D’YOUVILLE COLLEGE
BIOLOGY 307/607 - PATHOPHYSIOLOGY
Lecture 14 - GASTROINTESTINAL DISORDERS
Chapter 13
1.
Review of GI Anatomy & Physiology:
• alimentary canal (fig. 13 - 1 & ppt. 1):
- consists of oral cavity, pharynx, esophagus, stomach, small & large
intestines & anus; functions: digestion & absorption of nutrients from food, aided by
secretions from auxiliary glands (salivary glands, liver, and pancreas)
- small intestine: consists of duodenum, jejunum, & ileum -- main site of
digestion and absorption
- features maximizing absorptive surface area: longest section of tubular
digestive tract, folds in wall (involving submucosa & mucosa), villi, microvilli (fig.
13 - 2 & ppts. 2 to 4)
- digestion: facilitated by secretions & wall motility
- secreted enzymes (provided by pancreas, gastric & intestinal mucosas +
some from saliva) achieve breakdown of foodstuffs into absorbable particles
- other secretions, e.g., acid in stomach, bicarbonate in small intestine
(from pancreas) & bile from liver potentiate enzyme effectiveness: acid denatures
proteins, bicarbonate buffers acidity, & bile emulsifies lipids (secretions accomplish
chemical digestion)
- physical digestion is accomplished by muscular activity including
mastication & salivary secretions in oral cavity and motility of muscularis layer of
alimentary canal (peristalsis & mixing contractions)
- regulated by neural (mostly parasympathetic) and endocrine reflexes
(e.g., gastrin from stomach, cholecystokinin & secretin from small intestine) that
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modulate intrinsic activity of enteric nervous system (myenteric plexus regulates
motility, submucous plexus regulates secretions) (fig. 13 - 3 & ppt. 5)
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2.
- p. 3 -
Gastrointestinal Disorders:
• vomiting (emesis): retrograde expulsion from stomach &/or small intestine
triggered by vomiting center of medulla, which activates various reflexes to ensure
expulsion pathway is out the mouth
- stimulates powerful contractions of abdominal & gastric wall muscles,
resulting in expulsion of stomach (and intestinal) contents
- stimulates sensation of nausea (warning of impending emesis)
- chronic vomiting may result in loss of fluids, loss of electrolytes,
increased blood pH (as stomach replaces acid deficiency)
- inputs to vomiting center, such as emotional upset, irritations from drugs
or chemicals (excessive spices or alcohol, bacterial toxins), upset equilibrium signals,
gastric stretching due to overfilling, -- are mediated by higher brain levels, via
'chemotactic trigger zone' in the brain (fig. 13 - 4 & ppt. 6)
• diarrhea: watery stools, heavy mucus production stimulate increased
frequency of defecation reflex
- excessive fluid stems from: (fig. 13 - 5 & ppt. 7)
- factors that stimulate secretion: irritants such as bacterial toxins,
impaired fat digestion, poor recycling of bile salts, excessive use of laxatives, tumors
- factors that impose osmotic retention of water in colon: increased
content of indigestible or undigested materials in colon, overuse of antacids
containing poorly absorbed ions such as Mg+
- factors that impair water absorption by colon: malabsorption
diseases, irritable bowel syndrome (disturbed motility and accelerated clearance)
- chronic diarrhea may lead to fluid loss, electrolyte loss, acidosis; treat
with inhibitors of motility, promoters of fluid absorption
• gastrointestinal inflammations: esophagitis most often stems from
weakened lower esophageal sphincter that facilitates acid reflux from stomach with
resultant inflammation & damage to esophageal mucosa (GERD); may be associated
with sliding hiatal hernia or (less frequently) with paraesophageal hiatal hernia (fig.
13 - 6 & ppt. 8)
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- gastroenteritis often results from bacterial infection or autoimmune
condition; may be exacerbated by aspirin, NSAIDs, or alcohol abuse; usually
produces symptoms of 'indigestion', but serious cases may lead to ulcers or tumors
- appendicitis: obstruction to opening of appendix facilitates infection,
swelling, & potential perforation (sequel to ischemia & necrosis) with risk of
peritonitis (figs. 13 - 7, 13 - 8 & ppts. 9 & 10); more prevalent in young people (10 - 20)
- peritonitis: irritants of endogenous origin (from perforations of abdominal
organs) or of exogenous origin (wounds, surgical incisions, sexually transmitted
infections) cause local abscesses, scarring, and adhesions that may disrupt bowel
motility, and may cause fistulas (abnormal connections between lumina of unrelated
organs, e.g. colon with vagina); generalized peritonitis is associated with
widespread damage to abdominal organs with high risk of septicemia & shock
- diverticulitis: sequel to diverticulosis (pouch of mucosa extruded through
muscularis, usually in sigmoid colon), which results from elevated pressure in the
colon (fig. 13 - 10 & ppt. 11); diverticula may lead to entrapped, hardened feces
(fecaliths), which lead to the inflammatory condition; risk of bleeding and/or
perforation; adequate fiber in diet is preventive
- inflammatory bowel disease (IBD): cause not well understood, but genetic
predisposition and autoimmune attack on mucosa may be involved
- most cases characterized by episodic attacks followed by periods of
remission, but some are more severe
- two patterns are recognized (Crohn's disease that afflicts terminal
ileum and colon, & ulcerative colitis, which is confined to colon) (table 13 - 1)
- antidiarrheals, immunosuppressants, & anti-inflammatories are used,
but total bowel resection is often a necessary treatment
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- ulceration: large majority are gastric and duodenal; more prevalent in males
than females
- normal mucosal defenses involve mucus production (including
bicarbonate ion content) + disposal of damaged cells via cell renewal system
- impaired defenses (likely of genetic origin) coupled with gastric
hypersecretion of acid and pepsin (also likely genetic) lead to mucosal erosion followed
by digestion of submucosal tissues (peptic ulcer)
- condition is exacerbated by smoking, NSAIDs, and often present
bacterial infection (Helicobacter pylori) (fig. 13 - 13 & ppt. 12)
- normally self-resolving, but more severe cases may result in bleeding
(potential hypovolemic shock) and perforation (potential serious peritonitis)
- antibiotic therapy may eliminate the infection and facilitate healing
• bleeding: from severe ulcers, mucosal inflammations, violent vomiting (table
13 - 3)
- blood in vomitus has coffee ground appearance, in stools, a tar-like
appearance; severe bleeding requires treatment to prevent hypovolemic shock
• obstructions (= ileus): mechanical and adynamic types (arrest of peristalsis)
- mechanical obstructions include loops entrapped in hernias or adhesions
(with resulting strangulation -- figs. 13 - 14, 13 - 15 & ppts. 13 & 14); stricture (fig. 13 16 & ppt. 15), volvulus (fig. 13 - 17), and intussusception (fig. 13 - 18)
- sequelae include obstipation, fluid & electrolyte loss due to vomiting,
necrosis & possible perforation due to vascular compression (fig. 13 - 19 & ppt. 16)
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• malabsorption: consequence of impaired digestion, impaired absorption,
&/or impaired transit
- impaired digestion results from enzyme insufficiencies, bile insufficiency
(due to pancreatic &/or liver disorders) or bowel resections
- impaired absorption may involve immune sensitivity (to certain food
nutrients, e.g. gluten from grains) that destroys villi (= celiac disease) or infections
that destroy villi (tropical sprue)
- impaired transit involves disturbances to normal lymphatic delivery of
absorbed fats to the circulation (lipoprotein deficit or collapsed lacteal due to
infiltration of villus with macrophages)
- consequences summarized in fig. 13 - 20 (& ppt. 17)
• cancer: tumors, e.g. carcinomas, adenomas, polyps, may be found (in order
of frequency) in colon, stomach, esophagus, and small intestine
- may cause obstructions, bleeding, pain
- polyp removal is most often achieved during colonoscopy