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Pathophysiology.ENH 220
The Gastrointestinal Tract
Learning Objectives (1 of 2)
• Identify major types of cleft lip and cleft palate
deformity
• Explain pathogenesis and prevention of dental caries
and periodontal disease
• Describe common congenital anomalies of the GIT,
clinical manifestations, diagnosis, treatment
• Describe three most common lesions of the esophagus
that lead to esophageal obstruction
• Explain pathogenesis, complications, and treatment of
peptic ulcer
• Describe types and clinical manifestations of acute and
chronic enteritis
enh220 | Foundations of Pathophysiology
Learning Objectives (2 of 2)
• Differentiate acute appendicitis and Meckel’s
diverticulitis in terms of pathogenesis, clinical
manifestations, and treatment
• Describe pathogenesis of diverticulitis and the role of
diet in its development
• Discuss causes, clinical manifestations, complications
– Intestinal obstruction
– Colon cancer
– Diverticulosis
enh220 | Foundations of Pathophysiology
Gastrointestinal Tract
• Digestion and absorption of food
• Oral cavity
• Esophagus, stomach, small and large intestines,
anus

enh220 | Foundations of Pathophysiology
Cleft Lip and Cleft Palate
• Embryologically, face and palate formed by
coalescence of cell masses that merge to form facial
structures
• Palate formed by two masses of tissues that grow
medially and fuse at midline to separate as nose and
mouth
• Maldevelopment leads to defects
– 1 per 1000 births
– Multifactorial inheritance pattern

• Surgical correction (cheiloplasty)
– Cleft lip: soon after birth
– Cleft palate:

enh220 | Foundations of Pathophysiology
Types of cleft lip and palate abnormalities
viewed from below

enh220 | Foundations of Pathophysiology
Abnormalities of Tooth Development
• Teeth: specialized structures that develop in tissues of
the jaws
• Two sets
– Temporary or deciduous teeth (20 teeth)
– Permanent teeth (32 teeth)

• Missing teeth or extra teeth: common abnormality
• Enamel forms at specific times during embryologic
period
• Tetracycline: administered during enamel formation
causes permanent yellow-gray to brown discoloration
of the crown

enh220 | Foundations of Pathophysiology
Abnormalities of Tooth Development
enh220 | Foundations of Pathophysiology
Dental Caries and Periodontal Disease
• Oral cavity: diverse collection of aerobic and anaerobic bacteria
that mix with saliva, forming sticky film on teeth (dental plaque)
• Plaque and action of bacteria result in tooth decay (caries)
• Dental cavity: loss of tooth structure from bacterial action
• Gingivitis: inflammation of the gums due to masses of bacteria
and debris accumulating around base of teeth
• Periodontal disease: inflammation extends to tissues that
support teeth; forms small pockets of infection between teeth
and gums
– Two types:
enh220 | Foundations of Pathophysiology
The Stomach
• Is normally a very acid environment (pH 1.53.5)
• Digests proteins
• Breaks down, mixes and puts chyme into
duodenum
• Produces one essential protein: intrinsic factor
used in Vitamin B12 absorption
• Absorbs some compounds like
Histology of the stomach
The Gastric Wall
The gastric wall
The Bottom of the Pit
• Parietal cell: secretes HCl and
intrinsic factor
• Chief cell: secretes
pepsinogen and a bit of
lipase (fat digestion).
Pepsinogen is converted to
pepsin in the presence of HCl
• Enteroendocrine (or G) cell:
releases hormones such as
A stylized view of the gastric mucosa
Why doesn’t the stomach autodigest?
• About 2-3L of gastric fluids are released into the stomach
daily
• In response, the stomach wall secretes protective mucus
• The most common of the epithelial cells forming the
stomach wall are mucous cells.
• 500,000 epithelial cells of the surface lining are shed
every minute, thereby protecting the deeper layers of
the stomach wall.
• This surface layer is replaced completely every three days
and the entire lining regenerates itself every two weeks.
Regulation of gastric emptying
Control of gastric emptying
• Neural: the presence of neuronal NO (nitric oxide) allows the
stomach to relax to accommodate up to 1 litre of food
• Hormonal: gastrin and serotonin stimulate, VIP (vasoactive
intestinal peptide), GIP (gastric inhibitory peptide) and
somatostatin inhibit
• The duodenum controls the emptying based on content:
– Carbohydrates, water easy
– Small amounts of acid
– Fats enter very slowly
Stomatitis
• Inflammation of the oral cavity
• Causes
– Irritants: alcohol, tobacco, hot or spicy foods
– Infectious agents: Herpes virus, Candida albicans
fungus, bacteria that cause trench mouth

enh220 | Foundations of Pathophysiology
Carcinoma of the Oral Cavity
• Arises from squamous epithelium
– Lips
– Cheek
– Tongue
– Palate
– Back of throat

enh220 | Foundations of Pathophysiology
Esophagus (1 of 3)
• Muscular tube that extends from pharynx to stomach
with sphincters at both upper and lower ends
– Upper sphincter relaxes to allow passage of swallowed food
– Lower (gastroesophageal or cardiac) sphincter relaxes to
allow passage of food to the stomach

• Diseases
– Failure of cardiac sphincter to function properly
– Tears in lining of esophagus from retching and vomiting
– At gastroesophageal junction from repetitive, intermittent,
vigorous contractions that increase intraabdominal pressure
– Esophageal obstruction from carcinoma, food impaction, or
stricture
enh220 | Foundations of Pathophysiology
Esophagus (2 of 3)
• Symptoms
– Difficulty swallowing (dysphagia)
– Substernal discomfort or pain
– Inability to swallow (complete obstruction)
– Regurgitation of food into trachea
– Choking and coughing

• Two major disturbances of cardiac sphincter
– Cardiospasm: sphincter fails to open properly due to malfunction of
nerve plexus; esophagus becomes dilated proximal to constricted
sphincter from food retention
– Treatment: periodic stretching of sphincter; surgery
– Incompetent cardiac sphincter: sphincter remains open; gastric juices
leak back into esophagus
enh220 | Foundations of Pathophysiology
Esophagus (3 of 3)
• Complications of incompetent cardiac sphincter
– Reflux esophagitis: inflammation
– Ulceration and scarring of squamous mucosal lining
– Barrett’s esophagus: glandular metaplasia; change from
squamous to columnar epithelium; increased risk for cancer

• Esophageal obstruction
– Carcinoma: can arise anywhere in esophagus
– Tumor narrows lumen of esophagus, infiltrates surrounding
tissue, invades trachea (tracheoesophageal fistula)
– Food impaction: distal part
– Stricture:
enh220 | Foundations of Pathophysiology
Gastric mucosal tear caused by
retching and vomiting

enh220 | Foundations of Pathophysiology
Acute Gastritis
• Inflammation of the gastric lining
• Self-limited inflammation of short duration
• May be associated with mucosal ulceration or
bleeding
• Alcohol:

enh220 | Foundations of Pathophysiology
H. Pylori Gastritis (1 of 2)
• Small, curved, gram-negative organisms that colonize
surface of gastric mucosa
• Grow within layer of mucus covering epithelial cells
• Produce urease that decomposes urea, a product of
protein metabolism, into ammonia
• Ammonia neutralizes gastric acid allowing organisms
to flourish; organisms also produce enzymes that
break down mucus layer

enh220 | Foundations of Pathophysiology
H. Pylori Gastritis (2 of 2)
• Common infection that increases with age (50%
by age 50)
• Spreads via person-to-person through close
contact and fecal-oral route
• Increased risk of gastric carcinoma: intestinal
metaplasia
• Increased risk of malignant lymphoma (mucosaassociated lymphoid tissue, MALT)
enh220 | Foundations of Pathophysiology
Peptic Ulcer
• Pathogenesis
– Digestion of mucosa due to increased acid secretions and
digestive enzymes (gastric acid and pepsin)
– Helicobacter pylori injures mucosa directly or through increased
acid secretion by gastric mucosa
– Common sites: distal stomach or proximal duodenum

• Complications: hemorrhage, perforation, peritonitis,
obstruction from scarring
• Treatment
– Antacids: block acid secretion by gastric epithelial cells
– Antibiotic therapy: against H. pylori
– Surgery if medical therapy fails

enh220 | Foundations of Pathophysiology
Gastric ulcer, eroded a blood
vessel at base of ulcer causing
profuse bleeding

enh220 | Foundations of Pathophysiology

Large, chronic
duodenal ulcer
Carcinoma of the Stomach
• Manifestations
– Vague upper abdominal discomfort
– Iron-deficiency anemia (chronic blood loss from ulcerated
surface of tumor)

• Diagnosis: biopsy by means of gastroscopy
• Treatment: surgical resection of affected part,
surrounding tissue and lymph nodes
• Long-term survival:

enh220 | Foundations of Pathophysiology
Carcinoma of the Stomach

enh220 | Foundations of Pathophysiology
Inflammatory Diseases of the Intestines
• Acute enteritis
– Intestinal infections; common; of short duration
– Nausea, vomiting, abdominal discomfort, loose stools

• Chronic enteritis: less common, more difficult to treat
• Regional enteritis or Crohn’s disease: distal ileum
– Chronic inflammation and ulceration of mucosa with
thickening and scarring of bowel wall
– Inflammation may be scattered with normal intervening
areas or “skip areas”
– Treatment:

enh220 | Foundations of Pathophysiology
Ulcerative Colitis (1 of 2)
• Ulcerative colitis: large intestines and rectum
– Inflammation is limited to mucosa, bowel not
thickened unlike in Crohn’s
– Frequently begins in rectal mucosa and spreads
until entire colon is involved

• Complications
– Bleeding; bloody diarrhea
– Perforation: from extensive inflammation with
leakage of intestinal contents into peritoneal cavity
– Long-standing disease may develop cancer of colon
and/or rectum
enh220 | Foundations of Pathophysiology
Ulcerative Colitis (2 of 2)
• Treatment
– Symptomatic and supportive measures
– Antibiotics, corticosteroids to control flare-ups
– Immunosuppressive drugs
– Surgical resection

enh220 | Foundations of Pathophysiology
Inflammatory Diseases of the Intestines (1
of 3)
• Antibiotic-associated colitis: broad-spectrum antibiotics
destroy normal intestinal flora
– Allows growth of anaerobic spore-forming bacteria,
Clostridium difficile not inhibited by antibiotic taken
– Organisms produce toxins causing inflammation and necrosis
of colonic mucosa
– Diarrhea, abdominal pain, fever

• Diagnosis: stool culture, toxin in stool
• Treatment: stop antibiotic treatment; give vancomycin
or metronidazole
enh220– Foundations of Pathophysiology intestinal motility will prolong illness
| Drugs that decrease
Inflammatory Diseases of the Intestines (2
of 3)
• Appendicitis: most common inflammatory lesion of
the bowel
– Narrow caliber of appendix may be plugged with fecal
material
– Secretions of appendix drain poorly, create pressure in
appendiceal lumen, compressing blood supply
– Bacteria invade appendiceal wall causing inflammation

• Manifestations
– Generalized abdominal pain localizing in right lower
quadrant; rebound tenderness; rigidity

• Treatment:

enh220 | Foundations of Pathophysiology
Inflammatory Diseases of the Intestines (3
of 3)
• Meckel’s diverticulum
– Outpouching at distal ileum, 12-18 inches proximal to cecum
– From persistence of a remnant of the vitelline duct, narrow
tubular channel connecting small intestine with yolk sac
embryologically
– Found in 2% of population; usually asymptomatic

• May become infected causing features and
complications similar to acute appendicitis
• Lining may consist of ectopic acid-secreting gastric
mucosa and may cause peptic ulcer
enh220 | Foundations of Pathophysiology
Regional enteritis, mucosa
ulcerated and covered with
inflammatory exudate

enh220 | Foundations of Pathophysiology
Inflammatory Disease Intestines

enh220 | Foundations of Pathophysiology
Disturbances in Bowel Function
• Food intolerance: Crampy abdominal pain, distention,
flatulence, loose stools
• Lactose intolerance
– Unable to digest lactose into glucose and galactose for
absorption due to lactase deficiency
– Enzyme abundant in infants and young children
– Unabsorbed lactose remains in intestinal lumen and raises
osmotic pressure of bowel contents
– Fermented by bacteria in colon, yielding lactic acid that
further increases intraluminal pressure
enh220 –Foundations of Pathophysiology
| Common in
Irritable Bowel Syndrome
• Also known as spastic colitis or mucous colitis
• Episodes of crampy abdominal discomfort, loud gurgling
bowel sounds, and disturbed bowel function without
structural or biochemical abnormalities
• Alternating diarrhea and constipation
• Excessive mucus secreted by colonic mucosal glands
• Diagnosis: by exclusion
– Rule out pathogenic infections, food intolerance, and
inflammatory conditions

• Treatment
– Reduce emotional tension
– Improve intestinal motility

enh220 | Foundations of Pathophysiology
Obesity
• Calorie intake exceeds requirement
– Cardiovascular disease
– Musculoskeletal problems
– Impaired pulmonary function
– Operation carries high risk
– Higher death rate from cancer

• Treatment
– Medical management often ineffective
– Surgical treatment:
enh220 | Foundations of Pathophysiology
Anorexia nervosa
• False perception of being fat despite marked weight
loss
• Food intake restricted to lose weight
• Self-induced vomiting and laxatives may be used to
promote weight loss
• Organ system abnormalities occur related to food
restriction
• Requires psychiatric-medical treatment by persons
experienced in dealing with eating disorders
enh220 | Foundations of Pathophysiology
Bulimia nervosa
• Binge eating followed by self-induced vomiting
• Usually weight maintained. Family and friends may
not be aware of behavior
• Risk of gastric mucosa tears from retching and
vomiting
• Dental problems and metabolic alkalosis from
vomiting-induced loss of gastric acid
• Treatment similar to treatment of anorexia nervosa

enh220 | Foundations of Pathophysiology
Binge eating disorders
• Characterized by binge eating without selfinduced vomiting leading to weight gain
• Affects older adults and complicates problems
of person trying to lose weight
• Treatment requires patient motivation, as
when dealing with overeating problems

enh220 | Foundations of Pathophysiology
Colon Diverticulosis and Diverticulitis
• Diverticulosis: outpouchings or diverticula of colonic
mucosa through weak areas in the muscular wall of
large intestine
– Low-residue diet predisposes to condition as increased
intraluminal pressure must be generated to propel stools
through colon
– Acquired, usually asymptomatic, seen in older people
– Common site: sigmoid colon

• Diverticulitis: inflammation incited by bits of fecal
material trapped within outpouchings
• Complications:

enh220 | Foundations of Pathophysiology
Diverticulosis of colon. Exterior of colon,
illustrating several diverticula projecting through
the wall of the colon.

enh220 | Foundations of Pathophysiology
Diverticula of colon demonstrated by
injection of barlum contrast material into
colon (barium enema)

enh220 | Foundations of Pathophysiology
Intestinal Obstructions (1 of 5)
• Conditions blocking normal passage of
intestinal contents
• Always considered as a serious condition
• Severity depends on location of obstruction,
completeness, interference with blood supply
• High intestinal obstruction
– Severe, crampy abdominal pain from vigorous
peristalsis
– Vomiting with loss of H2O and electrolytes, may
result in dehydration
enh220 | Foundations of Pathophysiology
Intestinal Obstructions (2 of 5)
• Low intestinal obstruction
– Symptoms less acute
– Mild, crampy abdominal pain
– Moderate distention of abdomen

• Common causes of intestinal obstruction
– Adhesions
– Hernia
– Tumor
– Volvulus
– Intussusception

enh220 | Foundations of Pathophysiology
Intestinal Obstructions (3 of 5)
• Adhesions
– Adhesive bands of connective tissue
– May cause loop of bowel to become kinked,
compressed, twisted
– Causes obstruction proximal to site of adhesion

• Hernia
– Protrusion of loop of bowel through a small
opening, usually in abdominal wall
– Herniated loop pushes through peritoneum to
form hernial sac

enh220 | Foundations of Pathophysiology
Intestinal Obstructions (4 of 5)
• Hernia
– Inguinal hernia: common in men; loop of small
bowel protrudes through a weak area in inguinal
ring and descends downward into scrotum
– Umbilical and femoral hernia: common in both
sexes
– Umbilical hernia: loop of bowel protrudes into umbilicus
through defect in the abdominal wall
– Femoral hernia:
enh220 | Foundations of Pathophysiology
Intestinal Obstructions (5 of 5)
• Reducible hernia: herniated loop of bowel can be pushed
back into abdominal cavity
• Incarcerated hernia: cannot be pushed back
• Strangulated hernia: loop of bowel is tightly constricted
obstructing the blood supply to the herniated bowel;
requires prompt surgical intervention
• Volvulus: rotary twisting of bowel impairing blood supply;
common site: sigmoid colon
• Intussusception: telescoping of a segment of bowel into
adjacent segment; from vigorous peristalsis or tumor
– Common site: terminal ileum
enh220 | Foundations of Pathophysiology
Fibrous adhesions between
a loop of small intestine and
omentum

enh220 | Foundations of Pathophysiology
Inguinal hernia,
bilateral, extending
into scrotum
enh220 | Foundations of Pathophysiology

Umbilical hernia,
infant
Intussusception resulting from a colon
tumor

enh220 | Foundations of Pathophysiology
Volvulus
A. Rotary twisting of sigmoid colon on its mesentery
B. Obstruction of colon and interruption of blood
supply
Tumors of the Colon
• Benign pedunculated polyps
– Frequent
– Tip may erode causing bleeding
– Removed by colonoscopy

• Carcinoma
– Cecum and right half of colon
– Does not cause obstruction as caliber is large and bowel contents are
relatively soft
– Tumor can ulcerate, bleed; leads to chronic iron-deficiency anemia
– Symptoms of anemia: weakness and fatigue
– Left half of colon
– Causes obstruction and symptoms of lower intestinal obstruction
Colon Carcinoma

enh220 | Foundations of Pathophysiology
Hemorrhoids
• Varicose veins of hemorrhoidal venous plexus that
drains rectum and anus
• Constipation and straining predispose to development
• Relieved by high-fiber diet rich in fruits and vegetables,
stool softeners, rectal ointment, or surgery
– Internal hemorrhoids
– Veins of the lower rectum
– May erode and bleed, become thrombosed, or prolapse
– External hemorrhoids
– Veins of anal canal and perianal skin
– May become thrombosed, causing discomfort
Diagnosis of GI Disease
• Endoscopic procedures
– To directly visualize and biopsy abnormal areas such as
esophagus, stomach, intestines

• Radiologic examination
– To examine areas that cannot be readily visualized
– To evaluate motility problems
– To visualize contours of GIT mucosa
– To identify location and extent of disease
– Examples: Upper gastrointestinal tract – UGI
– Colon – BE (barium enema)

enh220 | Foundations of Pathophysiology
Colon carcinoma demonstrated by barium
enema

enh220 | Foundations of Pathophysiology
Discussion
• A 45-year-old patient has a large right-sided
colon carcinoma with iron deficiency anemia.
The anemia is most likely due to:
A. Impaired absorption of nutrients due to the tumor
B. Chronic blood loss from ulcerated surface of the tumor
C. Poor appetite
D. Metastases to the liver
E. Obstruction of the colon by the tumor
enh220 | Foundations of Pathophysiology

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Chapter 17 git-mod

  • 2. Learning Objectives (1 of 2) • Identify major types of cleft lip and cleft palate deformity • Explain pathogenesis and prevention of dental caries and periodontal disease • Describe common congenital anomalies of the GIT, clinical manifestations, diagnosis, treatment • Describe three most common lesions of the esophagus that lead to esophageal obstruction • Explain pathogenesis, complications, and treatment of peptic ulcer • Describe types and clinical manifestations of acute and chronic enteritis enh220 | Foundations of Pathophysiology
  • 3. Learning Objectives (2 of 2) • Differentiate acute appendicitis and Meckel’s diverticulitis in terms of pathogenesis, clinical manifestations, and treatment • Describe pathogenesis of diverticulitis and the role of diet in its development • Discuss causes, clinical manifestations, complications – Intestinal obstruction – Colon cancer – Diverticulosis enh220 | Foundations of Pathophysiology
  • 4. Gastrointestinal Tract • Digestion and absorption of food • Oral cavity • Esophagus, stomach, small and large intestines, anus enh220 | Foundations of Pathophysiology
  • 5. Cleft Lip and Cleft Palate • Embryologically, face and palate formed by coalescence of cell masses that merge to form facial structures • Palate formed by two masses of tissues that grow medially and fuse at midline to separate as nose and mouth • Maldevelopment leads to defects – 1 per 1000 births – Multifactorial inheritance pattern • Surgical correction (cheiloplasty) – Cleft lip: soon after birth – Cleft palate: enh220 | Foundations of Pathophysiology
  • 6. Types of cleft lip and palate abnormalities viewed from below enh220 | Foundations of Pathophysiology
  • 7. Abnormalities of Tooth Development • Teeth: specialized structures that develop in tissues of the jaws • Two sets – Temporary or deciduous teeth (20 teeth) – Permanent teeth (32 teeth) • Missing teeth or extra teeth: common abnormality • Enamel forms at specific times during embryologic period • Tetracycline: administered during enamel formation causes permanent yellow-gray to brown discoloration of the crown enh220 | Foundations of Pathophysiology
  • 8. Abnormalities of Tooth Development enh220 | Foundations of Pathophysiology
  • 9. Dental Caries and Periodontal Disease • Oral cavity: diverse collection of aerobic and anaerobic bacteria that mix with saliva, forming sticky film on teeth (dental plaque) • Plaque and action of bacteria result in tooth decay (caries) • Dental cavity: loss of tooth structure from bacterial action • Gingivitis: inflammation of the gums due to masses of bacteria and debris accumulating around base of teeth • Periodontal disease: inflammation extends to tissues that support teeth; forms small pockets of infection between teeth and gums – Two types: enh220 | Foundations of Pathophysiology
  • 10. The Stomach • Is normally a very acid environment (pH 1.53.5) • Digests proteins • Breaks down, mixes and puts chyme into duodenum • Produces one essential protein: intrinsic factor used in Vitamin B12 absorption • Absorbs some compounds like
  • 11. Histology of the stomach
  • 12. The Gastric Wall The gastric wall
  • 13. The Bottom of the Pit • Parietal cell: secretes HCl and intrinsic factor • Chief cell: secretes pepsinogen and a bit of lipase (fat digestion). Pepsinogen is converted to pepsin in the presence of HCl • Enteroendocrine (or G) cell: releases hormones such as
  • 14. A stylized view of the gastric mucosa
  • 15. Why doesn’t the stomach autodigest? • About 2-3L of gastric fluids are released into the stomach daily • In response, the stomach wall secretes protective mucus • The most common of the epithelial cells forming the stomach wall are mucous cells. • 500,000 epithelial cells of the surface lining are shed every minute, thereby protecting the deeper layers of the stomach wall. • This surface layer is replaced completely every three days and the entire lining regenerates itself every two weeks.
  • 17. Control of gastric emptying • Neural: the presence of neuronal NO (nitric oxide) allows the stomach to relax to accommodate up to 1 litre of food • Hormonal: gastrin and serotonin stimulate, VIP (vasoactive intestinal peptide), GIP (gastric inhibitory peptide) and somatostatin inhibit • The duodenum controls the emptying based on content: – Carbohydrates, water easy – Small amounts of acid – Fats enter very slowly
  • 18. Stomatitis • Inflammation of the oral cavity • Causes – Irritants: alcohol, tobacco, hot or spicy foods – Infectious agents: Herpes virus, Candida albicans fungus, bacteria that cause trench mouth enh220 | Foundations of Pathophysiology
  • 19. Carcinoma of the Oral Cavity • Arises from squamous epithelium – Lips – Cheek – Tongue – Palate – Back of throat enh220 | Foundations of Pathophysiology
  • 20. Esophagus (1 of 3) • Muscular tube that extends from pharynx to stomach with sphincters at both upper and lower ends – Upper sphincter relaxes to allow passage of swallowed food – Lower (gastroesophageal or cardiac) sphincter relaxes to allow passage of food to the stomach • Diseases – Failure of cardiac sphincter to function properly – Tears in lining of esophagus from retching and vomiting – At gastroesophageal junction from repetitive, intermittent, vigorous contractions that increase intraabdominal pressure – Esophageal obstruction from carcinoma, food impaction, or stricture enh220 | Foundations of Pathophysiology
  • 21. Esophagus (2 of 3) • Symptoms – Difficulty swallowing (dysphagia) – Substernal discomfort or pain – Inability to swallow (complete obstruction) – Regurgitation of food into trachea – Choking and coughing • Two major disturbances of cardiac sphincter – Cardiospasm: sphincter fails to open properly due to malfunction of nerve plexus; esophagus becomes dilated proximal to constricted sphincter from food retention – Treatment: periodic stretching of sphincter; surgery – Incompetent cardiac sphincter: sphincter remains open; gastric juices leak back into esophagus enh220 | Foundations of Pathophysiology
  • 22. Esophagus (3 of 3) • Complications of incompetent cardiac sphincter – Reflux esophagitis: inflammation – Ulceration and scarring of squamous mucosal lining – Barrett’s esophagus: glandular metaplasia; change from squamous to columnar epithelium; increased risk for cancer • Esophageal obstruction – Carcinoma: can arise anywhere in esophagus – Tumor narrows lumen of esophagus, infiltrates surrounding tissue, invades trachea (tracheoesophageal fistula) – Food impaction: distal part – Stricture: enh220 | Foundations of Pathophysiology
  • 23. Gastric mucosal tear caused by retching and vomiting enh220 | Foundations of Pathophysiology
  • 24. Acute Gastritis • Inflammation of the gastric lining • Self-limited inflammation of short duration • May be associated with mucosal ulceration or bleeding • Alcohol: enh220 | Foundations of Pathophysiology
  • 25. H. Pylori Gastritis (1 of 2) • Small, curved, gram-negative organisms that colonize surface of gastric mucosa • Grow within layer of mucus covering epithelial cells • Produce urease that decomposes urea, a product of protein metabolism, into ammonia • Ammonia neutralizes gastric acid allowing organisms to flourish; organisms also produce enzymes that break down mucus layer enh220 | Foundations of Pathophysiology
  • 26. H. Pylori Gastritis (2 of 2) • Common infection that increases with age (50% by age 50) • Spreads via person-to-person through close contact and fecal-oral route • Increased risk of gastric carcinoma: intestinal metaplasia • Increased risk of malignant lymphoma (mucosaassociated lymphoid tissue, MALT) enh220 | Foundations of Pathophysiology
  • 27. Peptic Ulcer • Pathogenesis – Digestion of mucosa due to increased acid secretions and digestive enzymes (gastric acid and pepsin) – Helicobacter pylori injures mucosa directly or through increased acid secretion by gastric mucosa – Common sites: distal stomach or proximal duodenum • Complications: hemorrhage, perforation, peritonitis, obstruction from scarring • Treatment – Antacids: block acid secretion by gastric epithelial cells – Antibiotic therapy: against H. pylori – Surgery if medical therapy fails enh220 | Foundations of Pathophysiology
  • 28. Gastric ulcer, eroded a blood vessel at base of ulcer causing profuse bleeding enh220 | Foundations of Pathophysiology Large, chronic duodenal ulcer
  • 29. Carcinoma of the Stomach • Manifestations – Vague upper abdominal discomfort – Iron-deficiency anemia (chronic blood loss from ulcerated surface of tumor) • Diagnosis: biopsy by means of gastroscopy • Treatment: surgical resection of affected part, surrounding tissue and lymph nodes • Long-term survival: enh220 | Foundations of Pathophysiology
  • 30. Carcinoma of the Stomach enh220 | Foundations of Pathophysiology
  • 31. Inflammatory Diseases of the Intestines • Acute enteritis – Intestinal infections; common; of short duration – Nausea, vomiting, abdominal discomfort, loose stools • Chronic enteritis: less common, more difficult to treat • Regional enteritis or Crohn’s disease: distal ileum – Chronic inflammation and ulceration of mucosa with thickening and scarring of bowel wall – Inflammation may be scattered with normal intervening areas or “skip areas” – Treatment: enh220 | Foundations of Pathophysiology
  • 32. Ulcerative Colitis (1 of 2) • Ulcerative colitis: large intestines and rectum – Inflammation is limited to mucosa, bowel not thickened unlike in Crohn’s – Frequently begins in rectal mucosa and spreads until entire colon is involved • Complications – Bleeding; bloody diarrhea – Perforation: from extensive inflammation with leakage of intestinal contents into peritoneal cavity – Long-standing disease may develop cancer of colon and/or rectum enh220 | Foundations of Pathophysiology
  • 33. Ulcerative Colitis (2 of 2) • Treatment – Symptomatic and supportive measures – Antibiotics, corticosteroids to control flare-ups – Immunosuppressive drugs – Surgical resection enh220 | Foundations of Pathophysiology
  • 34. Inflammatory Diseases of the Intestines (1 of 3) • Antibiotic-associated colitis: broad-spectrum antibiotics destroy normal intestinal flora – Allows growth of anaerobic spore-forming bacteria, Clostridium difficile not inhibited by antibiotic taken – Organisms produce toxins causing inflammation and necrosis of colonic mucosa – Diarrhea, abdominal pain, fever • Diagnosis: stool culture, toxin in stool • Treatment: stop antibiotic treatment; give vancomycin or metronidazole enh220– Foundations of Pathophysiology intestinal motility will prolong illness | Drugs that decrease
  • 35. Inflammatory Diseases of the Intestines (2 of 3) • Appendicitis: most common inflammatory lesion of the bowel – Narrow caliber of appendix may be plugged with fecal material – Secretions of appendix drain poorly, create pressure in appendiceal lumen, compressing blood supply – Bacteria invade appendiceal wall causing inflammation • Manifestations – Generalized abdominal pain localizing in right lower quadrant; rebound tenderness; rigidity • Treatment: enh220 | Foundations of Pathophysiology
  • 36. Inflammatory Diseases of the Intestines (3 of 3) • Meckel’s diverticulum – Outpouching at distal ileum, 12-18 inches proximal to cecum – From persistence of a remnant of the vitelline duct, narrow tubular channel connecting small intestine with yolk sac embryologically – Found in 2% of population; usually asymptomatic • May become infected causing features and complications similar to acute appendicitis • Lining may consist of ectopic acid-secreting gastric mucosa and may cause peptic ulcer enh220 | Foundations of Pathophysiology
  • 37. Regional enteritis, mucosa ulcerated and covered with inflammatory exudate enh220 | Foundations of Pathophysiology
  • 38. Inflammatory Disease Intestines enh220 | Foundations of Pathophysiology
  • 39. Disturbances in Bowel Function • Food intolerance: Crampy abdominal pain, distention, flatulence, loose stools • Lactose intolerance – Unable to digest lactose into glucose and galactose for absorption due to lactase deficiency – Enzyme abundant in infants and young children – Unabsorbed lactose remains in intestinal lumen and raises osmotic pressure of bowel contents – Fermented by bacteria in colon, yielding lactic acid that further increases intraluminal pressure enh220 –Foundations of Pathophysiology | Common in
  • 40. Irritable Bowel Syndrome • Also known as spastic colitis or mucous colitis • Episodes of crampy abdominal discomfort, loud gurgling bowel sounds, and disturbed bowel function without structural or biochemical abnormalities • Alternating diarrhea and constipation • Excessive mucus secreted by colonic mucosal glands • Diagnosis: by exclusion – Rule out pathogenic infections, food intolerance, and inflammatory conditions • Treatment – Reduce emotional tension – Improve intestinal motility enh220 | Foundations of Pathophysiology
  • 41. Obesity • Calorie intake exceeds requirement – Cardiovascular disease – Musculoskeletal problems – Impaired pulmonary function – Operation carries high risk – Higher death rate from cancer • Treatment – Medical management often ineffective – Surgical treatment: enh220 | Foundations of Pathophysiology
  • 42. Anorexia nervosa • False perception of being fat despite marked weight loss • Food intake restricted to lose weight • Self-induced vomiting and laxatives may be used to promote weight loss • Organ system abnormalities occur related to food restriction • Requires psychiatric-medical treatment by persons experienced in dealing with eating disorders enh220 | Foundations of Pathophysiology
  • 43. Bulimia nervosa • Binge eating followed by self-induced vomiting • Usually weight maintained. Family and friends may not be aware of behavior • Risk of gastric mucosa tears from retching and vomiting • Dental problems and metabolic alkalosis from vomiting-induced loss of gastric acid • Treatment similar to treatment of anorexia nervosa enh220 | Foundations of Pathophysiology
  • 44. Binge eating disorders • Characterized by binge eating without selfinduced vomiting leading to weight gain • Affects older adults and complicates problems of person trying to lose weight • Treatment requires patient motivation, as when dealing with overeating problems enh220 | Foundations of Pathophysiology
  • 45. Colon Diverticulosis and Diverticulitis • Diverticulosis: outpouchings or diverticula of colonic mucosa through weak areas in the muscular wall of large intestine – Low-residue diet predisposes to condition as increased intraluminal pressure must be generated to propel stools through colon – Acquired, usually asymptomatic, seen in older people – Common site: sigmoid colon • Diverticulitis: inflammation incited by bits of fecal material trapped within outpouchings • Complications: enh220 | Foundations of Pathophysiology
  • 46. Diverticulosis of colon. Exterior of colon, illustrating several diverticula projecting through the wall of the colon. enh220 | Foundations of Pathophysiology
  • 47. Diverticula of colon demonstrated by injection of barlum contrast material into colon (barium enema) enh220 | Foundations of Pathophysiology
  • 48. Intestinal Obstructions (1 of 5) • Conditions blocking normal passage of intestinal contents • Always considered as a serious condition • Severity depends on location of obstruction, completeness, interference with blood supply • High intestinal obstruction – Severe, crampy abdominal pain from vigorous peristalsis – Vomiting with loss of H2O and electrolytes, may result in dehydration enh220 | Foundations of Pathophysiology
  • 49. Intestinal Obstructions (2 of 5) • Low intestinal obstruction – Symptoms less acute – Mild, crampy abdominal pain – Moderate distention of abdomen • Common causes of intestinal obstruction – Adhesions – Hernia – Tumor – Volvulus – Intussusception enh220 | Foundations of Pathophysiology
  • 50. Intestinal Obstructions (3 of 5) • Adhesions – Adhesive bands of connective tissue – May cause loop of bowel to become kinked, compressed, twisted – Causes obstruction proximal to site of adhesion • Hernia – Protrusion of loop of bowel through a small opening, usually in abdominal wall – Herniated loop pushes through peritoneum to form hernial sac enh220 | Foundations of Pathophysiology
  • 51. Intestinal Obstructions (4 of 5) • Hernia – Inguinal hernia: common in men; loop of small bowel protrudes through a weak area in inguinal ring and descends downward into scrotum – Umbilical and femoral hernia: common in both sexes – Umbilical hernia: loop of bowel protrudes into umbilicus through defect in the abdominal wall – Femoral hernia: enh220 | Foundations of Pathophysiology
  • 52. Intestinal Obstructions (5 of 5) • Reducible hernia: herniated loop of bowel can be pushed back into abdominal cavity • Incarcerated hernia: cannot be pushed back • Strangulated hernia: loop of bowel is tightly constricted obstructing the blood supply to the herniated bowel; requires prompt surgical intervention • Volvulus: rotary twisting of bowel impairing blood supply; common site: sigmoid colon • Intussusception: telescoping of a segment of bowel into adjacent segment; from vigorous peristalsis or tumor – Common site: terminal ileum enh220 | Foundations of Pathophysiology
  • 53. Fibrous adhesions between a loop of small intestine and omentum enh220 | Foundations of Pathophysiology
  • 54. Inguinal hernia, bilateral, extending into scrotum enh220 | Foundations of Pathophysiology Umbilical hernia, infant
  • 55. Intussusception resulting from a colon tumor enh220 | Foundations of Pathophysiology
  • 56. Volvulus A. Rotary twisting of sigmoid colon on its mesentery B. Obstruction of colon and interruption of blood supply
  • 57. Tumors of the Colon • Benign pedunculated polyps – Frequent – Tip may erode causing bleeding – Removed by colonoscopy • Carcinoma – Cecum and right half of colon – Does not cause obstruction as caliber is large and bowel contents are relatively soft – Tumor can ulcerate, bleed; leads to chronic iron-deficiency anemia – Symptoms of anemia: weakness and fatigue – Left half of colon – Causes obstruction and symptoms of lower intestinal obstruction
  • 58. Colon Carcinoma enh220 | Foundations of Pathophysiology
  • 59. Hemorrhoids • Varicose veins of hemorrhoidal venous plexus that drains rectum and anus • Constipation and straining predispose to development • Relieved by high-fiber diet rich in fruits and vegetables, stool softeners, rectal ointment, or surgery – Internal hemorrhoids – Veins of the lower rectum – May erode and bleed, become thrombosed, or prolapse – External hemorrhoids – Veins of anal canal and perianal skin – May become thrombosed, causing discomfort
  • 60. Diagnosis of GI Disease • Endoscopic procedures – To directly visualize and biopsy abnormal areas such as esophagus, stomach, intestines • Radiologic examination – To examine areas that cannot be readily visualized – To evaluate motility problems – To visualize contours of GIT mucosa – To identify location and extent of disease – Examples: Upper gastrointestinal tract – UGI – Colon – BE (barium enema) enh220 | Foundations of Pathophysiology
  • 61. Colon carcinoma demonstrated by barium enema enh220 | Foundations of Pathophysiology
  • 62. Discussion • A 45-year-old patient has a large right-sided colon carcinoma with iron deficiency anemia. The anemia is most likely due to: A. Impaired absorption of nutrients due to the tumor B. Chronic blood loss from ulcerated surface of the tumor C. Poor appetite D. Metastases to the liver E. Obstruction of the colon by the tumor enh220 | Foundations of Pathophysiology

Notas do Editor

  1. Animated picture pans in window with fade-in captions (Advanced) Tip: For best results, select a high-resolution, vertically oriented picture, where the picture height is larger than the slide height. The picture in the example above is 15” high and 10” wide. (Normal slide dimensions are 7.5” high and 10” wide.) To reproduce the picture effects on this slide, do the following: On the Home tab, in the Slides group, click Layout, and then click Blank. On the Insert tab, in the Images group, click Picture. In the Insert Picture dialog box, select a picture, and then click Insert. Select the picture. Under Picture Tools, on the Format tab, in the Size group, click the Size and Position dialog box launcher. In the Format Picture dialog box, resize or crop the image so that the height is set to 15” and the width is set to 10”. To crop the picture, click Crop in the left pane, and in the right pane, under Crop position, enter values into the Height, Width, Left, and Top boxes. To resize the picture, click Size in the left pane, and in the right pane, under Size and rotate, enter values into the Height and Width boxes. On the Home tab, in the Drawing group, click Arrange, point to Align, and then do the following: Click Align to Slide. Click Align Top. Click Align Center. The remainder of picture will extend beyond the bottom edge of the slide area. You may need to zoom out to view your slide. To zoom out, on the View tab, in the Zoom group, click Zoom. In the Zoom dialog box, select 33%. To reproduce the shape effects on this slide, do the following: On the Home tab, in the Drawing group, click Shapes, and then under Rectangles click Rounded Rectangle (second option from the left). On the slide, drag to draw a rounded rectangle. Select the rounded rectangle. Under Drawing Tools, on the Format tab, in the Size group, do the following: In the Shape Height box, enter 2.5”. In the Shape Width box, enter 8”. Also on the Format tab, in the Shape Styles group, do the following: Click the arrow next to Shape Fill, and then click No Fill. Click the arrow next to Shape Outline, and then under Theme Colors click White, Background 1 (first row, first option from the left). Also on the Format tab, in the bottom right corner of the Shape Styles group, click the Format Shape dialog box launcher. In the Format Shape dialog box, in the left pane, click Line Style. In the Line Style pane, in the Width box, enter 12.5 pt. Also in the Format Shape dialog box, in the left pane, click 3-D Format, and then do the following in the 3-D Format pane: Under Bevel, click the button next to Top, and then under Bevel click Circle (first row, first option from the left). Under Surface, click the button next to Material, and then under Standard click Warm Matte (second option from the left). Click the button next to Lighting, and then under Cool click Freezing (second option from the left). On the Home tab, in the Drawing group, click Arrange, point to Align, and then do the following: Click Align to Slide. Click Align Middle. Click Align Center. On the Home tab, in the Drawing group, click Shapes, and then under Rectangles click Rectangle (first option from the left). On the slide, drag to draw a rectangle. Select the rectangle. Under Drawing Tools, on the Format tab, in the Size group, do the following: In the Shape Height box, enter 2.51”. In the Shape Width box, enter 10”. Also on the Format tab, in the Shape Styles group, click the arrow next to Shape Outline, and then click No Outline. Also on the Format tab, in the Shape Styles group, click the arrow next to Shape Fill, point to Gradient, and then click More Gradients. In the Format Shape dialog box, click Fill in the left pane, select Gradient fill in the Fill pane, and then do the following: In the Type list, select Linear. Click the button next to Direction, and then click Linear Down (first row, second option from the left). Under Gradient stops, click Add gradient stops or Remove gradient stops until two stops appear in the slider. Also under Gradient stops, customize the gradient stops as follows: Select the first stop from the left in the slider, and then do the following: In the Position box, enter 0%. Click the button next to Color, and then under Theme Colors click Black, Text 1 (first row, second option from the left). In the Transparency box, enter 0%. Select the second stop from the left in the slider, and then do the following: In the Position box, enter 100%. Click the button next to Color, and then under Theme Colors click Black, Text 1, Lighter 25% (fourth row, second option from the left). In the Transparency box, enter 0%. On the Home tab, in the Drawing group, click Arrange, point to Align, and then do the following: Click Align to Slide. Click Align Top. Click Align Center. Select the rectangle. On the Home tab, in the Clipboard group, click the arrow next to Copy, and then click Duplicate. On the Home tab, in the Drawing group, click Arrange, point to Rotate, and then click Flip Vertical. Also on the Home tab, in the Drawing group, click Arrange, point to Align, and then do the following: Click Align to Slide. Click Align Bottom. Click Align Center. Also on the Home tab, in the Drawing group, click Shapes, and then under Rectangles click Rectangle (first option from the left). On the slide, drag to draw a rectangle. Select the rectangle. Under Drawing Tools, on the Format tab, in the Size group, do the following: In the Shape Height box, enter 2.55”. In the Shape Width box, enter 1.06”. Under Drawing Tools, on the Format tab, in the bottom right corner of the Shape Styles group, click the Format Shape dialog box launcher. In the Format Shape dialog box, in the left pane, click Line Color. In the Line Color pane, select No line. Also in the Format Shape dialog box, in the left pane, click Fill. In the Fill pane, select Solid fill, click the button next to Color, and then under Theme Colors click Black, Text 1, Lighter 25% (fourth row, second option from the left). On the Home tab, in the Drawing group, click Arrange, point to Align, and then do the following: Click Align to Slide. Click Align Right. Click Align Middle. Select the rectangle. On the Home tab, in the Clipboard group, click the arrow next to Copy, and then click Duplicate. Select the duplicate rectangle. On the Home tab, in the Drawing group, click Arrange, point to Align, and then do the following: Click Align to Slide. Click Align Left. Click Align Middle. On the Home tab, in the Editing group, click Select, and then click Selection Pane. In the Selection and Visibility pane, select the rounded rectangle. On the Home tab, in the Drawing group, click Arrange, and then click Bring to Front. In the Selection and Visibility pane, press and hold CTRL, and then select the rounded rectangle and four rectangles. On the Home tab, in the Drawing group, click Arrange, and then click Group. To reproduce the text effects on this slide, do the following: On the Insert tab, in the Text group, click Text Box. On the slide, drag to draw a text box. Type the text you want to appear in the text box, and then select the text. Format the text in the textbox using the following steps: On the Home tab, in the Font group, choose the Calibri font and a font size of 26. Click the arrow next to Font Color, and then under Theme Colors click White, Background 1 (first row, first option from the left). In the Paragraph group, click Align Text Left. Drag the text box to the lower left part of the rounded rectangle. To reproduce the animation effects for the picture on this slide, do the following: On the slide, select the picture. On the Animations tab, in the Advanced Animation group, click Add Animation, and then, under Entrance, click Fade. Also on the Animations tab, in the Timing group, in the Start list, select With Previous. Also on the Animations tab, in the Timing group, in the Duration box, type 2. On the Animations tab, in the Advanced Animation group, click Add Animation, and then click More Motion Paths. In the Add Motion Paths dialog box, under Lines and Curves, click Up. Also on the Animations tab, in the Timing group, in the Start list, select With Previous. Also on the Animations tab, in the Timing group, in the Duration box, type 20. On the slide, select the Up motion path, and then do the following: Press and hold SHIFT, and then drag the end point (red arrow) of the motion path to the top edge of the slide. Press and hold Shift, and then drag the starting point (green arrow) of the motion path to the bottom edge of the slide. To reproduce the animation effects for the text on this slide, do the following: On the slide, select the text box. On the Animations tab, in the Advanced Animation group, click Add Animation, and then, under Entrance, click Fade. Also on the Animations tab, in the Timing group, in the Start list, select With Previous. Also on the Animations tab, in the Timing group, in the Duration box, type .5. Also on the Animations tab, in the Timing group, in the Delay box, type 3.0. Also on the Animations tab, in the Advanced Animation group, click Add Animation, and then, under Exit, click Fade. Also on the Animations tab, in the Timing group, in the Start list, select With Previous. Also on the Animations tab, in the Timing group, in the Duration box, type .5. Also on the Animations tab, in the Timing group, in the Delay box, type 8.0. On the slide, select the text box. On the Home tab, in the Clipboard group, click the arrow next to Copy, and then click Duplicate. On the slide, click in the second text box and edit the text. On the Animations tab, in the Advanced Animation group, click Animation Pane. In the Animation Pane, do the following: Select the entrance animation on the second text box. Click the arrow to the right of the effect, and then click Timing. In the Fade dialog box, on the Timing tab, in the Delay box, enter 8.5, and then click OK. Select the exit animation on the second text box. Click the arrow to the right of the effect, and then click Timing. In the Fade dialog box, on the Timing tab, in the Delay box, enter 13.0, and then click OK. On the slide, select the second text box. On the Home tab, in the Clipboard group, click the arrow next to Copy, and then click Duplicate. On the slide, click in the third text box and edit the text. In the Animation Pane, do the following: Select the entrance animation on the third text box. Click the arrow to the right of the effect, and then click Timing. In the Fade dialog box, on the Timing tab, in the Delay box, enter 13.5, and then click OK. Select the exit animation on the third text box. Click the arrow to the right of the effect, and then click Timing. In the Fade dialog box, on the Timing tab, in the Delay box, enter 19.5, and then click OK. On the slide, press and hold CTRL, and then select the three text boxes. On the Home tab, in the Drawing group, click Arrange, point to Align, and then do the following: Click Align Selected Objects. Click Align Middle. Click Align Center. To reproduce the animation effects for the shapes on this slide, do the following: On the slide, select the rounded rectangle and the group of shapes that form the background of the slide. On the Animations tab, in the Advanced Animation group, click Add Animation, and then click More Emphasis Effects. In the Add Emphasis Effect dialog box, under Basic, click Grow/Shrink. Also on the Animations tab, in the Timing group, in the Start list, select After Previous. Also on the Animations tab, in the Timing group, in the Duration box, type 2. On the Animations tab, in the Animation group, click Effect Options, and then click Horizontal. On the Animations tab, in the Advanced Animation group, click Add Animation, and then click More Exit Effects. In the Add Emphasis Effect dialog box, under Basic, click Fade. Also on the Animations tab, in the Timing group, in the Start list, select With Previous. Also on the Animations tab, in the Timing group, in the Duration box, type 1.