Gastrointestinal                                                                                    ...
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Gastrointestinal Disorders . Disorders of Nutrition. Alterations in: Ingesting Digesting Absorbing Eliminating. Anorexia Pica

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Disorders of Nutrition

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Gastrointestinal Disorders

Disorders of Nutrition

Alterations in: Ingesting Digesting Absorbing Eliminating



Nausea & Nausea

Esophageal Atresia

Tracheoesopheal fistula

Cleft lip/palate

Anorexia Nervosa

Pyloric Stenosis

Projectile Vomiting



  • Lactic Deficiency

  • Pancreatitis

  • Cystic Fibrosis


  • 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)


  • Diarrhea Osmotic Changes Secretory Changes Mucosal Damage Altered Motility

  • Crohn’s Disease

  • Ulcerative Colitis

Basic Structure of the GI tract







Circular muscle





Enteric Nervous System Influenced by ANS








Myenteric Submucosal









Gastric Motility







approx 3 contractions

per minute

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

VagusMast CellsG cells

AchHistamine Gastrin



H2 receptor



Gastric Parietal Cell

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

Lactase:lactoseglucose, galactose

Sucrase:sucrosefructose, glucose

Dextrinase:cleaves amylose branch points

Glucoamylase: maltoseglucoses

Only Monosaccharides are Absorbed

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


  • 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

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

Oropharyngeal vs Esophageal


  • 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


  • 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

High fever?

Bloody diarrhea?






large volume



small volume

LLQ pain

+ fecal leukocytes

Shigella, Salmonella,

C. difficile, E. coli (bad)

Campylobacter, HIV-


Viral: rotavirus, Norwalk

S. aureus food poisoning


Rehydrate, symptomatic

Culture and treat

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

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 ColitisContinuous ulcerationof mucosa of colonColon, rectum – distalWatery diarrhea – has mucus/pus – may be bloody – commonProned to develop colon carcinomarare abcess/fistula formation

Compare and Contrast – CD & UC

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


  • 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

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

Functional Obstruction * Bowel Manipulation (surgery) * Narcotic Anesthesia * Peritonitis

Types of Bowel Obstruction

“Itis” from TOP to BOTTOM

“itis”EtiologyClinical Findings

esophagitisreflux (GERD)- pain after meals

- “heartburn”

gastritis -PUDASA, ETOH- epigastric pain

H. pylori

regional enteritis? Etiology- diarrhea with

(Crohn) blood and mucus

ulcerative colitis? Etiology- bloody diarrhea

“Itis” from TOP to BOTTOM

“itis”EtiologyClinical Findings

diverticulitislow fiber dietlow abdominal

pain, fever

appendicitisobstruction- RLQ pain, fever

“fecalith”- rebound pain

peritonitisperforation- severe pain, ileus

bowel ischemia- guarding, rigid

pancreatitisbiliary disease- pain to back, shock

ETOH- high lipase, amylase

“Itis” from TOP to BOTTOM

“itis”EtiologyClinical Findings

cholecystitischolelithiasis- RUQ pain

- steatorrhea

hepatitisviral, acute ETOH- jaundice, big liver

- high AST, ALT

- flu-like symptoms


  • 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


  • 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

During first 48 hours

HCT drop of >10%

BUN rise >5 mg/dl

PaO2 < 60

Calcium < 8 mg/dl

Fluid sequestration of > 6 liters

Severity Scale: Pancreatitis


  • Age over 55

  • WBC > 16,000

  • Blood glucose > 200

  • Base deficit > 4

  • Serum LDH >350

  • AST > 250

Pancreatitis Severity

Number of criteria

Mortality Rate










  • 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


  • 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 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


Transmissionoral-fecalblood andblood andoral-fecal

body fluids body fluids

Riskcontaminatedsexual, IVsexual, IVwaterborne


Prognosisgoodmore severe85% chronic?

5% carrier

B+D more


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

cell failure

From GI




low albumin


immune deficient

estrogen excess


Portal vein

To vena


portal hypertension


esophageal varices



Hepatic vein

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

The End…..

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