Chapter 38: Alterations of Digestive Functions

Osmotic diarrhea

Undigested solutes (ex; lactose) pull water into the lumen.

Secretory diarrhea

Infections (ex; bacterial toxins) stimulate excessive chloride & water secretion.

Motility diarrhea

Rapid intestinal transit -> decreased contact time -> decreased absorption.

Primary constipation

Functional, slow transit, pelvic floor dysfunction.

Secondary constipation

Caused by low fiber, opiates, iron, hypothyroidism, aging.

Primary & Secondary Constipation

Lead to hard stools, straining <BMs/week

Abdominal Pain

• Stretching of organs leads to distention

• Ischemia of GI organs

• Inflammation of serosal surfaces

Parietal Pain

Sharp & localized from peritoneal irritation.

Visceral Pain

Dull, poorly localized from organ distention.

Referred Pain

Felt distant from organ due to shared nerve pathways.

Upper GI Bleeding Symptoms

Hematemesis, Melena (black, tarry stools), which may be from varices, ulcers.

Lower GI Bleeding

Hematochezia (bright red blood).

Occult Bleeding

Not visible, positive FOBT, iron-deficiency anemia.

Physiologic Response to GI Bleeding

Depends on Rate/Amount: Tachycardia, Hypotension, lowered Hgb/Hct, Dizziness, Fatigue, Severe blood loss leading to shock.

Disorders of GI Tract Motility

GERD, Gastroparesis, IBD, Constipation, Diarrhea, Obstructions

GERD

Incompetent LES leads to reflux, erosion, inflammation

GERD Pathogenesis

Resting tone of the lower esophageal sphincter tends to be lower than normal (or an incompetent LES) so it opens more frequently and for longer periods

GERD Clinical Manifestations

Heartburn, indigestion, chest pain, hoarseness / laryngitis, cough, asthma attacks, globus (sensation of something in the back of the throat), dysphagia

GERD History

Occurring 30-90 minutes after a meal, sleeping with multiple pillows and worsening with reclining, improves with antacids, sitting, or standing

GERD Treatment

Weight loss, head elevation, avoidance of eating 2-3 hours before bed, elimination of trigger foods, medications (proton-pump inhibitors, H-2 antagonists, antacids), laparoscopic fundoplication surgery

GERD Workup

Clinical diagnosis / history, upper endoscopy with biopsy, 24-hour pH test, esophageal manometry

Gastroparesis

Delayed gastric emptying (diabetes, vagal nerve damage).

IBD

Inflammation affects motility (diarrhea, urgency).

Functional Constipation

Slow colonic transit.

Obstructions

Tumors, adhesions lead to distention/upstream hypermotility.

Peptic Ulcer

Disease resulting from the damage of or breaking of mucosal barrier of the stomach and duodenum

Peptic Ulcer Etiology

Non-steroidal anti-inflammatory agents, helicobacter pylori

Non-Steroidal Anti-Inflammatory Agents

Has a system anti-prostaglandin effect, loss of cytoprotection which minimizes mucosal secretion and stops bicarbonate, less blood flow

Helicobacter Pylori Infection

Gram negative rod found in gastric epithelium, produces ammonia to decrease acid production and protease to allow bacteria to burrow into mucosa, produces auto-antibodies

Peptic Ulcer Complications - Hemorrhage

Caused by erosion of blood vessels and may be the first sign of a peptic ulcer

Peptic Ulcer Complications - Perforation

Ulcer erodes through the wall and results in chemical peritonitis

Peptic Ulcer Complications - Obstruction

May result later due to the formation of scar tissue

Peptic Ulcer Signs

Epigastric burning or localized pain usually following stomach emptying

Peptic Ulcer Treatment

Determine the cause, reduce exacerbating factors, antimicrobial + proton pump inhibitor for H.pylori infection

Duodenal Ulcers

Most common, pain is 2-3 hours after eating. Caused by H. Pylori or NSAIDS & is relieved by food/antacids.

Gastric Ulcers

Located in the antrum, pain immediately after eating. Caused by mucosal barrier breakdown and is not relieved by antacids.

Stress Ulcers

Rapid onset from severe illness, trauma, burns, sepsis. Risks for perforation & hemorrhage.

Pancreatic Insufficiency

Decreased enzymes (lipase, amylase, protease).

Pancreatic Insufficiency Clinical Effects

Steatorrhea, weight loss, fat soluble vitamin deficiencies (A, D, E, K).

Lactase Deficiency

Inability to digest lactose

Lactase Deficiency Clinical Effects

Bloating, gas, cramps, osmotic diarrhea

Bile Salt Deficiency

Poor micelle formation leads to poor fat absorption

Bile Salt Deficiency Clinical Effects

Steatorrhea, fat-soluble vitamin deficiency, liver disease, biliary obstruction

Ulcerative Colitis

Located in the rectum to colon (continuous lesions) that only affects mucosa layer

Ulcerative Colitis Stools

Frequent, watery, bloody, mucus

Ulcerative Colitis Complications

Toxic megacolon, malabsorption is less common

Crohn Disease

Located anywhere from the mouth to the anus (terminal ileum, common ex) that skips lesions making it transmural

Crohn Disease Stools

Loose and semi-formed

Crohn Disease Complications

Fistulas, fissures, abscesses. Malabsorption is common, especially B12 & folate

Portal Hypertension

Increased pressure in the portal system that causes varices, splenomegaly. Esophageal varices leads to massive bleeding

Ascites

Fluid accumulation in peritoneal cavity that is caused mainly by cirrhosis. Managed with paracentesis

Hepatic Encephalopathy

Increased ammonia buildup leading to astrocyte dysfunction that causes confusion, irritability, asterixis, coma

Jaundice

Hyperbilirubinemia (bilirubin accumulation) causing dark urine, yellow sclera, pale stools

Prehepatic Jaundice

Transfusion reactions, sickle cell anemia, thalessemia and autoimmune disease

Intrahepatic Jaundice

Hepatitis, cancer, cirrhosis, congenital disorders, and drugs, alcohol abuse

Posthepatic Jaundice

Gallstones, inflammation, scar tissue, or tumors block the flow of bile into intestines, pancreatic cancer

Hepatorenal Syndrome

Functional renal failure in end-stage liver disease. Oliguria and hypotension. Can be acute or gradual onset

Hepatic Encephalopathy

Spectrum of neuropsychiatric abnormalities in patients with liver dysfunction after exclusion of brain disease

Hepatic Encephalopathy Clinical Manifestations

Personality change & irritability, intellectual impairment & memory loss, depressed consciousness, flapping tremor of hands (asterixis)

Alcoholic Cirrhosis

Caused by long-term alcohol use

Alcoholic Cirrhosis Stages

Fatty liver (reversible) -> Alcoholic hepatitis -> Cirrhosis (fibrosis, irreversible)

Alcoholic Cirrhosis Manifestations

Ascites, varices, RUQ pain, jaundice, encephalopathy

Alcoholic Cirrhosis Treatment

Stop drinking alcohol, transplant in severe disease

Biliary Cirrhosis

Autoimmune destruction of bile ducts is primary while chronic obstruction from stones or tumors is secondary

Biliary Cirrhosis Symptoms

Pruritus, jaundice, fat soluble vitamin deficiency

Cholelithiasis

Gallstones from supersaturated bile; 4 F's (Female, forty, fertile, fat). Hypomotility -> stone growth

Cholecystitis

Stone obstructs the cystic duct leading to RUQ pain radiating to shoulder, rebound tenderness

Acute Pancreatitis

Autodigestion from enzyme leakage, severe epigastric pain radiating to back, N/V fever. Caused by gallstones and alcohol. Hypovolemia leads to shock while there's an increase in amylase/lipase

Chronic Pancreatitis

Recurrent inflammation leading to fibrosis

Chronic Pancreatitis Manifestations

Chronic abdominal pain, pancreatic insufficiency, malabsorption, steatorrhea, possibility of diabetes from loss of islets

Emesis

Forceful emptying of stomach and intestinal contents through the mouth

Melena

Dark/black, tarry stool