such as:

Laboratory tests for H. pylori.

H. pylori is detected using the urea breath test, this is the most accurate method.

H. pylori–specific serum immunoglobulin G (IgG) and immunoglobulin A (IgA) antibodies.

Measurement of H. pylori stool antigen levels

Diagnosis

Endoscopy.  An endoscopy with biopsy is the standard diagnostic procedure for PUD. It confirms the diagnosis and documents the type and extent of tissue damage.

Upper gastrointestinal series (barium swallow): creates images of your esophagus, stomach, and small intestine. During the X-ray, you swallow a white liquid (containing barium) that coats your digestive tract and makes an ulcer more visible.

Peptic Ulcer Disease

GERD

Gastritis

Nonulcer Dyspepsia

Cholecystitis

Pancreatitis

Diverticulosis

IBS

Differential Diagnosis

Peptic Ulcer Disease

Treatment for peptic ulcers depends on the cause.

If Patient is positive for H. pylori an antibiotic combination therapy is ordered for two weeks

(amoxicillin, clarithromycin, metronidazole, tinidazole, tetracycline and levofloxacin)

The antibiotics used will be determined by patient characteristics and current antibiotic resistance rates.

Eliminating or reducing use of injurious drugs, alcohol consumption and smoke cessation

Help the ulcer to heal with medication.

Proton pump inhibitor to block acid production and promote healing

(omeprazole, lansoprazole, rabeprazole, esomeprazole and pantoprazole)

Histamine H2-receptor antagonist to reduce acid production

(famotidine, cimetidine and nizatidine)

Antacids to neutralize stomach acid it can provide symptom relief

Cytoprotective agents to protect the lining of GI Tract

(sucralfate and misoprostol)

Surgery

The primary objectives are to reduce stimuli for acid secretion, decrease the number of acid-secreting cells in the stomach, and correct complications of ulcer disease.

Treatment

Peptic Ulcer Disease

Bleeding. Bleeding can occur as slow blood loss that leads to anemia or as severe blood loss that may require hospitalization or a blood transfusion. Severe blood loss may cause black or bloody vomit or black or bloody stools (hematemesis or melena)

Perforation. Peptic ulcers can eat a hole through (perforate) the wall of your stomach or small intestine, putting you at risk of serious infection of your abdominal cavity (peritonitis).

Obstruction. Peptic ulcers can block passage of food through the digestive tract, causing you to become full easily, to vomit and to lose weight either through swelling from inflammation or through scarring.

Gastric cancer. Studies have shown that people infected with H. pylori have an increased risk of gastric cancer.

Complications

Peptic Ulcer Disease

Protect yourself from infections: You can take steps to protect yourself from infections, such as H. pylori, by frequently washing your hands with soap and water and by eating foods that have been cooked completely.

Use caution with pain relievers drugs: for instance, take medication with meals and find the lowest dose possible that still gives you pain relief. If you need an NSAID, you may need to also take additional medications such as an antacid, a proton pump inhibitor, or acid blocker

Prevention

Peptic Ulcer Disease

Cirrhosis

Is an irreversible inflammatory, fibrotic liver disease. Structural changes result from injury (alcoholism, viruses (hepatitis), steatosis, chemicals) and fibrosis. The liver may be larger or smaller than normal and is usually firm or hard when palpated. Cirrhosis develops slowly over a period of years. Its severity and rate of progression depend on the cause.

Hepatitis virus B and C

Excessive alcohol intake

Idiopathic

Nonalcoholic fatty liver disease (NAFLD), also known as nonalcoholic steatohepatitis (NASH)

Autoimmune disorders

Hereditary metabolic disorder

Prolonged exposure to chemicals

Right-sided heart failure

Definition

Causes

Earliest symptoms pruritus, weight loss, fatigue, weakness, malaise, dark urine, pale stool.

Advanced Symptoms anorexia, nausea, vomiting, hematemesis, abdominal pain, chest pain, menstrual abnormalities, impotence, sterility, neuropsychiatric symptoms (difficulty concentrating, irritability, and confusion)

Late-stage: Jaundice

Cirrhosis

Signs and Symptoms:

Complications

Jaundice, portal hypertension, ascites, hepatic encephalopathy, varices with gastrointestinal bleeding, hepatorenal syndrome, hepatopulmonary syndrome, and portopulmonary syndrome.

Cirrhosis

Diagnostic

The diagnosis is based on the individual’s history and clinical manifestations.

The results of liver function tests are abnormal, and serologic studies show elevated levels of serum enzymes (i.e., alanine aminotransferase (ALT), aspartate aminotransferase (AST), and γ-glutamyltransferase) and bilirubin, and decreased serum albumin levels.

Prolonged prothrombin time cannot easily be corrected with vitamin K therapy. Malnutrition is often present.

Liver biopsy can confirm the diagnosis of cirrhosis, but biopsy is not necessary if clinical manifestations of cirrhosis are evident.

US, CT scan, MRE

Treatment

There is no specific treatment, but many of the complications are treatable. Rest, nutritious diet, corticosteroids, antioxidants, drugs that slow fibrosis, and management of complications such as ascites, gastrointestinal bleeding, anemia, infection, and encephalopathy slow disease progression. Liver transplant is the treatment for liver failure, and artificial liver support systems are being developed.

Cirrhosis

Management

Immunizations (Pneumococcal, influenza, Hepatitis A and B)

Ascites (Paracentesis, sodium restriction of 1 to 2 g/day, Spironolactone, Furosemide, Monitor electrolytes, BUN, and creatinine level. The serum-ascites albumin gradient (SAAG) paracentesis to remove 1 or 2 L of ascitic fluid and relieve respiratory distress.

Encephalopathy (Lactulose is useful for reducing urea production in the colon, thus lowering blood ammonia levels in patients with portal systemic encephalopathy d/d cirrhosis. Rifaximin decreases intestinal production of ammonia and is used for lactulose non responders.

Jaundice (total plasma bilirubin concentrations greater than 2.5 to 3 mg/dL). The treatment for jaundice consists of correcting the cause). Refractory edema (thiazide, loop diuretic and sodium restriction)

Cessation of alcohol consumption slows the progression of liver damage, improves clinical symptoms, and prolongs life.

Cirrhosis

Primary biliary cirrhosis

Secondary biliary cirrhosis

Hepatocellular carcinoma

Hemochromatosis

NASH

Primary sclerosing cholangitis

Parasitic infection (e.g., Schistosoma mansoni)

Differential Diagnoses

Cholelithiasis (Gallstones) and Cholecystitis

Gallstone formation is termed cholelithiasis. Inflammation of the gallbladder or cystic duct is known as cholecystitis.

Definition

is Inflammatory or infectious conditions causing gallstone formation and bile duct obstruction. Stone formation in the gallbladder occurs when certain substances reach a high concentration in bile and produce crystals.

Gallstones are formed from impaired metabolism of cholesterol, bilirubin, and bile acids. All gallstones contain cholesterol, unconjugated bilirubin, bilirubin calcium salts, fatty acids, calcium carbonates and phosphates, and mucin glycoproteins. Gallstones are of three types depending on chemical composition: cholesterol (70% cholesterol and the most common [70% to 80% of gallstones]); pigmented (black [hard] and brown [soft] with less than 30% cholesterol); and mixed.

Cholelithiasis (Gallstones) and Cholecystitis

Risk factors

Obesity; rapid weight loss in obese individuals; middle age; female sex; use of oral contraceptives; Native American ancestry; genetic predisposition; gallbladder, pancreatic, or ileal disease; low high density lipoprotein (HDL) cholesterol level and hypertriglyceridemia; and gene-environmental interactions.

Clinical Manifestations

Heartburn, flatulence, epigastric discomfort, pruritus, jaundice, and food intolerances, particularly to fats and cabbage. The pain (biliary colic) is most characteristic, occurs 30 minutes to several hours after eating a fatty meal, and is caused by the lodging of one or more gallstones in the cystic or common duct with obstruction and distention. It can be intermittent or steady and usually is located in the right upper quadrant and radiates to the mid-upper back. Jaundice indicates that the stone is located in the common bile duct. Abdominal tenderness and fever indicate cholecystitis.

Cholelithiasis (Gallstones) and Cholecystitis

Complications

Can include pancreatitis from obstruction of the pancreatic duct.

Diagnosis

Is based on the medical history, physical examination, and imaging evaluation. Imaging techniques include transabdominal ultrasound, endoscopic ultrasound, and magnetic resonance cholangiopancreatography.

Cholelithiasis (Gallstones) and Cholecystitis

Evaluation and Treatment: Cholelithiasis

Oral bile acids (ursodeoxycholic acid or chenodeoxycholic acid) may dissolve cholesterol stones, but the stones may recur when the drug is discontinued.

Laparoscopic cholecystectomy is the preferred treatment for gallstones that cause obstruction or inflammation. Use of transluminal endoscopic surgery is advancing rapidly. Endoscopic retrograde cholangiopancreatography and sphincterotomy with stone retrieval are used for the treatment of bile duct stones. Large stones, or intrahepatic stones, may be managed with open surgery or lithotripsy.

Ursodiol

Gallstone dissolution: 8 to 10 mg/kg/day in two or three divided doses

Gallstone prevention: 300 mg 1 tablet PO BID

Patients with stones larger than 2 mm, acute condition in the abdomen, known sensitivity to the drug, acute pancreatic gallstones, or acute cholecystitis are not candidates for the drug.

Milk Thistle: has been shown to protect the liver after exposure to hepatotoxins such as acetaminophen, ethanol, and halothane, and to restore liver function in patients with hepatitis and cirrhosis

Cholelithiasis (Gallstones) and Cholecystitis

Treatment more specific for Cholecystitis

Treatment includes pain control, replacement of fluid and electrolytes, and fasting. Antibiotics (penicillin and aminoglycoside) are often prescribed to manage bacterial infection in severe cases. Acute attacks usually require laparoscopic gallbladder resection (cholecystectomy). Obstruction also may lead to reflux of bile into the pancreatic duct, causing acute pancreatitis.

Cholelithiasis (Gallstones) and Cholecystitis

CBC with differential

UA

LFTs

Serum pancreatic enzymes

Serum electrolyte values

BUN and creatinine

Blood cultures

hCGs

Electrocardiography

Ultrasound

CT scan with contrast

Diagnostics

Bowel obstruction

Chronic cholecystitis

Diverticulitis

Gastroenteritis

Irritable bowel syndrome

Pancreatitis

Renal colic

Appendicitis

Differential Diagnostics

Ulcerative colitis

Is a chronic inflammatory disease that causes ulceration of the colonic mucosa, in the inner lining of Colon and rectum.

Those ulcers produce pus and mucous, which cause abdominal pain and the need to frequently empty your colon.

Definition

Causes of Ulcerative Colitis

Abnormal immune response

Genetics

Environmental factors (Diet, stress, viral/bacterial infection, NSAID use)  

Ulcerative Colitis

Frequent bloody diarrhea with passage of purulent mucus

Abdominal cramps and pain

Persistent diarrhea accompanied by abdominal pain and blood in the stool

Fever

Elevated heart rate

Urgent bowel movements

Bloody stools

Dehydration

Weight loss

Anemia

Ulcerative colitis

Signs and Symptoms

Types of Ulcerative Colitis

Ulcerative colitis

Types of Ulcerative Colitis

Ulcerative Proctitis

Bowel inflammation limited to less than six inches of the rectum

Symptoms

Rectal bleeding

Rectal pain

Urgency in your bowel movements

Left-Sided Colitis

Continuous inflammation begins at the rectum and extends as far into the colon as the splenic flexure

It also includes proctosigmoiditis, which affects rectum and the sigmoid colon.

Symptoms

Loss of appetite

Weight loss

Bloody diarrhea

Pain on the left side of the abdomen

Ulcerative colitis

Types of Ulcerative Colitis

Extensive Colitis

Affects the entire colon.

Continuous inflammation begins at the rectum and extends beyond the splenic flexure.

Symptoms

Loss of appetite

Bloody diarrhea

Abdominal pain

Weight loss

Diagnostic test

Colonoscopy

Barium enema

X-ray, CT scan

Blood test: It shows low hemoglobin values, hypoalbuminemia, and low serum potassium levels.

Stool studies: White blood cells or certain proteins in your stool can indicate ulcerative colitis

Ulcerative colitis

Rupture of bowel

Toxic Megacolon

Weigh loss, dehydration

Anemia

Loss of form of haustra (“lead-pipe sign”)

Complications

Differential diagnosis

Crohn Disease

Infectious colitis

Chronic schistosomiasis

Amebiasis

Intestinal tuberculosis

Infectious, ischemic, or radiation colitis

Acute self-limiting colitis (ASLC)

Colon cancer

Ulcerative colitis

Treatment

Anti-inflammatory drugs:

Aminosalicylates:5-aminosalicylic acid (5-ASA)First line ttx Sulfasalazine (Others: Mesalamine, Balsalazide, Olsalazine)

Corticosteroids:  (Prednisone, Budesonide, Hydrocortisone, Methylprednisolone)

Immunosuppressors/modulators: To reduce immune system activity when other drugs don’t work/off steroids. Take several weeks to 3 months to start working.

Immunosuppressors(azathioprine, cyclosporine, methotrexate)

Immunomodulators: Target proteins made by the immune system. Neutralizing these proteins decreases inflammation in the intestines. (Adalimumab, Infliximab, etc)

Treatment UC

Antibiotic, antidiarrheal, tylenol (NO NSAIDS)

Severe cases: Surgery

Proctocolectomy: removal of colon and rectum, patient will have permanent ileostomy

or

Ileorectal anastomosis:Colon and rectum removal, and pouch created that attaches to ileum which allows stool to pass from small intestine to anus.

Crohn Disease

Signs and Symptoms

Right lower quadrant intermittent abdominal pain.

Ulcers (mouth and GI tract)

Lower abdominal pain 1 hour after eating.

Diarrhea (may have pus, blood, or mucus).

Fever

Fissure (anal that bleeds)

Bloating

Weight loss.

Abnormal liquid stools.

Types of Crohn Disease

Ileocolitis: Inflammation in the ileum and colon, is the most common type of Crohn’s disease.

Ileitis: Inflammation in the small intestine (ileum).

Gastroduodenal: Inflammation affect the stomach and the duodenum’

Jejunoileitis: Patchy areas of inflammation develop in jejunum).

Crohn Disease

Diagnostic test

Complications

Differential diagnosis

Colonoscopy

Barium Enema (BE, Lower GI Series)

CT scan

Small bowel series or a capsule endoscopy (camera pill)

Anti–Glycan Antibodies (Crohn Disease Prognostic Panel)

Intestinal obstruction. 

Fistulas. 

Abscesses. 

Anal fissures. 

Ulcers. 

Malnutrition. 

Sepsis

Amebiasis

Appendicitis

Bacterial Gastroenteritis

Diverticulitis

Giardiasis

Irritable Bowel Syndrome

Ulcerative Colitis

Viral Gastroenteritis

Crohn Disease

Treatment

Anti-inflammatory drugs:

Aminosalicylates:5-aminosalicylic acid (5-ASA)First line ttx Sulfasalazine (Others: Mesalamine, Balsalazide, Olsalazine)

Corticosteroids:  (Prednisone, Budesonide, Hydrocortisone, Methylprednisolone)

Immunosuppressors/modulators: To reduce immune system activity when other drugs don’t work/off steroids. Take several weeks to 3 months to start working Immunosuppressors(azathioprine, cyclosporine, methotrexate)

Immunomodulators: Target proteins made by the immune system. Neutralizing these proteins decreases inflammation in the intestines. (Adalimumab, Infliximab, etc)

Acetaminophen for mild pain

Antibiotics to prevent or treat complications that involve infection, such as abscesses and fistulas.

Loperamide: severe diarrhea.

Surgery is generally performed to manage complications

Crohn Disease

Non-pharmacological intervention

Avoid carbonated drinks, popcorn, vegetable skins, nuts, and other high-fiber foods, lactose

Drink more fluids

Eat smaller meals more often

Keep a food diary to help identify foods that cause problems

High calorie, low fat, low fiber, and low salt diet

Crohn Disease

Differences

Ulcerative Colitis

Only the colon and rectum (large intestine) are affected

Affects the inner-most lining of the large intestine (submucosa to mucosa)

Cure is surgery

Continuous lesions

Crohn Disease

Can affect any part of the GI tract from the mouth to the anus

Can affect the entire lining of the intestinal wall to serosa

No cure, surgery helps with quality of life

Skip lesions

Irritable Bowel Syndrome

Definition

Disorder of brain-gut interaction characterized by abdominal pain with altered bowel habits.

Causes

Still unknown but some factors can lead to IBS like:

Dysmotility: Problems with how your GI muscles contract and move food through the GI tract.

Visceral hypersensitivity: Extra-sensitive nerves in the GI tract.

Brain-gut dysfunction: Miscommunication between nerves in the brain and gut.

Factors associate

Stressful or difficult early life events.

Depression/anxiety

Alcohol consumption/smoking

Irritable Bowel Syndrome

Signs and Symptoms

Abdominal pain or cramps, usually in the lower half of the abdomen.

Bloating.

Bowel movements that are harder or looser than usual.

Diarrhea, constipation or alternating between the two.

Excess gas.

Mucus in the stool(may look whitish).

Irritable Bowel Syndrome

Types of IBS

Irritable Bowel Syndrome

Differential diagnosis

Celiac disease

Lactose intolerance

Ulcerative Colitis.

Microscopic Colitis.

Differential diagnosis

Rome IV Criteria: Recurrent abdominal pain, on average, at least 1 day per week in the last 3 months, associated with two or more of the following criteria:

1. Related to defecation

2. Associated with a change in frequency of stool

3. Associated with a change in form (appearance) of stool

CBC

C-reactive protein

Fecal calprotectin

Colonoscopy, X-ray, CT scan

Stool test

Lactose intolerant test

Crohn’s Disease.

Stress.

Diverticulitis.

Gallstones.

Irritable Bowel Syndrome

Treatment

Pharmacotherapy is based on severity and is targeted at specific symptoms.

All patients with alternating constipation/diarrhea:

Increased dietary fiber (25 g/day)

Pain

Antispasmodic (anticholinergic) medication—short term

TCAs—long term

Diarrhea

Loperamide—short term; often used for breakthrough diarrhea

Antidepressants (TCAs)—long term

Alosetron (ordered by GI specialists) if resistant to all other interventions

Constipation

Fiber

Laxatives

Irritable Bowel Syndrome

Non-pharmacologic Treatment

Dietary changes:

Fluids should not be taken with foods

Increase fiber in the diet (fruits, vegetables, grains and nuts).

Drink plenty of water

Avoid : caffeine, chocolate, teas and sodas.

Limit cheese and milk. 

Make sure to get calcium from other sources, such as broccoli, spinach, salmon or supplements.

symptoms.

Activity changes:

Exercise regularly.

Don’t smoke.

Try relaxation techniques.

Eat smaller meals more often.

Food diary to know which foods trigger flare-ups. Common triggers are red peppers, green onions, red wine, wheat and cow’s milk.

Behavioral and psychological therapies, stress management, and meditation.

Cancer of the Digestive System

Esophagus : (2.6 percentage of deaths)

Stomach: (1.8 percentage of deaths)

Colorectal: (8.25 percentage of death)

Cancer of the tube that runs from the throat to the stomach (esophagus).

Definition

The most common cells are Squamous cells and Adenocarcinoma. Chronic inflammation, intestinal metaplasia, and dysplasia (Barrett esophagus [columnar rather than squamous epithelium in the lower esophagus]) induced by gastroesophageal reflux accelerates the formation of esophageal adenocarcinoma. Both adenocarcinoma and squamous cell carcinoma develop neoplastic transformation after long-term exposure to environmental irritants (basal and squamous cell hyperplasia).

Pathogenesis

Esophageal Cancer

Causes

Factors that can increase your risk of esophageal cancer include:

Smoking

Heavy alcohol consumption

Chronic heartburn or acid reflux

Gastroesophageal reflux disease (GERD)

Malnutrition

Barrett’s esophagus, a condition that sometimes develops in people with GERD

Achalasia, a rare disorder of muscles in the lower esophagus

Not eating enough fruit and vegetables

Undergoing radiation treatment to the chest or upper abdomen

Signs and symptoms

Difficulty swallowing (dysphagia)

Weight loss without trying.

Chest pain, pressure or burning.

Worsening indigestion or heartburn.

Coughing or hoarseness.

Esophageal Cancer

Diagnostic Tests

Barium swallow test. If you’re having trouble swallowing, sometimes a barium swallow is the first test done.

Computed tomography (CT) scan.

Magnetic resonance imaging (MRI) scan.

Positron emission tomography (PET) scan.

Upper endoscopy.

Endoscopic ultrasound.

Bronchoscopy.

Thoracoscopy and laparoscopy.

Treatment

Treatment of gastroesophageal reflux is essential for the prevention of Barrett esophagus.

Esophageal carcinoma is treated with endoscopic radiofrequency mucosal ablation.

Radiation therapy: The use of X-rays, gamma rays and charged particles to fight cancer

Chemotherapy: The use of anticancer drugs to treat cancerous cells

Surgery: The use of an operation to remove the cancerous tissue from the body.

Combination of therapies.

Esophageal Cancer

Esophageal Cancer

Obstruction of the esophagus. Cancer may make it difficult for food and liquid to pass through your esophagus.

Pain. Advanced esophageal cancer can cause pain.

Bleeding in the esophagus. Esophageal cancer can cause bleeding. Though bleeding is usually gradual, it can be sudden and severe at times.

Complications

Prevention

You can take steps to reduce your risk of esophageal cancer. For instance:

Quit smoking. If you smoke, talk to your doctor about strategies for quitting. Medications and counseling are available to help you quit. If you don’t use tobacco, don’t start.

Drink alcohol in moderation, if at all. If you choose to drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women and up to two drinks a day for men.

Eat more fruits and vegetables. Add a variety of colorful fruits and vegetables to your diet.

Maintain a healthy weight. If you are overweight or obese, talk to your doctor about strategies to help you lose weight. Aim for a slow and steady weight loss of 1 or 2 pounds a week.

Cancer that occurs in the stomach.

Definition

Pathogenesis

Environmental factors and genetic predisposition combine to cause injury, inflammation, and the progression to gastric adenocarcinoma. About 1% to 3% of gastric cancers are familial. Gastric adenocarcinoma usually begins in the glands of the stomach mucosa, commonly in the prepyloric antrum. Atrophic gastritis progresses to intestinal metaplasia, dysplasia, and adenocarcinoma.

Stomach Cancer

Causes

Signs and symptoms

Infection with H. pylori that carry selected virulence factors. H. pylori is causatively linked to mucosa- associated lymphoid tissue (MALT) lymphoma (a low-grade B-cell lymphoma) that can originate in the stomach.

Dietary factors, such as salt added to food, food additives in pickled or salted foods and low intake of fruits and vegetables. Dietary salt enhances the conversion of nitrates to carcinogenic nitrosamines in the stomach. Salt is also caustic to the stomach and can cause chronic atrophic gastritis.

Lifestyle factors, such as alcohol consumption and cigarette smoking. Smokers have a higher incidence of H. pylori infection.

The early stages of gastric cancer are generally asymptomatic or produce vague symptoms such as loss of appetite (especially for meat), malaise, and indigestion.

Later manifestations include unexplained weight loss, upper abdominal pain, vomiting, change in bowel habits, and anemia caused by persistent occult bleeding.

Stomach Cancer

Stomach Cancer

Diagnostic Tests

Treatment

Barium x-ray film shows the lesion.

Direct endoscopic visualization (microscopic examination of exfoliated cells obtained by lavage during endoscopy).

Biopsy usually establish the diagnosis.

Surgery is the only curative treatment for early stages of disease.

Screening and eradication of H. pylori infection are the best preventive approaches to gastric cancer.

Early diagnosis and chemotherapy combined with radiation improve post-surgical outcomes.

Abstinence from alcohol and smoking improves outcomes.

Dietary modifications include high intake of fruits and vegetables, vitamin C, carotenoids, and fiber and reduced intake of salt, salted food, and red meat.

Small Intestine Cancer

Definition

Small intestine carcinoma is rare and represents less than 3% of gastrointestinal cancers. The most prevalent tumor type is adenocarcinoma, which is followed by carcinoid tumors (neuroendocrine serotonin-producing tumors), sarcomas, and lymphomas (neuroendocrine serotonin-producing tumors). Carcinoma is more common in people who have familial adenomatous polyposis or Crohn’s disease.

Abdominal pain

Yellowing of the skin and the whites of the eyes (jaundice)

Feeling unusually weak or tired

Nausea/Vomiting

Losing weight without trying

Blood in the stool, which might appear red or black

Watery diarrhea

Skin flushing

Signs and symptoms

Small Intestine Cancer

Risk factors

Gene mutations passed through families. Some gene mutations that are inherited from your parents can increase your risk of small bowel cancer and other cancers.

Other bowel diseases. Other diseases and conditions may increase the risk of small bowel cancer, including Crohn’s disease, inflammatory bowel disease and celiac disease.

Weakened immune system. If your body’s germ-fighting immune system is weakened.

Small Intestine Cancer

Diagnosis

CT

MRI

Positron emission tomography (PET)

X-rays of the upper digestive system and small bowel after drinking a solution containing barium (upper gastrointestinal series with small bowel follow-through)

Nuclear medicine scans, which use a small amount of radioactive tracer to enhance imaging tests

Endoscopic tests involve placing a camera inside your small intestine so that your doctor can examine the inside walls. Endoscopic tests may include:

Surgical resection followed by tumor types specific treatment. Surgery can involve one large incision in your abdomen (laparotomy), or several small incisions (laparoscopy).

Chemotherapy. Chemotherapy uses powerful drugs to kill cancer cells.

Targeted drug therapy. Targeted drug treatments focus on specific weaknesses present within cancer cells.

Immunotherapy. Immunotherapy is a drug treatment that helps your immune system to fight cancer.

Treatment

It’s not clear what may help to reduce the risk of small bowel cancer, since it’s very uncommon.

Eat a variety of fruits, vegetables and whole grains.

Drink alcohol in moderation

Stop smoking.

Exercise most days of the week at 30 min.

Maintain a healthy weight.

Small Intestine Cancer

Complications

Prevention

An increased risk of other cancers. People who have small bowel cancer run a higher risk of having other types of cancers

Cancer that spreads to other parts of the body.

Colon and Rectum Cancer

A cancer of the colon or rectum, located at the digestive tract’s lower end. Is the third most common cause of cancer and cancer death.

Stage 0 (carcinoma in situ): involves only the mucosal lining.

Stage I: Extension of cancer to the middle layers of the colon wall, no spread to lymph nodes.

Stage II: Extension beyond the colon wall to nearby tissues around the colon or rectum, and through the peritoneum.

Stage III: Spread beyond the colon into lymph nodes and nearby organs and through the peritoneum.

Stage IV: Spread to nearby lymph nodes and has spread to other parts of the body, such as the liver or lungs.

Definition

Colon and Rectum Cancer

Risk Factors

Hereditary and Medical Factors

Family history of colorectal cancer

Familial adenomatous polyposis

Hereditary non-polyposis colorectal cancer

Inflammatory bowel disease after 10 years

Type 2 diabetes mellitus

Modifiable Risk Factors

Smoking or chewing tobacco
Obesity
Physical inactivity
Moderate to heavy alcohol consumption

High consumption of processed meat

Red meat consumption (large variations among studies) High-fat, low-fiber diet

Lower Risk

Diets high in cereal grains, vegetables, milk; fish; folic acid, calcium, and vitamin D; magnesium and selenium; and low in fat.

Postmenopausal estrogen use Physical activity

Use of NSAIDs

Colon and Rectum Cancer

Signs and symptoms

A change in bowel habits.

Blood in or on your stool (bowel movement).

Diarrhea, constipation, or feeling that the bowel does not empty all the way.

Abdominal pain, aches, or cramps that don’t go away.

Weight loss and Anemia.

Diagnosis

Blood tests (Complete blood count, tumor markers and liver enzymes)

Imaging tests (X-rays, CT scan, MRI scan, PET scan ultrasound, angiography)

Biopsy

Diagnostic colonoscopy (done after you show symptoms, not as a routine screening test)

Proctoscopy.

Colon and Rectum Cancer

Treatment for colon cancer usually involves surgery to remove the cancer. Removing polyps during a colonoscopy (polypectomy).

Endoscopic mucosal resection.

Minimally invasive surgery (laparoscopic surgery).

Other treatments, such as radiation therapy and chemotherapy, might also be recommended.

Treatment

Anal carcinoma

Definition

Is very uncommon cancer. Anal cancer is a disease in which malignant (cancer) cells form in the tissues of the anus.

The squamous cell carcinoma is the most prevalent tumor type. Other anal malignancies include adenocarcinoma, lymphoma, and sarcoma.

Most common, infection with the human papillomavirus (93 percent).

Followed by anal involvement in Crohn’s disease.

Squamous cell anal cancer is more likely in people who have been infected with the human immunodeficiency virus.

Having a personal history of vulvar, vaginal, or cervical cancers.

Having many sexual partners or repetitive anal intercourse.

Risk factor

Anal carcinoma

Signs and symptoms

Diagnosis

Bleeding from the anus or rectum.

A lump near the anus.

Pain or pressure in the area around the anus.

Itching or discharge from the anus.

A change in bowel habits

Physical exam and health history.

Digital rectal examination (DRE).

Anoscopy.

Proctoscopy.

Endo-anal or endorectal

ultrasound.

Biopsy: The removal of cells or tissues with signs of cancer

Surgery and combination chemoradiation are used to treat anal carcinomas, depending on their stage.

Treatment

Burisch J, Munkholm P. Inflammatory bowel disease epidemiology. Current Opinion in Gastroenterology. 2013;29(4):357–362.

Edmunds, M., & Mayhew, M. (2013). Pharmacology for the Primary Care Provider (4th Edition). Elsevier Health Sciences (US). https://online.vitalsource.com/books/9780323087902

Kappelman MD, Moore KR, Allen JK, Cook SF. Recent trends in the prevalence of Crohn’s disease and ulcerative colitis in a commercially insured U.S. population. Digestive Diseases and Sciences. 2013;58:519–525.

McCance, S.H. K. ([Insert Year of Publication]). Pathophysiology (8th Edition). Elsevier Health Sciences (US). https://online.vitalsource.com/books/9780323583473

Molodecky NA, Soon IS, Rabi DM, et al. Increasing incidence and prevalence of the inflammatory bowel diseases with time, based on systematic review. Gastroenterology. 2012;142(1):46–54.

Pagana, K.P.T.P. T. ([Insert Year of Publication]). Mosby’s Manual of Diagnostic and Laboratory Tests (7th Edition). Elsevier Health Sciences (US). https://online.vitalsource.com/books/9780323697057

References

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