ingestion of food; propulsion of food & waste from waste -> anus; secretion of mucous, water, & enzymes; digestion (mechanical & chemical) of food; absorption of digested food; elimination of waste products; immune & microbial protection against infection.

chewing, swallowing, & defecation

GI motility and secretion of digestion aiding substances

mouth, esophagus, stomach, duodenum

small intestine, large intestine, colon

descending aorta -> celiac artery and mesenteric artery; then celiac artery feeds the stomach, spleen, and pancreas and also branches into hepatic artery going to the liver; the mesenteric artery branches into the superior mesenteric feeding the pancreas, small intestine, and colon, and the inferior mesenteric feeding the colon.

stomach, spleen, pancreas, small intestine, colon all flow into portal vein -> liver -> inferior vena cava.

portal vein -> liver sinusoids -> kupffer cells (remove waste and toxins) -> inferior vena cava

Ions (Mag, Phos), sugars (sorbitol), lactose, tube feeds

Viruses (rotavirus) enterotoxins (E Coli, Vibrio cholera, Shiga toxin), exotoxins (C Diff), small bowel overgrowth, IBD (UC and Chron’s), constipation (increase of mucous and fluid)

shortened intestine (surgery), neuropathy, laxatives, hyperthyroidism, IBD, fistula

ingestion of high osmolar substances that pull water in and increase stool weight and volume -> large volume diarrhea

increase secretion of chloride or bicarbonate or decrease sodium absorption

excessive motility, decreases transit time and decreased fluid absorption-> negative effects include dehydration, fluid electrolyte and acid-base balance (metabolic acidosis), weight loss.

Osmotic

>\= 3 loose watery stools per day

>\= 3 loose watery stools per day less than 14 days

>\= 3 loose watery stools per day for 30+ days

dehydration, electrolyte imbalance, (Hyponatremia, hypokalemia), metabolic acidosis, weight loss

acute infection

IBS

malabsorption

esophageal or gastric varices, Mallory-Wise Tear, cancer, peptic ulcer, medications

polyps, IBD, Diverticulitis, cancer, hemorrhoids

Occult Bleeding

Upper GI Bleed

Lower GI Bleed

Peptic Ulcer Disease

Peptic Ulcer Disease

Because plasma volume and red cell volume are lost porportionately

50-70 yo, no family Hx, stress, cancer risk, H pylori (60-80%), increased gastrin (associated with gastritis)

increased pain when patient eats a meal and relieved by antacids (associated with gastritis)

Intermittent, nocturnal pain that has phases of remission and exacerbation (not associated with gastritis) with almost a 100% association with H pylori

unknown but risk factors include 10-40 yo with no family Hx

Continuous lesions common in colon or rectum (lower GI) but can effect the entire large intestine and effects the mucosal layer only

Diarrhea with bloody stools and presence of antineutrophil cytoplasmic antibodies

Severe malnutrition may require TPN

Both genetic and environmental with risk factors 10-30 yo with family Hx

Abdominal pain, mucoid diarrhea, abdominal mass, malabsorption

“Skip” lesions common in ileocecal region, small intestine and colon. Effects entire intestinal wall along any portion of the GI tract. Common to have fistulae, strictures, and obstructions.

Diet management

Brain gut interaction, visceral hypersensitivity; abnormal GI permeability, motility, secretion, and sensitivity; post-inflammatory; alteration in gut microbiota, psychosocial factors (epigenetic)

Pain, bloating, fecal urgency, incomplete emptying, doesn’t impact sleep

Unknown

Fiber and pre- and probiotics

Older age, genetics, obesity, smoking, lack of activity, NSAIDS, low fiber diet

Herniation, constriction (adhesions), volvulus (twisting), intussuseption (fold into itself) -> distension

Adolescence but can occur at any age

Cramping pain, diarrhea, constipation, distension, flatulence, fever, leukocytosis, LLQ tenderness

SBO - colicky pain associated with peristalsis, distension, emesis, dehydration, and electrolyte abnormalities LBO - hypogastric pain and distension (bowel sounds often present), vomiting (late sign r/t cancer)

Epigastric or periumbilical pain increasing in intensity over time. May subside then RLQ pain with rebound tenderness (when it ruptures), and N/V and fever

Hernias of mucosal layer of colon through muscle wall

Decreased absorption and increased fluid accumulation proximal to obstruction leading to emesis, dehydration, and electrolyte abnormalities

Inflammation of diverticula

Unclear

Obstruction and inflammation of gallbladder

Epigastric pain (30 mins -> hours after eating), intolerable of fatty foods, vague (heartburn, epigastric pain, jaundice), obstruction (jaundice, fever)

Constant epigastric and mid-abdominal pain, fever and Leukocytosis, N/V, abdominal distension (paralytic ileus) , jaundice (obstructed bile duct). Systemic effects (pleural effusion, ALI, abscess, sepsis, SIRS)

If obstruction in the cyst duct = cholecystitis

Stones result from impaired metabolism of cholesterol, unconjugated bilirubin, fatty foods, calcium carbonates, and phosphates (pigmented gallstones). Hepatocytes secrete bile that is supersaturated in cholesterol.

Obstructive biliary disease, alcoholism, hyperlipidemia, genetics

Inflammation of pancreas (acute or chronic) from autodigestion of pancreatic cells

Amylase, Lipase (key for diagnosis), CRP (shows level of severity)

Acute pancreatitis is the direct result of pancreatic duct obstruction. Chronic pancreatitis is a result of progressive fibrosis and scarring of the pancreas.

Hypertrophy and hyperplasia of pyloric sphincter related to increased gastrin in 3rd trimester (genetic and family Hx), presents in 1st week of life- 6 months, projectile vomiting with eating. Repair with surgery.

The GI system in general slows down and looses function with aging leading to decreased sense of taste/smell, decrease motility and secretion, altered microbiome, lactose intolerance, decreased absorption of nutrients and vitamins, increased constipation, and decreaed liver regeneration. In Anorexia of Aging this leads to decreased appetite and altered satiety control (high levels of ghrelin) leading to decreased intake.

Tylenol overdose, Hep B, Hep C, metabolic liver disease

Viral, autoimmune, ETOH, genetic (Alpha 1 antitrypsin and Wilson’s disease), NAFLD

Anorexia, N/V, abdominal pain, progressive jaundice -> ascities and GI bleeding

Severe acute hepatocyte necrosis without hepatic encephalopathy without previous liver disease or cirrhosis (neuro is intact)

Acute liver injury + coagulopathy and hepatic encephalopathy (neuro changes)

Kupper cells activate -> release inflammatory mediators -> ROS -> activate fibrotic hepatic stellate cells

Extrahepatic obstruction of bile (gall stones); intrahepatic obstruction (liver disease/ bile canaculi); pre-hepatic excessive production (RBC lysis) resulting in hyperbilirubinemia causing yellow/green skin pigmentation

Light colored stools (lack of bile pigment), yellow/green skin sclera first (excess bilirubin in circulation) -> skin xanthoma and pruitis.

Prehepatic - thrombosis and narrowing of portal vein Intrahepatic - vascular remodeling (cirrhosis, hepatitis, parasitic infection) Posthepatic - hepatic vein thrombosis or R HF

Varices (increased risk of rupture), splenomegaly (indication of severity) -> causing thrombocytopenia, hepatopulmonary syndrome (asymptomatic hypoxia r/t vasodilation and shunting), venous resistance to blood flow.

Splenic vasodilation-> decreased SVR -> triggers RAAS to increase ADH -> fluid retention and shifting -> increased risk of peritonitis and bacterial translocation

Accumulation of fluid in peritoneal cavity, R HF, nephrotic syndrome, hypoalbuminemia, cirrhosis, peritonitis, malnutrition

Alteration of neurotransmitters and increase in neurotoxins (cytokines, serotonin, tryptophan, ammonia) -> ammonia metabolizes to glutamine in the brain interfering with neurotransmitters -> results in cytotoxic edema, changes in BBB, increase in GABA -> decrease in LOC

Change in LOC, hand tremor (asterixis), slow speech, bradykinesia, stupor, seizure, coma

Duration and amount of alcohol intake and acetaldehyde

Cirrhosis

-Increased fat deposits in hepatocytes -> oxidative stress with lipid peroxidation and permanent hepatocyte injury -Alcoholic cirrhosis: acetaldehyde inhibits liver metabolism + autoantibodies to hepatic cells + increased bacterial translocation-> inflammation and cellular injury

Obesity, insulin resistance, high triglycerides and cholesterol, DMII, metabolic syndrome

Usually asymptomatic, may result in NASH, symptoms are similar to non-alcoholic Liver Fibrosis

Infiltration of hepatocytes with fat (from triglycerides) occurs without alcohol intake and inflammation

Middle-aged women, autoimmune T-lymphocyte, highly specific anti-mitochondrial antibody destruction of small intrahepatic bile ducts

Gallstones, tumors, strictures, chronic pancreatitis

Pruitis, hyperbilirubinemia, jaundice, light clay-colored stolls, portal HTN, encephalopathy

Primary + RUQ pain, low-grade fever

Progressive autoimmune reaction destroys bile ducts in liver

Prolonged (partial/complete) obstruction of the common bile ducts and it’s branches

Hep A

Hep B

Hep C

Hep D

Hep E

Prodromal Phase

Icteric Phase