Download - Gi+presentation+2014+ho (1)
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Gastrointestinal Gastrointestinal SystemSystem
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Before we beginBefore we begin• Important to know anatomy and normal function.
(Chapter 35)• This will need to be reviewed on your own to help
you understand normal functioning. • Test material will come from pathology and
pathological processes.
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Know anatomy of glandsKnow anatomy of glands
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Anatomy (Cont.)Anatomy (Cont.)• Lower esophageal sphincter
o 2-5 cm above the juncture of the lower esophagus and stomacho Remains constricted, preventing highly acidic gastric contents from
moving up from the stomach into the esophaguso If not working properly can lead to reflux or heartburn
Why do patients with type 2 diabetes have acid reflux?
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ApplicationApplication• What types of problems will present with a
dysfunctional LES?
• Will it vary by age group?
• What types of screening questions will you ask?
• Why do patients with type 2 diabetes have acid reflux?
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Anatomy (Cont.)Anatomy (Cont.)• Specialized cells in the
stomacho Chief cells
• Secrete pepsinogen (an inactive form of pepsin)
o Parietal cells• Produce HCl (activates
pepsinogen to pepsin)• Produce intrinsic factor
(enhances vitamin B12 absorption)
• Stimulated by acetylcholine, histamine, and gastrin
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Anatomy (Cont.)Anatomy (Cont.)• Specialized cells in the
stomacho Mucous cells
• Produce an alkaline mucus (HCO3 + mucus)
• Shields stomach wall and neutralizes acid in the immediate area of the lining
o G cells• Secrete gastrin into the
bloodstream• Gastrin increases gastric
motility and stimulates chief and parietal cell secretion
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Anatomy (Cont.)Anatomy (Cont.)• Small intestine
o Intestinal villi• Fingerlike projections
contained in the lining• Increase surface area for
digestion and absorption of nutrients
o Microvilli• Microscopic projections
covered with a fuzzy coat called brush border
• Contains many digestive enzymes
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Anatomy (Cont.)Anatomy (Cont.)• Small intestine
o Crypts of Lieberkühn• Intestinal glands that secrete about 2 L of fluid/day into lumen of
intestine• Fluid reabsorbed by villi
o Goblet cells and Brunner glands• Secrete large amounts of mucus to protect SI from damage of acidic
gastric juices
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MotilityMotility• Intestinal wall
o Skeletal muscle• Key role in motility at upper end and lower end of GI tract
o Muscular movements performed by close layers of smooth muscleo Neural control by CNS through the ANSo Modulated by numerous hormonal interactions
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Motility (Cont.)Motility (Cont.)• Intestinal wall
o Controlled by intrinsic nervous system• Responsible for many reflexes that occur locally in the GI tract
o Examples• Localized secretion of digestive juices by submucosal
glands• Increase in gut smooth muscle activity
• The enteric nervous system (ENS) is the intrinsic nervous system of the gastrointestinal tract.
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Motility Motility (Cont.)(Cont.)
• Two layers of intrinsic nervous systemo Submucosal plexus
• Controls secretion and sensory functions
o Myenteric plexus• Lies between longitudinal
and circular muscular layers
• Responsible for control of GI movements
• Stimulation increases GI tract activity
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Motility (Cont.)Motility (Cont.)• Two layers of intrinsic nervous system
o Myenteric plexus • Stimulation results in:
o Tonic contraction of intestinal wallo Rhythmic contractions; increase in intensityo Rhythmic contractions; increase in rateo Velocity of conduction of excitatory waves along wall; increases
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QuestionQuestion• What will happen if the intrinsic nervous system of
the GI tract is inhibited in some form?
A. Tonic contraction of intestinal wallB. Increase in rhythmic contraction strengthC. Decrease in rhythmic contraction rate
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• What might a patient present with who has a paralyzed enteric nervous system?
A.DiarrheaB. Digital paralysisC.Dark brown emesisD. Increased bowel sounds
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Motility (Cont.)Motility (Cont.)• Parasympathetic innervation
o Cranial• Transmitted with vagus nerves to provide extensive innervation to
esophagus, stomach, pancreas, first half of the large intestineo Sacral
• Originates in 2nd, 3rd, 4th sacral segments of spinal cord • Innervates the distal half of the large intestine• Key role in defecation reflex
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Motility (Cont.)Motility (Cont.)• Hormonal control
o Gastrin• Secreted by the mucosa of antrum in response to food
entering the stomach• Increases stomach motility
o Cholecystokinin• Secreted by mucosa of the jejunum in response to entry of
fatty substances; increases contractility of the gallbladdero Gastric inhibitory peptide
• Secreted by mucosa of upper portion of SI in response to the presence of fat; decreases stomach motility
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Movement of Nutrients Movement of Nutrients (Cont.)(Cont.)
• Small intestineo Segmental contractions (mixing)
• Back-and-forth action that breaks apart chyme and mixes with digestive juices
• As one set of contractions is completed, a new set begins• Contractions occur at rate of 7-12 times/min
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Movement of Nutrients Movement of Nutrients (Cont.)(Cont.)
• Ileocecal sphinctero Normally closedo Relaxes when intestinal
contents are present in terminal ileum
o Propulsive movement push contents into cecum
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Movement of Nutrients Movement of Nutrients (Cont.)(Cont.)
• Large intestine (colon)o Main function is fluid absorptiono Storage of fecal mass until expelled from bodyo Segmental contractions produce haustral churningo Defecation
• Takes about 18 hours to reach distal endo One to three mass movements per day
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Movement of Nutrients Movement of Nutrients (Cont.)(Cont.)
• Regulation of colonic motilityo Initiated by distention in colonic wallso Proximal portion of colon initiated by distention in colonic walls
• Stimulates contractions by triggering short reflexes through intrinsic nerve plexuses
o Distal portion of colon dependent on extrinsic nerve supply• Voluntary control• Inhibits defecation until voluntarily relaxed
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Gastrointestinal Gastrointestinal Hormones Hormones
• Gastrin (stomach)o Stimulates gastric glands to secrete substances produced by different
specialized cells
• Secretin (duodenum)o Release stimulated by HCl and chymeo Increases rate of bile secretion
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Gastrointestinal Hormones (Cont.)Gastrointestinal Hormones (Cont.)
Enterochromaffin-like cells (ECL)
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Gastrointestinal Hormones (Cont.)Gastrointestinal Hormones (Cont.)• Cholecystokinin (duodenum)
o Stimulates release of digestive enzymeso Gallbladder contraction and emptying
• Gastric inhibitory peptide (duodenum)o Slows gastric emptying by decreasing activity
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Gastrointestinal Hormones (Cont.)Gastrointestinal Hormones (Cont.)
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Read about digestion of food on your Read about digestion of food on your
own, please.own, please.
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Summary of Digestive Summary of Digestive FunctionFunction
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Aging Effects on GI Aging Effects on GI SystemSystem
• Decreased parietal and chief cellso Leads to decreased HCl and pepsin in stomach causing
an increased pH (alkalinity)• Epithelial membrane changes
o Decreased absorption of lipids, amino acids, glucose, Ca, and Fe
• Decreased smooth muscle and strengtho Decreased emptying time o Decreased anal sphincter toneo Increased nonperistaltic waves and decreased peristalsis
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Gastrointestinal Gastrointestinal DisordersDisorders
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Common Manifestations of Common Manifestations of
Gastrointestinal Tract Disorders Gastrointestinal Tract Disorders • Dysphagia
o Difficulty in swallowing• Inability to initiate swallowing• Sensation that swallowed solids/liquids “stick” in esophagus• Pain with swallowing (odynophagia) may accompany
o Problems in delivery of food/fluid into esophagus• Causes
o R/T neuromuscular incoordination o Normal sequence is altered or absent
o Symptoms• May cough and expel the ingested food/fluids through mouth or nose• Aspirate when attempting to swallow• Worse with liquids than solids
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Common Manifestations of Gastrointestinal Common Manifestations of Gastrointestinal
Tract Disorders (Cont.)Tract Disorders (Cont.)
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Common Manifestations of Gastrointestinal Common Manifestations of Gastrointestinal
Tract Disorders (Cont.)Tract Disorders (Cont.)• Esophageal pain
o Heartburn (pyrosis)• Cause
o Reflux of gastric contents into esophagus• High acidic contents are an irritant to sensory afferent
nerve endings in mucosa• Causes spasms of esophageal muscle
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Common Manifestations of Gastrointestinal Common Manifestations of Gastrointestinal
Tract Disorders (Cont.)Tract Disorders (Cont.)• Esophageal pain
o Heartburn (pyrosis)• Symptoms
o Substernal burning sensation that may radiate to neck or throat
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Common Manifestations of Gastrointestinal Common Manifestations of Gastrointestinal
Tract Disorders (Cont.)Tract Disorders (Cont.)• Esophageal pain
o Chest pain (esophageal distention or obstruction)• Symptoms
o Similar to angina pectoris (radiates to neck, shoulder, arm, and jaw)
o Brought on by swallowing
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Common Manifestations of Gastrointestinal Common Manifestations of Gastrointestinal
Tract Disorders (Cont.)Tract Disorders (Cont.)• Vomiting
o Forceful expulsion of gastric contents through moutho Accompanied by nauseao Characteristics of vomitus may suggest nature of disorder
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Common Manifestations of Gastrointestinal Common Manifestations of Gastrointestinal
Tract Disorders (Cont.)Tract Disorders (Cont.)• Vomiting
o Causes• Coordinated sequence of abdominal muscle contraction with reverse
esophageal peristalsis• Alterations in the integrity of GI tract wall (gastroenteritis)• Alterations in motility (obstruction)
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Common Manifestations of Gastrointestinal Common Manifestations of Gastrointestinal
Tract Disorders (Cont.)Tract Disorders (Cont.)• Bowel pattern alterations
o Constipation• Small, infrequent, or difficult bowel movements• Causes
o Dietary (low in fiber)o Lack of exerciseo Pathologic conditions (ex: diverticulitis, obstruction)
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Chemical DigestionChemical Digestion
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Common Manifestations of Gastrointestinal Common Manifestations of Gastrointestinal
Tract DisordersTract Disorders• Bowel pattern alterations
o Diarrhea• Increased frequency and fluidity of bowel movements caused by
decreased transit time in SI• Acute
o Acute infectiono Emotional stresso Leakage of stool around impacted feces
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Common Manifestations of Gastrointestinal Common Manifestations of Gastrointestinal
Tract Disorders (Cont.)Tract Disorders (Cont.)• Bowel pattern alterations
o Diarrhea• Chronic
o Chronic GI tract infectiono Alterations in motility or integrity of GI tracto Malabsorptiono Certain endocrine disordero Food allergy o Ingestion of irritantso Caffeine
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Common Manifestations of Gastrointestinal Common Manifestations of Gastrointestinal
Tract Disorders (Cont.)Tract Disorders (Cont.)• Pathophysiologic mechanisms
o Osmotic• Increased amounts of poorly, absorbed solutes in the intestine
o Secretory• Due to toxins that stimulate intestinal fluid secretion and impair
absorption
• Pathophysiologic mechanismso Exudative (mucus, blood, protein)
• Results from inflammatory processeso Diarrhea related to motility disturbances
• Example: dumping syndrome
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GI Disorders Head to GI Disorders Head to “Toe”“Toe”
BRAIN•Remember the brain’s role in GI symptoms.•The GI system is greatly influenced by stress.•Hypothalmic-Pituitary-Adrenal-Axis (HPA axis):
o Corticotropin releasing factor (CRF) released from the hypothalamus
o Pituitary responds to CRF by releasing ACTH (adrenocorticotropic hormone).
o ACTH stimulates adrenals to release cortisolo Cortisol promotes fluid and salt retention, impairs inflammation,
decreases gastric emptying.
•Intestinal sensitivity increases with stress, increased mast cell activity. •IBS patients have increased sensitivity to stress in the gut.
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Esophageal Disorders - GERDEsophageal Disorders - GERD• Patho:
o Closure strength of the lower esophageal sphincter (LES) is adversely affected.• Medications, fatty foods, caffeine, ETOH, smoking, sleep position,
obesity.• Increased intraabdominal pressure - Pregnancy
o Backflow of gastric contents into esophagus through LESo Inflammation caused by reflux of highly acidic materialo Progression can lead to ulceration, fibrotic scarring, strictures, Barrett
esophagus
• Clinical Manifestations:o Severity of clinical manifestations depends on the frequency,
duration, volume, and acidity of material being refluxed.o Heartburn, regurgitation, chest pain, dysphagia.
• Complications:o Reflux esophagitis – inflammation of esophageal mucosa,
esophageal strictures, cough, asthma, laryngitis.o Barrett’s esophagitis – columnar tissue replaces the normal
squamous epithelium of the distal esophagus. Increases risk of esophageal CA.
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Esophageal Disorders Esophageal Disorders (Cont.)(Cont.)
• Esophagitiso Barrett esophagus
• Complication when columnar tissue replaces normal squamous epithelium of the distal esophagus
• Carries a significant risk for esophageal cancer
•
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Hiatal HerniaHiatal Hernia• Patho: Defect in the diaphragm that allows a
portion of the stomach to pass through the diaphragmatic opening in the thorax.
o Risk increases with age o Women more than meno Signs and symptoms
• Similar to GERD• Heartburn• Chest pain• Dysphagia
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• Hiatal herniao Sliding hernia (most common)
• Portion of stomach and gastroesophageal junction slip up into thorax above diaphragm
o Paraesophageal hernia (rolling)• Part of greater curvature of stomach rolls through the diaphragmatic
defecto Mixed
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Hiatal HerniaHiatal Hernia• Patho: Defect in the diaphragm that allows a
portion of the stomach to pass through the diaphragmatic opening in the thorax.
• Two Types:o Sliding hernia: 3-10x more common incidence in women. Both a
portion of the stomach and the gastroesophageal junction is above the diaphragmatic opening.
o Paraesophageal hernia: A greater part of the curvature of the stomach rolls through the diaphragmatic defect.
• Clinical Manifestations:o Predisposition to GERD: heartburn, chest pain, dysphagiao Cameron ulcers may develop on the mucosal surface of the
stomach.o If part of the stomach gets stuck above the diaphragm, could
become incarcerated – life threatening.
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Mallory-Weiss Mallory-Weiss SyndromeSyndrome
• Patho: Tear in the mucosa or submucosa of the caria or lower portion of the esophagus. Primarily caused by prolonged or forceful vomiting in which the upper esophageal sphincter fails to relax during the vomiting process.
• Risk Factors: o 75% are men who ingest excessive ETOH or salicylates. o coughing, straining with BM, trauma, hiatal hernia,
esophagitis, and gastritis.
• Clinical Manifestations:o Vomiting of blood and passing large amounts of blood rectally after
vomiting episode. o Epigastric or back pain may also be present.
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Esophageal VariciesEsophageal Varicies• Patho: Complication of portal hypertension
caused by cirrhosis of the liver. Normal blood flow to the liver is obstructed. Blood flows into the smaller blood vessels that are not designed to carry large amounts of blood. The vessels may leak or rupture causing life-threatening bleeding.
• Risk Factors: ETOH or cirrhosis of any cause. Chronic hepatitis B infection.
• Clinical Manifestations: o Vomiting of blood, o dark tarry stools.
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Esophageal Disorders Esophageal Disorders (Cont.)(Cont.)
• Esophageal variceso Complication of portal hypertension resulting from alcoholic or
posthepatitis cirrhosiso Affects more than half of cirrhotic patients
• 30% have variceal hemorrhage within 2 years of diagnosiso High mortality rate
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Inflammation of the Inflammation of the
Stomach and IntestinesStomach and Intestines• Gastritis
o Acute• Precipitated by ingestion of irritating substances
o Example: alcohol and aspirin• Signs and symptoms
o Anorexiao Nauseao Vomitingo Postprandial discomforto Hematemesis
o Chronic• Helicobacter pylori is nearly always a factor
o Complications• Peptic ulcer disease• Atrophic gastritis• Gastric adenocarcinoma• Mucosa-associated lymphoid tissue lymphoma
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Inflammation of the Inflammation of the
Stomach and Intestines (Cont.)Stomach and Intestines (Cont.)• Gastroenteritis
o Inflammation of stomach and small intestineo Usually a result of another GI disordero Acute is caused by direct infection of tract by pathogenic virus or
bacterial toxin o May be caused by imbalance in normal bacterial flora by introduction of
unusual bacteria (travel)
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Inflammation of the Inflammation of the
Stomach and Intestines (Cont.)Stomach and Intestines (Cont.)• Gastroenteritis
o Signs and symptoms• Diarrhea• Abdominal discomfort and pain• Nausea• Vomiting• Fever• Malaise
o Treatment• Replace fluid and electrolytes
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Inflammation of the Inflammation of the
Stomach and Intestines (Cont.)Stomach and Intestines (Cont.)• Peptic ulcer disease
o Causes• H. pylori• Stress• Smoking• Alcohol• Spicy foods• Smoking• Genetic
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Inflammation of the Inflammation of the
Stomach and Intestines (Cont.)Stomach and Intestines (Cont.)• Peptic ulcer disease
o Gastric• Due to breakdown of protective mucous layer that prevents diffusion
of acids into gastric epithelia• Barrier of epithelial layer and slightly alkaline layer of mucus
interrupted with chronic irritations
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Inflammation of the Inflammation of the
Stomach and Intestines (Cont.)Stomach and Intestines (Cont.)• Peptic ulcer disease
o Duodenal• Inappropriate excess secretion of acid• Increased basal activity of vagus nerve
o Stimulates pyloric antrum cells to release gastrin to act on gastric parietal cells to release HCl
o Results in high level of HCl
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Inflammation of the Inflammation of the
Stomach and Intestines (Cont.)Stomach and Intestines (Cont.)
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Ulcerative ColitisUlcerative ColitisPatho:• Chronic inflammatory disease of the mucosa of the rectum
and colon• Large ulcers form in mucosal layer of colon and rectum • Begins as inflammation at base of crypts of Lieberkühn;
damage results; abscess formation in crypts; abscesses begin to coalesce, large ulcerations develop in epithelium
• Associated with increased cancer • risk after 7 to 10 years of disease• Have exacerbations and remissions• Hallmark clinical manifestations • are bloody diarrhea and lower• abdominal pain
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Inflammatory Bowel Disease Inflammatory Bowel Disease
(Cont.)(Cont.)• Crohn disease
o Affects proximal portion of the colon or terminal ileumo Inflammation of all layers of the intestinal wall resulting from blockage and
inflammation of lymphatic vesselso Suggestive findings are ulcerations, strictures, and fistulas
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Patho:• Affects proximal portion of the colon or terminal ileum• Chronic inflammation of all layers of intestinal wall resulting
from blockage and inflammation of lymphatic vessels• Suggestive findings are ulcerations, strictures, fibrosis, and
fistulasClinical manifestations• Intermittent bouts of fever, diarrhea, if bloody, not as
severe as ulcerative colitis; • constant, chronic RLQ pain, • may have RLQ mass, tenderness
CrohnCrohn’s Disease’s Disease
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EnterocolitisEnterocolitis• Antibiotic-associated colitis (AAC) (also called
Pseudomembranous enterocolitis)o Acute inflammation and necrosis of small and large intestine o Caused by Clostridium difficile (exposure to antibiotics)o Signs and symptoms
• Diarrhea (often bloody), abdominal pain, fever, colonic perforation (rare)
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Enterocolitis (Cont.)Enterocolitis (Cont.)• Necrotizing enterocolitis (NEC)
o Occurs in premature infants (<34 wk) and infants with low birth weight (<5 lb)
o Characterized by diffuse or patchy intestinal necrosis with sepsiso Signs and symptoms
• Distended abdomen and stomach, intestinal perforationo Treatment: surgical with antibiotics
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Enterocolitis (Cont.)Enterocolitis (Cont.)• Appendicitis
o Obstruction by fecalith, inflammationo Signs and symptoms
• RLQ pain (“McBurney’s point”) (classic, but may be anywhere), nausea, vomiting, fever, diarrhea, RLQ tenderness, systemic signs of inflammation
o Treatment: immediate surgical removal
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Enterocolitis (Cont.)Enterocolitis (Cont.)• Diverticular disease (diverticulosis)
o Presence of diverticula in the colono Results in low intake of dietary fibero Signs and symptoms
• Diverticulosis—asymptomatic• Diverticulitis—fever, acute lower abdominal pain
o Treatment: antibiotics and surgery for complicated diverticulitis
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Alterations in MotilityAlterations in Motility• Irritable bowel syndrome
o Chronic (>3 months) functional disorder o Fluctuations in stool frequency and consistency (no nocturnal diarrhea)o Cause: unclear but slow wave activity of bowel in increased.o Often associated with anxiety or depression
o Signs and symptoms• Diarrhea or constipation or alteration of both, abdominal cramping
pain, mucus in stool, nausea, bloating
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Alterations in Motility Alterations in Motility (Cont.)(Cont.)
• Intestinal obstructiono Mechanical
• Adhesions, hernia, tumors, impacted feces, volvulus, intussusception o Functional
• Conditions that inhibit peristalsis such as narcotics, anesthesia, surgery, peritonitis, hypokalemia, spinal cord injuries
o Signs and symptoms• Depend on site and duration: dehydration, vomiting, electrolyte
depletion, constipation, abdominal distention
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Alterations in Motility Alterations in Motility (Cont.)(Cont.)
• Volvuluso Twisting of bowel on itself causing intestinal obstruction and blood vessel
compression (ischemia)o Results from anomaly of rotation, ingested foreign body, or adhesion;
cannot always be determinedo Common sites are cecum and sigmoid colono Sudden, tight, twisting of bowel impedes blood flow to bowel
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Alterations in Motility Alterations in Motility (Cont.)(Cont.)
• Volvuluso Impeded blood flow leads to gangrene, necrosis, and perforationo Life-threatening conditiono Signs and symptoms
• Depend on site and duration: dehydration, vomiting, electrolyte depletion
o Treatment• Varies according to severity and location: surgical intervention or
decompression
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Alterations in Motility Alterations in Motility (Cont.)(Cont.)
• Intussusceptiono Telescoping/invagination of a portion of bowel into adjacent (usually
distal) bowel causing intestinal obstructiono Males more than femaleso Signs and symptoms
• Increased bowel sounds, abdominal pain, varieso Treatment: surgical treatment
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Alterations in Motility Alterations in Motility (Cont.)(Cont.)
• Hirschsprung diseaseo Familial, congenital disorder of the large intestine in which the autonomic
ganglia are reduced or absento Occurs 1:5000 live birthso Most commonly found in infants and childreno Males more than females
• Signs and symptoms• Profuse diarrhea, hypovolemic shock, intestinal perforation
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Malabsorption DisordersMalabsorption Disorders• Failure of GI tract to absorb or normally digest one
or more dietary constituents• Causes
o Enzyme abnormalitieso Infectiono Radiation enteritis
• Signs and symptomso Diarrheao Passage of inappropriately processed intestinal contents
• Types (celiac diseases, tropical sprue)
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Malabsorption Disorders (Cont.)Malabsorption Disorders (Cont.)• Celiac disease (celiac spruce)
o Familial intolerance of gluten-containing foodso Leads to inflammation and atrophy of the intestinal villio Impaired nutrient absorption
• Reduced surface area • Decreased brush border enzymes
o 2x increase for intestinal malignancy
o Diagnosis• Intestinal biopsy• Anti-tissue transglutaminase antibody (anti-ttg)• Immunoglobulin A (IgA) endomysial antibody
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Malabsorption Disorders after Surgical Malabsorption Disorders after Surgical
InterventionIntervention• Dumping syndrome
o Dumping of stomach contents into small intestine due to impaired gastric emptying
o Common after gastrectomyo Large volume of hyperosmolar food
is dumped rapidly into small intestine leading to increased bowel motility
o Rapid absorption of large amount of glucose leads to an excessive rise in plasma insulin
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Malabsorption Disorders after Surgical Malabsorption Disorders after Surgical
Intervention (Cont.)Intervention (Cont.)• Dumping syndrome
o Signs and symptoms• Diarrhea, abdominal pain, • Rapid fall in blood glucose level 1-3 hr after meal (rebound
hypoglycemia)o Treatment
• Eating small meals throughout day instead of large meals, carbohydrate restriction, medications to reduce bowel motility
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Malabsorption Disorders after Surgical Malabsorption Disorders after Surgical
Intervention (Cont.)Intervention (Cont.)• Short-bowel syndrome
o Severe diarrhea and significant malabsorption o Develops after surgical removal of large portions of SIo Rapid transit time and reduced surface area for absorptiono Diminished ability to absorb H2O, electrolytes, protein, fat, carbohydrates,
vitamins, and trace elements
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Malabsorption Disorders after Surgical Malabsorption Disorders after Surgical
Intervention (Cont.)Intervention (Cont.)• Short-bowel syndrome
o Signs and symptoms• Diarrhea and malabsorption
o Treatment• Temporary or indefinite intravenous nutritional support
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Neoplasms of GI TractNeoplasms of GI Tract• Esophageal cancer
o Accounts for 1%-2% of all cancerso Men more than womeno Survival rate of <20% in men older than 60 yearso Risk factors
• Genetic, diet high in nitrosamine content, chronic severe reflux (Barrett esophagus), environmental, smoking, alcohol
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Neoplasms of GI Tract Neoplasms of GI Tract (Cont.)(Cont.)
• Esophageal cancero Prognosis: poor; spreads extensively to surrounding organso Very high degree of metastasiso Treatment
• Stent placement, tumor ablation through heat probe and laser
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Neoplasms of GI Tract Neoplasms of GI Tract (Cont.)(Cont.)
• Gastric carcinomao Prevalence in Japan 10x higher than U.S.o Men > 30 yearso Stages (early and advanced)
• Determined by penetration into major muscle layer of stomach, involvement of lymphatic system and surrounding organs
o Risk factors• H. pylori infection, genetic, dietary habits, environmental factors,
smoking
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Neoplasms of GI Tract Neoplasms of GI Tract (Cont.)(Cont.)
• Small intestinal neoplasmso Benign or malignanto Unusual
• Account for <5% GI tumorso > 50 yearso Causes partial or complete obstruction
• Depending on extent and type
o Signs and symptoms• Depends on type and extent; partial or complete obstruction of small
bowel may occur
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Neoplasms of GI Tract Neoplasms of GI Tract (Cont.)(Cont.)
• Colonic polypso Any protrusion into
the lumen of the GI tract
o Benign or malignanto Signs and symptoms
• Usually none; may cause occult or gross bleeding, abdominal pain
o Treatment• Varies according
to size, type, and location
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Neoplasms of GI Tract Neoplasms of GI Tract (Cont.)(Cont.)
• Colon cancer• Risk factors
o Increases after age 40o High-fat, low-fiber dieto Polyps, chronic irritation or inflammation
• Warning signs• Black, tarry, or pencil-shaped stool• Change in bowel habits• Urgent need to defecate on awakening
in morning• Alternating constipation and diarrhea• Sensation of rectal fullness• Dull ache may be felt in rectum/sacral
region
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Chapter 37Chapter 37
Alterations in Function of the Alterations in Function of the
Gallbladder and Exocrine PancreasGallbladder and Exocrine Pancreas
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Structure and Function of the Structure and Function of the
Pancreaticobiliary SystemPancreaticobiliary System
Please review on your own….!
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Physiology and Function of Bile Physiology and Function of Bile
FlowFlow• Bile produced by hepatocytes in liver; stored
in gallbladdero Primary bile acids: choli, chenodeoxycholic acido Secondary bile acids: deoxycholic acid,
ursodeoxycholic acid, lithocholic acido Composed primarily of H2O, electrolytes, organic solute; low
protein contento Additional components include pigment cholesterol
phospholipids
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Physiology and Function of Bile Physiology and Function of Bile
Flow (Cont.)Flow (Cont.)
Bile Compositiono Primarily H2O, electrolytes, organic
soluteo Low protein contento Additional components: pigment,
cholesterol, phospholipids
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Physiology and Function of Bile Physiology and Function of Bile
Flow (Cont.)Flow (Cont.)
Bile Functions• Aids in digestion of lipids• Transports waste products
o Bilirubino Immunoglobulins (IgA)o Toxinso Cholesterol
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Physiology and Function of Bile Physiology and Function of Bile
Flow (Cont.)Flow (Cont.)
Gallbladder• Concentrates and stores bile• Fasting state
o Muscular sphincter at ampulla of Vater is contracted; promotes flow of bile into gallbladder
o Half of bile stored; half flows into duodenumo Absorption: 90% of H2O in bile absorbed from bile in 4 hours
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Functional Anatomy of the Functional Anatomy of the
Pancreas (Cont.)Pancreas (Cont.)• Endocrine pancreas
o Insulino Glucagono Somatostatin into blood
• Exocrine pancreaso Secretes >1 L of digestive juice into duodenum every 24 hr
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Functional Anatomy of the Functional Anatomy of the
Pancreas (Cont.)Pancreas (Cont.)
Pancreas Components• Lobular; composed of two fused organs
o Dorsalo Ventral
• Pancreatic juiceso Active digestive enzymes: amylase, lipaseo Precursor or proenzymes: trypsinogeno Release stimulated by cholecystokinin and secretin
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Disorders of the Disorders of the GallbladderGallbladder
• Cholesterol gallstone formation (cholelithiasis)o Etiology
• 20 million (U.S.)o Incidence
• Native Americans > American Caucasians
• Women > men (2:1)o Risk factors
• Age• Sex• Obesity (also rapid
weight loss in obese)• Variety of medical
factors
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Disorders of the Gallbladder Disorders of the Gallbladder
(Cont.)(Cont.)• Cholesterol gallstone formation (cholelithiasis)
o Pathophysiology• Three phases
o Supersaturation of bile with cholesterolo Nucleation of crystalso Hypomotility allowing stone growth
• Cholecystitiso Inflammation of the gallbladder wallo Related to continued presence of gallstones
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Disorders of the Gallbladder Disorders of the Gallbladder
(Cont.)(Cont.)
Signs and Symptoms: ChronicCholelithiasis• Biliary colic
o Precipitated by a meal (infrequent schedule)o Persistent epigastric (right upper abdominal pain)o Often radiates to backo Increases steadily for >15 minutes, lasts several hours, then slowly
decreaseso Related to intermittent obstruction of cystic duct
• Nausea, vomiting, sweating, flatus
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Disorders of the Gallbladder Disorders of the Gallbladder
(Cont.)(Cont.)
Chronic Cholelithiasis• Diagnosis: ultrasound• Treatment
o Watchful waitingo Patients with significant recurrences of biliary colic
• Cholecystectomy• Chemical dissolution of gallstones• Lithotripsy
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Disorders of the Gallbladder Disorders of the Gallbladder
(Cont.)(Cont.)
Acute Cholecystitis: Acute Inflammationof the Gallbladder Wall• Etiology
o Cholelithiasis present in 90% of patientso Obstruction of cystic duct present in almost all patients: related
to stasis of bileo Bacterial infection may be present
• If untreated, escalates; gangrene may occuro Peritonitiso Septic shocko Localized abscesso Cholecystoenteric fistula (fistula between gallbladder and GI
tract)
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Disorders of the Gallbladder Disorders of the Gallbladder
(Cont.)(Cont.)
Acute Cholecystitis• Signs and symptoms
o Severe right upper abdominal pain: radiates to backo Abdominal tendernesso Fever
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Disorders of the Gallbladder Disorders of the Gallbladder
(Cont.)(Cont.)
Acute Cholecystitis • Acalculous cholecystitis
o Occurs in patients without preexisting gallstoneso Males >50 yearso Rapid development of gangrene, perforation, emphysematous
cholecystitis, and empyema develops rapidly
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Disorders of the Gallbladder Disorders of the Gallbladder
(Cont.)(Cont.)
Acute Cholecystitis • Risks
o Major surgery o Critical illnesso Traumao Burn-related injury
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Disorders of the Gallbladder Disorders of the Gallbladder
(Cont.)(Cont.)
Chronic Cholecystitis: ChronicInflammation of Gallbladder Wall • Related to persistent low-grade irritation from
gallstones• Related to recurrent attacks of acute
cholecystitis• Predisposing factors
o Diabetes mellituso Obesity
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Disorders of the Gallbladder Disorders of the Gallbladder
(Cont.)(Cont.)
Chronic Cholecystitis • Signs and symptoms
o Asymptomatico Leads to complications
• Biliary sepsis• Scarring (porcelain gallbladder)
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Acute Pancreatitis• Etiology: 1-5:10,000 in U.S. annually• Predisposing factors• Biliary tract disease
o Hypertriglyceridemiao Ethanol-associated (66%)
• Secretion of protein-rich pancreatic fluid• Deposition of inspissated protein plugs• Obstruction of small pancreatic ducts
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Acute Pancreatitis: Signs and Symptoms• Steady, boring pain in epigastrium or LUQ
o Increases in intensityo Severe tenderness on palpationo Radiates or penetrates to back
o Accompanied by nausea and vomiting• Abdominal distention
o Hypoactive or absent bowel tones
• Low-grade fever
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Acute Pancreatitis: Diagnosiso Laboratory• Increase in amylase and lipase during
first 12 hro Remain elevated for several dayso Lipase preferred test
• Elevated aminotransferases• Elevated alkaline phosphatase and
bilirubin• Leukocytosis• Hyperlipidemia• Hypocalcemia
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Acute Pancreatitis: Diagnosis • CT of abdomen
o Gold standard and allows remarkable detail: edema, abscess, cyst formation
o Prognostic assessment: Ranson’s criteria
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Acute Pancreatitis: Differential Diagnosis• Perforated peptic ulcer• Acute cholecystitis• Mesenteric vascular disease
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Acute Pancreatitis: Complications• Pseudocyst: collection of fluid within or
adjacent to pancreaso Signs and symptoms
• Fever• Tachycardia• Abdominal mass and tenderness
o Management: endoscopic or surgical drainage
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Acute Pancreatitis: Complications • Pancreatic ascites: persistent leak in
pancreatic duct into pleural space and mediastinumo Signs and symptoms: painless and massiveo Treatment
• Ultrasound• CT• Fluid analysis obtained by aspiration
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Acute Pancreatitis: Complications o Pancreatic ascites: management
• Prolonged parenteral nutrition• Endoscopic placement of a stent into main pancreatic duct
o Common bile duct obstructiono Portal or splenic vein thrombosiso Peptic ulcer diseaseo Chronic fistula formation
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Chronic Pancreatitis: Etiology• Mortality (3%-4% yearly)• Predisposing factors
o ETOH consumptiono Idiopathico Hereditaryo Hyperparathyroidism (hypercalcemia)o Trauma
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Chronic Pancreatitis: Pathophysiology • Presence of chronic inflammatory lesions in
pancreas• Key element: necrosis followed by fibrosis• Persistence of symptoms secondary to
pancreatic dysfunction over weeks and months
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)• Destruction of exocrine parenchyma and
fibrosiso Precedes destruction of endocrine parenchymao Leads to calcification
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Chronic Pancreatitis: Pathophysiology • Increase in protein concentration in
pancreatic juice with reduction in “pancreatic stone protein” (inhibits formation of pancreatic protein plugs)o Leads to calcification—obstruction in flow of pancreatic juice
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Chronic Pancreatitis: Signs andSymptoms• Bouts of acute pancreatitis with progressive
signs of persistent pancreatic dysfunction• Insidious onset of epigastric pain radiating to
back (first symptom)• No pain but sequelae of chronic
pancreatitis(10%-15%)
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Chronic Pancreatitis: Signs andSymptoms • Endocrine and exocrine pancreatic
insufficiencyo Diabetes: progressive loss of endocrine cells in pancreatic isletso Malabsorption
• Pancreatic enzyme output <10% of normal• Impairment of vitamins A, D, E, and K
o Weight loss: poor intake related to pain
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Chronic Pancreatitis: Complications• Pseudocyst• Pancreatic ascites• Obstruction of common bile duct: surgical or
endoscopic intervention• Thrombosis of portal and splenic veins may
lead to GI hemorrhage related to gastric varices
• Peptic ulcer disease
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Chronic Pancreatitis: Diagnosis• History• Physical examination• Laboratory: elevated LFTs, alkaline
phosphatase, and bilirubin levels• Abdominal x-ray• CT• ERCP: suspicious cases unconfirmed with
other tests
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Chronic Pancreatitis: Treatment• Pain control
o Absolute abstention from alcoholo Analgesicso Surgical interventiono Celiac plexus block
• Pancreatic sphincterotomy: management of single or multiple stones
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Chronic Pancreatitis: Treatment • Pseudocysts (adjacent to stomach or
duodenum): endoscopic drains• Obstruction of bile duct or main pancreatic
duct: biliary/pancreatic stents• Whipple procedure
(pancreaticoduodenectomy)
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)
Chronic Pancreatitis: Treatment• Management of endocrine/exocrine
insufficiencyo Low-fat dieto Pancreatic enzyme supplementationo Oral hypoglycemic agents/insulin
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Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)Chronic Pancreatitis: Treatment• Pancreatic enzyme replacement
o Steatorrhea controlo Chronic pain managemento 20%-30% ETOH-induced disease respond to therapyo Medications
• H2 blocker• Proton pump inhibitor
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Chapter 38Chapter 38• Test questions developed from guides provided to
you in content section.
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Hmmm….Hmmm….• What the heck is the difference between Chronic
Persistent Hepatitis and Chronic Active Hepatitis? • Does a patient have “gastritis” or “gastroenteritis?”
Are they the same or are they different?• How is UC and Chron’s the same? Different? What
types of symptoms would they present with that would help me differentiate between them?
• What is going on with Ascites?• How does Hepatitis A, B, C, D, E differentiate from
each other? How are they caused and what are the complications?
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Hmmm….Hmmm….• What is the difference between a duodenal ulcer and a
Peptic Ulcer? How are they caused? What questions do I need to ask as nurse practitioner to help me differentiate between them and help them? If I say the term “Gastric” ulcer, what am I referring to?
• Why am I always getting Psoriasis and Cirrhosis mixed up? They are two different systems!!!
• Does portal hypertension always occur when I embark from a ship? What is it and how does it occur?
• Why is the Lower Esophageal Sphincter important? What happens when it doesn’t work? How does it present? What causes it not to work?
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Hmmm….Hmmm….• Acute vs. Chronic Pancreatitis? Are they the same?
How will I tell them apart? Is there a difference in the cause? Is one just prettier than the other?