Gastrointestinal                                                                                                                                                            Disorders 
Disorders of Nutrition
 Alterations in:

   Ingesting

   Digesting

   Absorbing

   Eliminating
Ingestion
•	Anorexia
•	Pica
•	Nausea & Nausea
•	Esophageal Atresia
•	Tracheoesopheal fistula
•	Cleft lip/palate
•	Anorexia Nervosa
•	Pyloric Stenosis
•	Projectile Vomiting
Maldigestion
•	Lactic Deficiency
•	Pancreatitis
•	Cystic Fibrosis

Malabsorption
•	Intestinal Parasites
•	Gastrectomy
  Loss of Stomach as  Reservoir 
  for Food
  Dumping Syndrome
  Loss of Intrinsic Factor
•	Celiac Disease (Sprue)
•	Cholecystitis/Cholelithiasis
•	Regional Enteritis (Crohn’s Disease)
Elimination
•	Diarrhea
  Osmotic Changes
  Secretory Changes
  Mucosal Damage
  Altered Motility
•	Crohn’s Disease
•	Ulcerative Colitis
Basic Structure of the GI tract 
Enteric Nervous System 
Influenced by ANS
Gastric Motility
Control of Gastric Emptying
Small and Large Bowel Motility
•	Small Intestine
•	2-4 hours to traverse
•	Segmental contractions to mix
•	Peristaltic waves to move forward
•	Large Intestine
•	Slow progression at 5-10 cm per hour
•	Segmental contractions produce haustra
•	1-3 mass movements per day
Secretion in the Stomach
•	Parietal Cells		
•	HCL
•	Intrinsic Factor
•	Chief Cells
•	Pepsinogen
•	Surface epithelia and mucous cells
•	HCO3- and mucus
Control of Acid Secretion
Secretion in the Small Intestine
•	Secretions from Pancreas
•	HCO3-, Proteases, Lipases, Amylases
•	Secretion from Gallbladder 
•	Bile acids, pigment, phospholipid
•	Secretions from intestinal epithelia
•	Brush border enzymes
Brush Border Enzymes
Digestion and 
Absorption of Proteins
•	Pepsin:  15% of peptide bonds broken
•	Pancreatic proteases
•	Trypsin
•	Chymotrypsin
•	Carboxypeptidases
•	Brush Border
•	Peptidases cleave into 1 to 4 aa chains
Digestion and Absorption of Fat
•	Bile salts are amphipathic molecules that break up large fat globs into droplet
•	Lipase are water soluble - only work at surface of droplet
•	Triglycerides --------> FFA and glycerol
•	Bile forms micelles with FFA to keep soluble. 
•	FFA are lipid soluble so absorb directly
Reabsorption of Bile
•	Bile is reabsorbed at terminal ileum
•	Passive diffusion and active transport
•	Transported to liver via portal blood
•	ALL reabsorbed bile is taken up on first pass by liver
•	Entire bile pool circulates 2 to 5 times per meal.  5-10% lost per day in stool
GI Disorders
Dysphagia
•	Neuromuscular:  pharynx
•	Stricture or tumor:  Progressive solid food dysphagia
•	Achalasia:  esophageal motility disorder, loss of peristalsis in lower 2/3 plus impaired LES relaxation
•	Mallory-Weiss syndrome:  mucosal tears at distal esophagus, bleeding, pain
Oropharyngeal vs Esophageal
•	Nasal regurgitation
•	Airway obstruction with eating
•	Coughing when swallowing
•	Immediate regurgitation
•	Hoarse voice
•	No airway distress
•	Late regurgitation
•	Chest pain @ meals
•	Frequent heartburn
•	Presence of collagen disease
•	Presence of Left supraclavicular node
Dyspepsia
•	Present with heartburn, indigestion, epigastric distress
•	Up to 2/3 will have no identifiable cause
•	One-half will have relief from placebo
•	Symptom profile does not differentiate between GERD, PUD, and non-ulcer dyspepsia (functional)
•	Physical exam is rarely helpful
Diagnosis
•	NSAID: suspect PUD and treat
•	Helicobacter pylori: urea breath test or biopsy during endoscopy
•	GERD: Trial of H2 therapy
•	Functional: may improve with agents that increase motility 
•	Zollinger-Ellison syndrome: gastrin level
PUD with H. pylori
•	H. pylori is nearly always a factor in non-NSAID peptic ulcer disease
•	Conventional therapy with H2 blockers or H+ pump inhibitors has a 75-80% one-year recurrence rate
•	Treatment for H. pylori reduced recurrence rate to less than 5%
Acute Infectious Diarrhea
Chronic Diarrhea: Stool Studies
•	Stool Osmolality: normal gap < 50
•	Laxative screen: Mg, PO4, SO4
•	Fecal leukocytes: Inflammatory disease
•	Ova and parasites: Giardia, cryptosporidium
•	Fecal Fat analysis:  > 10 g/24 hrs indicates malabsorption
•	Fecal weight: > 1000 g is secretory
Osmotic Diarrhea: Lactase Def.
•	Incidence
•	90% of Asian Americans
•	95% of Native Americans
•	50% of Mexican Americans
•	60% of Jewish Americans
•	25% of other Caucasians
•	DX: empiric trial of lactose-free diet for two weeks
Inflammatory Bowel Disease
•	Ulcerative Colitis
•	Involves only the colon and rectum
•	Mucosal layer is affected
•	Hallmark is bloody diarrhea and lower abdominal cramps
•	Associated with increased cancer risk after 8-10 years of disease
Assess UC Disease Severity
•	Number of stools per day
•	Hematocrit
•	Sed rate
•	Albumin level
Crohn Disease
•	Intermittent bouts of fever, diarrhea, 
and RLQ pain
•	May have RLQ mass, tenderness
•	Can affect any portion of GI tract
•	30% are small bowel only
•	50% are small and large bowel
•	15-20% are large bowel only
Crohn Disease
•	Transmural process in the intestinal wall predisposes to fistula formation
•	If suspected, obtain upper GI series with small bowel follow through plus either colonoscopy or barium enema
•	Suggestive findings are ulcerations, strictures, and fistulas
•	RX: stop smoking, drugs similar to UC
Compare and Contrast – CD & UC
•	Crohn’s Disease

  “Skip” Lesions
 (granulomatous)
  
  Terminal ileum
  Diarrhea/Constipation 
  Alternates – Less
  Bloody
  Malignant Potential
(not totally determined)
      Proned to Develop
  Abcesses & Fistula
  formation
•	Ulcerative Colitis

Continuous ulceration
of mucosa of colon

Colon, rectum – distal

Watery diarrhea – has mucus/pus – may be bloody – common

Proned to develop colon carcinoma

rare abcess/fistula formation
Motility Diarrhea: IBS
•	Irritable bowel syndrome is a chronic (>3months) functional disorder with no identifiable pathology
•	Fluctuations in stool frequency and consistency (no nocturnal diarrhea)
•	Perceived abd distention, bloating, pain
•	Often associated with anxiety or depression
IBS
•	It is not IBS if fever, bloody stools, nocturnal diarrhea, or weight loss are present
•	Consider checking CBC, sed rate, albumin, and stool for occult blood to rule out inflammatory disease, consider lactose-free trial.
•	RX:  restrict caffeine, gas producing food, high fiber. Rx depression
Occult GI Bleeding
•	Detected by FOBT: worry colorectal CA
•	Indicated for iron deficiency anemia in males or postmenopausal females
•	Unless S&S suggest Upper GI etiology (heartburn, dyspepsia PUD) start with colonoscopy (or barium enema)
•	If no source, follow with endoscopy
Acute Abdominal Pain
•	Tension:  spasm, associated with intense peristalsis (irritant, infection, obstruction)
•	Ischemia:  intense constant pain (bowel strangulation, volvulus adhesion)
•	Inflammation:  first localized to serosa covering inflamed part then extends to abdominal wall causing reflex muscle spasms (rigidity, involuntary guarding)
Assessment of the Pain
•	Is it nongastric? consider aortic aneurysm, ectopic pregnancy, PID, kidney
•	Is it an acute surgical abdomen?
•	Involuntary guarding, rigidity
•	Absent bowel sounds
•	Is there shock
Localization of Abdominal Pain
•	Stomach, duodenum:  mid epigastric
•	Small bowel:  periumbilical
•	Colon:  low abdomen, midline
•	Rectum:  sacrum and perineum
•	Gallbladder: mid epigastric radiates to RUQ or right scapula
•	Pancreas: mid epigastric radiate to back
•	Appendix: RLQ, but variable
Bowel Obstruction
•	Presentation
•	Pain, distention, vomiting, obstipation
•	Evaluation
•	Flat and upright abdominal film
•	Small bowel: less urgent
•	intestinal tube, decompression
•	Large bowel: urgent, danger of cecal perf
•	immediate surgical consult
Types of Bowel Obstruction
•	Mechanical Obstruction

  *  Adhesions
  *  Tumors
  *  Impaction
  *  Strangulated Hernia
  *  Volvulus “Twisting”
  *  Intussusception
       (telescoping)
•	Functional Obstruction

  *  Bowel Manipulation
        (surgery)
  *  Narcotic Anesthesia
  *  Peritonitis
“Itis” from TOP to BOTTOM
“Itis” from TOP to BOTTOM
“Itis” from TOP to BOTTOM
Appendicitis
•	Etiology:
•	Obstruction by fecalith, inflammation
•	Presentation:
•	RLQ pain (classic, but may be anywhere), N&V, fever, diarrhea, RLQ tenderness
•	Evaluation: CBC, abdominal ultrasound
•	RX: immediate surgical consult
Diverticulitis
•	Etiology: 
•	Microperforation with peridiverticular inflammation
•	Presentation:
•	Elderly with LLQ pain, severe constipation, nausea, fever
•	Evaluation:
•	CBC, abd film, CT if peritoneal signs
•	Rx: NPO, antibiotics, IV fluids
Liver, biliary, and pancreatic anatomy
Acute Pancreatitis
•	Etiology:  unknown
•	Associated with ETOH, biliary disease
•	Presentation:
•	Severe epigastric and back pain
•	Evaluation:
•	CBC, glucose, calcium, electrolytes, amylase, lipase (renal studies)
•	Severity index
Severity Scale: Pancreatitis
Initially
•	Age over 55
•	WBC > 16,000
•	Blood glucose > 200
•	Base deficit > 4
•	Serum LDH >350 
•	AST > 250
Pancreatitis Severity
Cholecystitis
•	Etiology:
•	95% associated with stone in cystic duct
•	Presentation:
•	Often obese female, fever, RUQ pain with scapular or epigastric pain, colicky, N&V
•	Evaluation:
•	CBC, RUQ ultrasound, HIDA scan
•	RX: Prompt cholecystectomy
Steatorrhea
•	Pancreatic steatorrhea:
•	> 90% of exocrine function lost
•	Bile salt deficiency:
•	decreased ileal reabsorption (Crohn)
•	blocked secretion (cholestasis)
•	Bacterial overgrowth syndromes:
•	stasis of small bowel contents
•	Mucosal defects: Celiac disease (sprue)
Jaundice
•	Jaundice occurs with bilirubin level > 3 mg/dl (normal 0.2-1.2)
•	Increased RBC breakdown
•	Impaired liver uptake of bilirubin
•	Impaired excretion of bilirubin
Functions of the Liver
•	Nutrient metabolism (glucose, protein, fat, fat soluble vitamins)
•	Production of serum proteins and enzymes (albumin, clotting factors etc.)
•	Detoxification of hormones, drugs
•	Bile synthesis (conjugation of bilirubin)
•	Urea synthesis
Structure of liver lobule
Manifestations of Liver Dysfunction
•	Impaired protein synthesis
•	bleeding (clotting factor deficiency)
•	edema (hypoproteinemia)
•	immune deficiency (substrate for antibody)
•	Accumulation of toxins and hormones
•	feminization (excess estrogens)
•	poor metabolism of drugs
•	spider nevi (estrogen)
Manifestations of Liver Dysfunction
•	Inadequate bile synthesis
•	increased bilirubin level
•	jaundice
•	Inadequate urea synthesis
•	increased blood ammonia level (NH3)
•	hepatic encephalopathy
•	Release of marker enzymes into blood
•	AST (SGOT)
•	ALT (SGPT)
High Direct Bilirubin
•	Hepatocellular injury: 
•	hepatitis
•	drugs
•	hemochromatosis
•	Alpha-1 antitrypsin deficiency
•	Cholestasis:
•	stones, tumors, strictures
•	cholangitis
Acute Hepatitis
•	Etiology: acute liver inflammation and cellular injury: viral, toxic
•	Presentation: jaundice, anorexia, fatigue, diffuse abd discomfort, dark urine
•	Evaluation: History of viral or toxin exposure, AST, ALT, Alk phos, bilirubin, serology for viral hepatitis
Viral Hepatitis
Acute Toxic Hepatitis
•	Etiology: exposure to hepatotoxin or its metabolite
•	Evaluation: No definitive tests:
•	history of exposure is important
•	negative viral serology screen
•	improvement after discontinuing drug
•	if alcohol is the toxin, AST > ALT, 2:1
Chronic Alcoholic Liver Disease
•	Etiology: chronic, heavy ETOH exposure 
•	Only 15-20% of alcoholics develop liver disease
•	Men > 4-6 drinks/day, Women > 3-4/day
•	Pathogenesis: unknown
•	Presentation:
•	fatty liver
•	hepatitis
•	cirrhosis
Cirrhosis of the Liver
•	Fibrotic liver
•	loss of hepatocellular functions
•	obstruction to bloodflow from the gut
•	Etiology
•	Chronic alcohol use (most common)
•	Biliary (obstruction in bile drainage)
•	Postnecrotic (viral, toxic hepatitis)
•	Cardiac (right heart failure, liver congestion)
Liver Cirrhosis
Treatment & Monitoring
•	Abstinence from alcohol
•	Restore nutrition: (high protein diet unless hepatic encephalopathy)
•	Monitor PT, AST, ALT, albumin, bilirubin
•	Vitamin K
•	Abnormal PT despite vitamin K indicates a severely compromised liver
Treatment & Monitoring
•	Ascites:
•	caput medusae: flow outward from navel
•	sodium restriction
•	spironolactone
•	monitor for spontaneous bacterial peritonitis
•	If ascites is present, high likelihood of esophageal varices
Treatment & Monitoring
•	Hepatic Encephalopathy
•	Altered mental status due to accumulation of toxins, including ammonia (NH3)
•	Precipitated by GI bleed, drugs, increased shunting of blood around liver
•	Monitor NH3 level
•	lactulose
•	withhold protein
Liver Cancer
•	May and usually does have similar clinical manifestations to cirrhosis. Liver cancer is almost always metastatic. The survival rate s less than 5%.
Balloon tamponade of esophageal varices
Study Well & Do GREAT Next Week
                      The End…..