Gi+presentation+2014+ho (1)

Gastrointestinal Gastrointestinal SystemSystem

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.

Know anatomy of glandsKnow anatomy of glands

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?

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?

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

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

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

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

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

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.

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

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

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

• What might a patient present with who has a paralyzed enteric nervous system?

A.DiarrheaB. Digital paralysisC.Dark brown emesisD. Increased bowel sounds

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

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

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


• Ileocecal sphinctero Normally closedo Relaxes when intestinal

contents are present in terminal ileum

o Propulsive movement push contents into cecum


• 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


• 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

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

Gastrointestinal Hormones (Cont.)Gastrointestinal Hormones (Cont.)

Enterochromaffin-like cells (ECL)

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

Gastrointestinal Hormones (Cont.)Gastrointestinal Hormones (Cont.)

Read about digestion of food on your Read about digestion of food on your

own, please.own, please.

Summary of Digestive Summary of Digestive FunctionFunction

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

Gastrointestinal Gastrointestinal DisordersDisorders

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

Common Manifestations of Gastrointestinal Common Manifestations of Gastrointestinal

Tract Disorders (Cont.)Tract Disorders (Cont.)


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



o Heartburn (pyrosis)• Symptoms

o Substernal burning sensation that may radiate to neck or throat



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


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


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)


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)

Chemical DigestionChemical Digestion


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


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


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

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.

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.

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

•

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

• 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

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.

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.

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.

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

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


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)


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


Stomach and Intestines (Cont.)Stomach and Intestines (Cont.)• Peptic ulcer disease

o Causes• H. pylori• Stress• Smoking• Alcohol• Spicy foods• Smoking• Genetic



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



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


Stomach and Intestines (Cont.)Stomach and Intestines (Cont.)

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

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

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

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)

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

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

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

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

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


• 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


• 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


• 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


• 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

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)

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

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


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


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


Intervention (Cont.)Intervention (Cont.)• Short-bowel syndrome

o Signs and symptoms• Diarrhea and malabsorption

o Treatment• Temporary or indefinite intravenous nutritional support

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

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


• 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


• 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


• 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


• 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

Chapter 37Chapter 37

Alterations in Function of the Alterations in Function of the

Gallbladder and Exocrine PancreasGallbladder and Exocrine Pancreas

Structure and Function of the Structure and Function of the

Pancreaticobiliary SystemPancreaticobiliary System

Please review on your own….!

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


Flow (Cont.)Flow (Cont.)

Bile Compositiono Primarily H2O, electrolytes, organic

soluteo Low protein contento Additional components: pigment,

cholesterol, phospholipids



Bile Functions• Aids in digestion of lipids• Transports waste products

o Bilirubino Immunoglobulins (IgA)o Toxinso Cholesterol



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

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

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

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

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


(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


(Cont.)(Cont.)

Chronic Cholelithiasis• Diagnosis: ultrasound• Treatment

o Watchful waitingo Patients with significant recurrences of biliary colic

• Cholecystectomy• Chemical dissolution of gallstones• Lithotripsy


(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)


(Cont.)(Cont.)

Acute Cholecystitis• Signs and symptoms

o Severe right upper abdominal pain: radiates to backo Abdominal tendernesso Fever


(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


(Cont.)(Cont.)

Acute Cholecystitis • Risks

o Major surgery o Critical illnesso Traumao Burn-related injury


(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


(Cont.)(Cont.)

Chronic Cholecystitis • Signs and symptoms

o Asymptomatico Leads to complications

• Biliary sepsis• Scarring (porcelain gallbladder)

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


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


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


Acute Pancreatitis: Diagnosis • CT of abdomen

o Gold standard and allows remarkable detail: edema, abscess, cyst formation

o Prognostic assessment: Ranson’s criteria


Acute Pancreatitis: Differential Diagnosis• Perforated peptic ulcer• Acute cholecystitis• Mesenteric vascular disease


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


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


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


Chronic Pancreatitis: Etiology• Mortality (3%-4% yearly)• Predisposing factors

o ETOH consumptiono Idiopathico Hereditaryo Hyperparathyroidism (hypercalcemia)o Trauma


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

Disorders of the Pancreas (Cont.)Disorders of the Pancreas (Cont.)• Destruction of exocrine parenchyma and

fibrosiso Precedes destruction of endocrine parenchymao Leads to calcification


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


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%)


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


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


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


Chronic Pancreatitis: Treatment• Pain control

o Absolute abstention from alcoholo Analgesicso Surgical interventiono Celiac plexus block

• Pancreatic sphincterotomy: management of single or multiple stones


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)


Chronic Pancreatitis: Treatment• Management of endocrine/exocrine

insufficiencyo Low-fat dieto Pancreatic enzyme supplementationo Oral hypoglycemic agents/insulin

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

Chapter 38Chapter 38• Test questions developed from guides provided to

you in content section.

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?

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?

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?

Gi+presentation+2014+ho (1)

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