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Alteration in Gastrointestinal functionsPEPTIC ULCER DISEASE

Peptic ulcer disease refers to ulcerations in the mucosa of the lower esophagus, stomach, or duodenum

Pathophysiology and Etiology

Stomach contains acidic secretions that can digest substances, intrinsic defenses protect the gastric mucosal membrane from injury. A thick, tenacious layer of gastric mucus protects the stomach from autodigestion,

Gastric ulcers may be a result of destruction of the mucosal barrier.

The duodenum is protected from ulceration by the function of Brunner's glands. These glands produce a viscid, mucoid,alkaline secretion that neutralizes the acid chyme. Duodenal ulcers appear to result from excessive acid protection.

Helicobacter pylori releases a toxin that destroys the gastric and duodenal mucosa, reducing the epithelium's resistance to acid digestion and causing gastritis and ulcer disease.

Salicylates and other NSAIDs inhibit the secretion of prostaglandins (substances that block ulceration).

Certain illnesses, such as pancreatitis, hepatic disease, Crohn's disease, preexisting gastritis, and Zollinger-Ellison syndrome, also contribute to ulceration.

blood type (gastric ulcers and type A; duodenal ulcers and type O) and other genetic factors.

Exposure to irritants, such as alcohol, coffee,and tobacco, may contribute by accelerating gastric acid emptying and promoting mucosal breakdown. Emotional stress also contributes to ulcer formation because of the increased stimulation of acid and pepsin secretion and decreased mucosal defense.

Physical trauma and normal aging are additional predisposing conditions.

Clinical Manifestations

Gnawing or burning epigastric pain occurring 1 to 3 hours after a meal due to stretching of the mucosa by food pain relieved by food or antacids, but usually recurring 2 to 4 hours later secondary to food acting as a buffer for

acid.

Nocturnal epigastric, abdominal pain or burning. May awaken patient at night, usually around midnight to 3 a.m. hunger like due to excessive acid production Epigastric tenderness on examination

Early satiety, anorexia, weight loss, heartburn, belching (may indicate reflux disease)

Dizziness, syncope, hematemesis, or melena (may indicate hemorrhage)

Anemia

Sudden, intense midepigastric pain radiating to the right shoulder may indicate ulcer perforation.

Diagnostic Evaluation

Upper GI endoscopy with possible tissue biopsy and cytology.

Upper GI radiographic examination (barium study)

Serial stool specimens to detect occult blood

Serology to test for H. pylori antibodies

Appendicitis

APPENDICITIS

Appendicitis is inflammation of the vermiform appendix caused by an obstruction of the intestinal lumen from infection, stricture, fecal mass, foreign body, or tumor.

Appendicitis may occur at any age and affects both sexes equally; however, between puberty and age 25,

Prevalent in men.

Since the advent of antibiotics, the incidence and the death rate of appendicitis have declined; if untreated, this disease is invariably fatal.

Causes

mucosal ulceration

fecal mass

stricture

barium ingestion

viral infection.

Pathophysiology

Mucosal ulceration triggers inflammation, which temporarily obstructs the appendix. The obstruction blocks mucus outflow. Pressure in the now distended appendix increases, and the appendix contracts.

Bacteria multiply, and inflammation and pressure continue to increase, restricting blood flow to the organ and causing severe abdominal pain.

Obstruction is followed by edema, infection, and ischemia.

As intraluminal tension develops, necrosis and perforation usually occur.


Generalized or localized abdominal pain in the epigastric or periumbilical areas and upper right abdomen. Within 2 to 12 hours, the pain localizes in the right lower quadrant and intensity increases.

Anorexia, moderate malaise, mild fever, nausea and vomiting.

Usually constipation occurs; occasionally diarrhea.

Rebound tenderness, involuntary guarding, generalized abdominal rigidity.

low-grade temperature from systemic manifestation of inflammation and leukocytosis

Complications

wound infection

intraabdominal abscess

fecal fistula

intestinal obstruction

incisional hernia

peritonitis

death.


WBC count reveals moderate leukocytosis (10,000 to 16,000/mm3) with shift to the left (increased immature neutrophils).

Urinalysis to rule out urinary disorders.

Abdominal X-ray may visualize shadow consistent with fecalith in appendix; perforation will reveal free air.

Abdominal ultrasound or CT scan can visualize appendix and rule out other conditions, such as diverticulitis and Crohn's disease. Focused appendiceal CT can quickly evaluate for appendicitis.

PERITONITIS

Peritonitis is a generalized or localized inflammation of the peritoneum, the membrane lining the abdominal cavity and covering visceral organs.


Primary Peritonitis

Acute, (rare)

Escherichia coli.

streptococci, pneumococci, or gonococci.

Secondary Peritonitis

Contamination of peritoneal cavity by GI fluid and microorganisms.


Initially, local type of abdominal pain tends to become constant, diffuse, and more intense.

Abdomen becomes extremely tender and muscles become rigid; rebound tenderness and ileus may be present; patient lies very still, usually with legs drawn up.

Percussion: resonance and tympany due to paralytic ileus; loss of liver dullness may indicate free air in abdomen.

Auscultation: decreased bowel sounds.

Nausea and vomiting often occur; peristalsis diminishes; anorexia is present.

Elevation of temperature and pulse as well as leukocytosis.

Fever; thirst; oliguria; dry, swollen tongue; signs of dehydration.

Weakness, pallor, diaphoresis, and cold skin are a result of the loss of fluid, electrolytes, and protein into the abdomen.

Hypotension, tachycardia, and hypokalemia may occur.

Shallow respirations may result from abdominal distention and upward displacement of the diaphragm.

Note: With generalized peritonitis, large volumes of fluid may be lost into abdominal cavity (can account for losses to 5 L/day).

Ascites

Complication of appendicitis

diverticulitis, peptic ulceration, biliary tract disease, colon inflammation, volvulus, strangulated obstruction, perforation, abdominal cancers.


WBC to show leukocytosis (leukopenia if severe).

ABG levels may show hypoxemia or metabolic acidosis with respiratory compensation.

Urinalysis may indicate urinary tract problems as primary source.

Peritoneal aspiration (paracentesis) to demonstrate blood, pus, bile, bacteria (Gram's stain), amylase.

Abdominal X-rays may show free air in peritoneal cavity, gas and fluid collection in small and large intestines, generalized bowel dilatation, intestinal wall edema.

CT scan of abdomen or sonography may reveal intra-abdominal mass, abscess, ascites.

Chest X-ray may show elevated diaphragm.

Exploratory laparotomy

CROHN'S DISEASE

Crohn's disease is a chronic idiopathic inflammatory disease that can affect any part of the GI tract, usually the small and large intestines.

As Crohn's disease progresses, fibrosis thickens the bowel wall and narrows the lumen. Narrowing or stenosis

can occur in any part of the intestine and cause varying degrees of intestinal obstruction


unknown

lymphatic obstruction, allergies, immune disorders, genetic predisposition.

Environmental agents, such as infections (viral or bacterial overload) or dietary factors,

Defect in the intestinal barrier that increases the permeability of the bowel.

Defect in the repair of mucosal injury leading to chronic condition.

Intestinal tissue is thickened and edematous; ulcers enlarge, and deepen.The deep penetration of these ulcers may form fissures, abscesses, and fistulae. The healing and fibrosis of these lesions may lead to stricture

The clinical presentation can be divided into three patterns:

Inflammatory

Fibrostenotic (stricturing)

Perforating (fistulizing)

Signs and symptoms

Signs and symptoms include:

steady, colicky pain in the right lower quadrant due to acute inflammation and nerve fiber irritation

cramping intermittent pain due to acute inflammation

tenderness due to acute inflammation

weight loss secondary to diarrhea and malabsorption

diarrhea due to bile salt malabsorption,

loss of healthy intestinal surface area, and bacterial growth

steatorrhea secondary to fat malabsorption

bloody stools secondary to bleeding from inflammation and ulceration.

Fever may indicate infectious complication such as abscess.

Fecal urgency and tenesmus (feeling of constantly needing to pass stools, despite an empty colon feeling of constantly needing to pass stools, despite an empty colon)

anorexia, weight loss, malaise, nausea, arthralgias, and hematochezia

Rectal examination may reveal a perirectal abscess, fistula, fissure, or skin tags (which represent healed perianal lesions).

Complications

anal fistula

perineal abscess

fistulas to the bladder or vagina or to the skin in an old scar area

intestinal obstruction

nutrient deficiencies from poor digestion and malabsorption of bile salts and vitamin B 12

fluid imbalances.

Diagnosis

Fecal occult test reveals minute amounts of blood in stools.

Small bowel X-ray shows irregular mucosa, ulceration, and stiffening.

Barium enema reveals the string sign (segments of stricture separated by normal bowel) and possibly fissures and narrowing of the bowel.

Sigmoidoscopy and colonoscopy reveal patchy areas of inflammation (helps to rule out ulcerative colitis), with cobblestone-like mucosal surface. With colon involvement, ulcers may be seen.

Biopsy reveals granulomas in up to half of all specimens.

Blood tests reveal increased white blood cell count and erythrocyte sedimentation rate, and decreased potassium, calcium, magnesium, and hemoglobin levels.Hemorrhoids

Hemorrhoids are varicosities in the superior(internal) or inferior (external) hemorrhoidal venous plexus. Dilation and enlargement

Incidence: both sexes.

highest between ages 20 and 50.

Pathophysiology

Hemorrhoids result from activities that increase intravenous pressure, causing distention and engorgement.

The exact pathogenesis remains controversial. Theories include:

Abnormal dilatation of veins of internal hemorrhoidal venous plexus.

Abnormal distension of the arteriovenous anastomoses.

Downward displacement or prolapse of anal cushions.

Destruction of the anchoring connective tissue system.

Increased intra-abdominal pressure causes engorgement in the vascular tissue lining the anal canal.

Loosening of vessels from surrounding connective tissue occurs with protrusion or prolapse into anal canal.

Predisposing factors include:

Pregnancy, prolonged sitting/standing.

Straining at stool, chronic constipation/diarrhea.

Anal infection, rectal surgery, or episiotomy.

Hereditary factor.

Exercise.

Coughing, sneezing, vomiting.

Loss of muscle tone due to age.

Anal intercourse.

Classification:

First-degree- anal canal.

Second-degree- prolapse during straining but reduce spontaneously.

Third-degree- prolapsed hemorrhoids that require manual reduction after each bowel movement.

Fourth-degree hemorrhoids are irreducible..


Bleeding during or after defecation, bright red blood on stool due to injury of mucosa covering hemorrhoid (most common)

Visible (if external) and palpable mass

Constipation, anal itching

Sensation of incomplete fecal evacuation

Infection or ulceration, mucus discharge

Pain noted more in external hemorrhoids

Sudden rectal pain due to thrombosis in external hemorrhoids

Complications

Constipation

Local infection

Thrombosis of hemorrhoids

Secondary anemia from severe or recurrent bleeding.

Diagnosis

Physical examination confirms external hemorrhoids.

Anoscopy and flexible sigmoidoscopy visualizes internal hemorrhoidsUlcerative colitis

Ulcerative colitis is a chronic idiopathic inflammatory disease of the mucosa and, less frequently, the submucosa of the colon and rectum. If only the rectum is involved, it may be called ulcerative proctitis.


The exact cause of ulcerative colitis is unknown. Possible theories include:

Genetic predisposition.

Environmental factors may trigger disease (viral or bacterial pathogens, dietary).

Immunologic imbalance or disturbances.

Defect in intestinal barrier causing hypersensitive mucosa and increased permeability.

Defect in repair of mucosal injury, which may develop into a chronic condition.

Multiple crypt abscesses develop in intestinal mucosa that may become necrotic and lead to ulceration and perforation

FIGURE 18-9 GI and systemic complications of ulcerative colitis.

May manifest as a systemic disease with inflammatory changes of connective tissue. Most common in young adulthood and middle-age, peak incidence at ages 20 to 40.

Incidence greatest in whites of Jewish descent.


Diarrhea may be bloody or contain pus and mucus.

Tenesmus (painful straining), sense of urgency, and frequency.

Increased bowel sounds; abdomen may appear flat, but, as condition continues, abdomen may appear distended.

There often is weight loss, fever, dehydration, hypokalemia, anorexia, nausea and vomiting, iron-deficiency anemia, and cachexia (general lack of nutrition and wasting with chronic disease).

Crampy abdominal pain.

The disease usually begins in the rectum and sigmoid and spreads proximally, at times, involving the entire colon. Anal area may be irritated and reddened; left lower abdomen may be tender on palpation.

There is a tendency for the patient to experience remissions and exacerbations.

Increased risk of developing colorectal cancer.

May inhibit extracolonic manifestations of eye (iritis, uveitis), joint (polyarthritis), and skin complaints (erythema nodosum, pyoderma gangrenosum).


Diagnosis is based on a combination of laboratory, radiologic, endoscopic, and histologic findings.

Laboratory Tests

Stool examination to rule out enteral pathogens; fecal analysis positive for blood during active disease.

Complete blood count hemoglobin and hematocrit may be low due to bleeding; WBC may be increased.

Elevated erythrocyte sedimentation rate (ESR).

Decreased serum levels of potassium, magnesium, and albumin may be present.

Other Diagnostic Tests

Barium enema to assess extent of disease and detect pseudopolyps, carcinoma, and strictures. May show absence of haustral markings; narrow, lead-pipe appearance; superficial ulcerations.

Flexible proctosigmoidoscopy/colonoscopy findings reveal mucosal erythema and edema, ulcers, inflammation that begins distally in the rectum and spreads proximally for variable distances. Pseudopolyps and friable tissue may be present.

Changes in crypt height, loss of crypts, crypt abscess with neutrophils infiltrates on biopsy.

CT scan can identify complications such as toxic megacolon.

Rectal biopsy differentiates from other inflammatory diseases or cancer.

Cholecystitis

Cholecystitis acute or chronic inflammation causing painful distention of the gallbladder is usually associated with a

gallstone impacted in the cystic duct. Cholecystitis accounts for 10% to 25% of all patients requiring gallbladder surgery.

The acute form is most common among middle-aged women; the chronic form, among the elderly. The prognosis is good

with treatment.

Causes

Gallstones (the most common cause)

Poor or absent blood flow to the gallbladder

Abnormal metabolism of cholesterol and bile salts.

Pathophysiology

In acute cholecystitis, inflammation of the gallbladder wall usually develops after a gallstone lodges in the cystic duct. When bile flow is blocked, the gallbladder becomes inflamed and distended.

Bacterial growth, usually Escherichia coli, may contribute to the inflammation. Edema of the gallbladder (and sometimes

the cystic duct) obstructs bile flow, which chemically irritates the gallbladder. Cells in the gallbladder wall may become oxygen starved and die as the distended organ presses on vessels and impairs blood flow. The dead cells slough off, and an exudate covers ulcerated areas, causing the gallbladder to adhere to surrounding structures.

Signs and symptoms

Acute abdominal pain in the right upper quadrant that may radiate to the back, between the shoulders, or to the

front of the chest secondary to inflammation and irritation of nerve fibers

Colic due to the passage of gallstones along the bile duct

Nausea and vomiting triggered by to the inflammatory response

Chills related to fever

Low-grade fever secondary to inflammation

Jaundice from obstruction of the common bile duct by stones.

Complications

Perforation and abscess formation

Fistula formation

Gangrene

Empyema

Cholangitis

Hepatitis

Pancreatitis

Gallstone ileus

Carcinoma.

Diagnosis

X-ray reveals gallstones if they contain enough calcium to be radiopaque; also helps disclose porcelain gallbladder

(hard, brittle gall bladder due to calcium deposited in wall), limy bile, and gallstone ileus.

Ultrasonography detects gallstones as small as 2 mm and distinguishes between obstructive and nonobstructive

jaundice.

Levels of serum alkaline phosphate, lactate dehydrogenase, aspartate aminotransferase, and total bilirubin are high; serum amylase slightly elevated; and icteric index elevated. White blood cell counts are slightly elevated during cholecystitis attack.

Vincent's angina:

A reoccurring periodontal disease which results in necrosis and ulceration of the gums.

Symptoms may include fever, bone loss, breath odor and enlarge neck and throat lymph nodes. Also called trench mouth, acute necrotizing ulcerative gingivitis or Vincent's infection.

An acute or chronic GINGIVITIS characterized by redness and swelling, NECROSIS extending from the interdental papillae along the gingival margins, PAIN; HEMORRHAGE, necrotic odor, and often a pseudomembrane. The condition may extend to the ORAL MUCOSA; TONGUE; PALATE; or PHARYNX.

Vincent gingivitis,also calledVincent infection,Vincent stomatitis,acute necrotizing ulcerative gingivitis,Vincent angina,ortrench mouth,

acute and painful infection of the tooth margins and gums that is caused by the symbiotic microorganismsBacillus fusiformisandBorrelia vincentii. The chief symptoms are painful, swollen, bleeding gums; small, painful ulcers covering the gums and tooth margins; and characteristic fetid breath. The ulcers may spread to the throat and tonsils. Fever and malaise may also be present. Vincent gingivitis can occur after a prolonged failure to brush ones teeth, though there are many other predisposing factors, such as vitamin deficiencies, emotional stress, and so on.

GASTROESOPHAGEAL REFLUX DISEASE AND ESOPHAGITIS

Gastric contents flow back into the esophagus in gastroesophageal reflux disease (GERD) due to incompetent lower esophageal sphincter (LES). Esophagitis, or inflammation of the esophageal mucosa, may result.


Gastroesophageal reflux associated with an incompetent LES gastric contents reflux (flow backward) through the LES into the esophagus.

Can be the result of impaired gastric emptying from gastroparesis or partial gastric outlet obstruction.

The acidity of gastric content and amount of time in contact with esophageal mucosa are related to the degree of mucosal damage.

Inflammation and ulceration of the esophagus may result, causing esophagitis.

May be caused by motility disorders achalasia, scleroderma, esophageal spasm.


GERD

The most common symptom is heartburn (pyrosis), typically occurring 30 to 60 minutes after meals and with reclining positions. May have complaints of spontaneous reflux (regurgitation) of sour or bitter gastric contents into the mouth.

Other typical symptoms include globus (sensation of something in throat), mild epigastric pain, dyspepsia, and nausea and/or vomiting.

Dysphagia is a less common symptom.

Atypical symptoms include chest pain, hoarseness, recurrent sore throat, frequent throat clearing, chronic cough, dental enamel loss, bronchospasm (asthma/wheezing), and odynophagia (sharp substernal pain on swallowing).

Symptoms that may suggest other disease etiologies need further evaluation: atypical chest pain (rule out possible cardiac causes), dysphagia, odynophagia, GI bleeding, shortness of breath, or weight loss (rule out cancer or esophageal stricture).

Esophagitis

Esophagitis is an acute or chronic inflammation of the esophagus. Severity of symptoms may be unrelated to the degree of esophageal tissue damage.

Symptoms vary according to etiology of esophagitis. Symptoms include dysphagia, odynophagia, severe burning, chest pain.

Causes of esophagitis other than GERD

Infectious Candida, herpes, human immunodeficiency virus, cytomegalovirus

Chemical (alkali or acid) or radiation therapy

Medication-induced may include doxycycline, ascorbic acid, quinidine, potassium chloride, bisphosphonates


Uncomplicated GERD may be diagnosed on patient history of typical symptoms.

Endoscopy can visualize inflammation, lesions, or erosions. Biopsy can confirm diagnosis.

Esophageal manometry measures LES pressure and determines if esophageal peristalsis is adequate. This study should be used before patients undergo surgical treatment for reflux. This test is also done before a pH probe for determination of correct catheter placement.

Acid perfusion (Bernstein test) onset of symptoms after ingestion of dilute hydrochloric acid and saline is considered positive. This test differentiates between cardiac and noncardiac chest pain.

Ambulatory 24-hour pH monitoring is frequently performed for diagnosing GERD or reflux esophagitis. It determines the amount of gastroesophageal acid reflux and has a 70% to 90% specificity rate. The Bravo pH capsule system is a catheter-free system in which a capsule containing a radiotelemetry pH sensor is inserted into the esophagus. This sensor transmits signals to an external pager-size receiver, allowing the patient to be catheter-free during the 24 hours of pH testing.

Barium esophagography use of barium with radiographic studies to diagnose mechanical and motility disorders. This test is rarely useful in diagnosing GERD.

ESOPHAGEAL DIVERTICULUM

An esophageal diverticulum is an outpouching of the esophageal wall, usually in the cervical posterior side, secondary to an obstructive or inflammatory process.


Zenker's diverticulum protrusion of pharyngeal mucosa at the pharyngoesophageal junction between the interior pharyngeal constrictor and cricopharyngeal muscle.

Mid or distal esophageal diverticula may develop above strictures or may be secondary to motility disorders.


Zenker's Diverticulum

Difficulty in swallowing, fullness in neck, throat discomfort, a feeling that food stops before it reaches the stomach, and regurgitation of undigested food

Belching, gurgling, or nocturnal coughing brought about by diverticulum becoming filled with food or liquid, which is regurgitated and may irritate the trachea

Halitosis and foul taste in mouth caused by food decomposing in a pouch (diverticulum)

Weight loss due to nutritional depletion

GERONTOLOGIC ALERT

Hoarseness, asthma, and pneumonitis may be the only signs of esophageal diverticula in elderly patients.

Mid or Distal Esophageal Diverticula

Generally no symptoms.


Barium esophagogram outlines diverticulum.

Endoscopy is not indicated and may be dangerous due to the possibility of rupture.

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