GI disorders

GI tract

also called alimentary canal; continuous tube from mouth to anus where food passes

secretion

cells within walls of GI trct and accessory organs release water, acid, buffers, and enzymes into lumen of the tract

motility

alternating contraction anf relaxation of smooth mucles withing walls of tract to mix and propel contents down

digestion

mechanical and chemical breaking down of food

absorption

end products of digestion pass from GI tract into blood or lymph for distribution to cells

elimination

emptying the rectum to eliminate indigestible substances from GI tract

mucosa

inner lining of the GI tract consisting of stratifies squamous epithelium, lamina propria, and thin layer of smooth muscle

submucosa

areolar connective tissue containing blood vessels, glands, and lymph tissue; consists of extensive network of neurons

muscularis

muscle layer of GI tract; contains skeletal muscle for controol of swallowing and defecation, and smooth muscle that controls peristalsis

serosa

outer layer of GI tract; connective tissue and epithelium forms part of peritoneum; route for blood vessels, lymph, nerves to enter/exit tract; anchors organds in place

segmentation

contractions of circular muscle that mix contents; contents do not move through

peristalsis

rhythmic propulsice contractions that propel chyme towards large intestine

anorexia

lack of desire to eat despite physiological stimuli that would normally produce hunger

nausea

subjective experience associated with different conditions; may be associated with anorexia and vomiting; common symptoms include hypersalivation and tachycardia

vomiting

forceful emptying of stomach/intestinal contents through mouth as a protective mechanism

constipation

infrequent or difficult defecation

diarrhea

increased frequency of bowel movements with inc volume and fluidity of feces; may be acute or chronic

acute abdominal pain

abdominal pain that may be caused by tension, ischemia, or inflammation

dyspepsia

chronic or recurrent pain in upper abdomen or feelings of upper abdominal fullness; may indicate GERD, indigestion, peptic ulcers, epigastric distress

hematemesis

vomiting of blood

hematochezia

passage of fresh blood through anus

melena

black feces associated with GI hemorrhage → dark colour due to oxidation of iron in hgb

occult bleeding

small amount of ‘hidden’ blood that is invisible to the naked eye

hemorrhoids

varicosed rectal veins that develop when blood pools and engorges the vessels; caused by chronic constipation/diarrhea, pregnancy, portal hypertension

dysphagia

difficulty swallowing resulting in choking, frequent (aspiration) pneumonia, unexplained weight loss, nasal regurgitation

odynophagia

pain when swallowing

achalasia

specific type of dysphagia where there is too much muscle tone and contractions of the LES resulting in progressive dysphagia, aperistalsis, vomiting, weight loss

achalasia pathophysiology

shift in balance between inhibitory and excitatory stimulation of the LES; decreased number of NO-releasing neurons (inhibitory) resulting in overexcitation by ACh → hypertonic LES

esophageal diverticulum

outpouching of the esophageal wall caused by a weakness of the muscularis layer; pouch tends to retain food resulting in gurgling, couching, belching, and bad breath; may cause esophagitis and ulcerations and require surgical intervention

hiatal hernia

protrusion of herniation of the stomach through the esophageal hiatus od the diaphragm; may be sliding or paraesophageal; causes indigestion and GERD, SOB, pain

gastroesophageal reflux disease

backflow of gastric contents from stomach into the esophagus through LES; chronic condition causing heartburn, dysphagia, regurgitation, upper abdominal pain; also results in esophageal damage over time due to esophagus not having protection from stomach acid

GERD etiology

caused by inadequate anti-reflux mechanisms such as dec LES closure strength, inc intra-abdominal pressure, or inc gastric fluid volume; or by inadequate esophageal clearance

mallory-weiss syndrome

bleeding caused by forceful or prolonged vomiting, resulting in a tear in the mucosa or submucosa of the cardia or lower esophagus; may see hematemesis or melena after an episode of forceful vomiting, or epigastric or back pain

esophageal varicies

dilation of submucosal esophageal veins caused by portal hypertension or schistosomiasis; has high mortality rate from bleeding

parietal cells

secretes hydrochloric acid and intrinsic factor needed for absorption of vitamin B12

G cell

secretes the hormone gastrin

chief cell

secretes pepsinogen and gastric lipase

gastric mucosal barrier

mechanisms that protect the gastric mucosa from stomach acid and enzymes

gastritis

inflammation of the gastric mucosa lining the stomach; can be acute or chronic

acute gastritis

also erosive or hemorrhagic gastritis; inflammatory disorder due to superficial erosion of epithelium

chronic gastritis

chronic inflammatory changes to glandular epithelia of the stomach lining; lacks grossly visible erosions

type A

also chronic fundal gastritis; characterized by antibodies produced against parietal cells or intrinsic factor, leading to absorption defects and possibly cancer; mucosal thinning and glandular atrophy

type B

also chronic antral gastritis; mainly caused by H. pylori infection; results in epithelial damage, glandular atrophy, mucin depletion, and metaplasia

peptic ulcer disease (PUD)

a break or ulcerarion in the mucosal lining of the GI tract, causing GI tract to be exposed to acid or pepsin; develops when aggressive factors overwhelm mucosal defenses

erosion

refers to superficial mucosal injury

ulcer

when injury extends through the mucosa and into deeper tissues

gastric ulcers

20-25% of PUD; occurs in lower stomach due to impaired mucosal defenses; associated with NSAIDs and H. pylori; causes epigastric pain that worsens with food

duodenal ulcers

75-80% of PUD; occurs in proximal duodenum due to excess acid exposure; strongly associated with H. pylori infection; causes epigastric pain that is relieved with food

helicobacter pylori

gram-negative, spiral bacterium; colonizes mucus layer overlying the gastric epithelium and produces urease to create more alkaline microenvironment and allow self survival in stomach

stress ulcers

acute mucosal erosions and ulcers that develop during severe physiologic stress, most commonly in fundus or body of the stomach; can be caused by shock, sepsis, major trauma, mechanical ventilation

curling ulcers

type of stress ulcer caused by severe burns; reduced blood flow to digestive tract, breaking down protective lining and leading to damage and ulcers

cushing ulcers

type of stress ulcer associated with head trauma or inc ICP → vagus nerve is stimulated in attempt to lower ICP → inc vagal stimulation inc gastric secretion → combo of excess acid and mucosal injury promotes ulcer formation

pyloric obstruction

blocking or narrowing of the pyloric sphincter (between stomach and duodenum); backing of contents causes epigastric pain and fullness, nausea and vomiting, malnutrition, dehydration

intestinal obstruction

any interruption of the normal flow of intestinal contents through the GI tract; can be mechanical or functional, causing abdominal distension, nausea/vomiting, dehydration and electrolyte imbalance, constipation

volvulus

twisting of bowel on itself, causing intestinal obstruction and blood vessel compression, commonly in small intestine, cecum, and sigmoid colon

intussusception

telescoping/invagination of a portion of bowel into adjacent bowel, causing intestinal obstruction; surgical treatment done to prevent gangrene, shock, perforation

hirschsprung disease

congenital disorder of the large intestine where enteric ganglion cells are absent in a segment of the distal intestine, resulting in stasis of the stool, bacterial overgrowth, and intestinal perforation

paralytic ileus

decreased motor activity og GI tract without mechanical obstruction → impaired peristalsis → accumulation and stasis of intestinal contents; results in inability to pass gas and absent or hypoactive BS

diverticula

herniations of mucosa through the muscle layers of the colon wall, primarily in the sigmoid colon

diverticulosis

when diverticula develop; low fiber diet → small stool volume → stronger contractions → inc colon lumen pressure → herniations through weak points in muscle wall

diverticulitis

inflammatory stage of diverticulosis, where fecaliths block diverticula, leading to inflammation; may also become necrotic and rupture, leading to local peritonitis

appendicitis

inflammation of the vermiform appendix caused by obstruction → inc pressure → dec blood flow and hypoxemia → ulcerations → bacterial invasion → inflammation and edema

inflammatory bowel disease (IBD)

general term; caused by failure of immune regulation, genetic predisposition, and environmental factors;mincludes ulcerative colitis and crohn’s disease

IBD pathogenesis

immune system abnormally and chronically activated without any pathogen → unregulated, exaggerated immune response against normal bacteria → tissue damage

ulcerative colitis

chronic inflammatory disease that causes ulceration of the colonic mucosa; characterized by WBCs, lots of watery diarrhea, abscess formation → purulent bloody mucus in stools

crohn’s disease

idiopathic, chroninc inflammatory disorder that can affect any part of the digestive tract; characterized by inflammatory fissures, skip lesions, cobblestone appearance, deep fissures → possible fistula formation

maldigestion

failure of the chemical proccess of digestion

malabsorption

failure of intestinal mucosa to absorb digested nutrients

celiac disease

immune mediated disorder triggered by ingestion of gluten; giladin induces intestinal lesions → malabsorption; T cell mediated reaction to gliadin → structural changes in intestinal mucosa

lactase deficiency

inability to break down lactose into monosaccharides; lactose is fermented by intestinal bacteria → pain, flatulence, osmotic diarrhea; may be primary (genetic) or secondary (injury)

pancreatic insufficiency

insufficient pancreatic enzyme production caused by pancreatitis, pancreatic carcinoma, pancreatic resection, cystic fibrosis; mainly manifested as fat maldigestion resulting in fatty stools and weight loss

bile salt deficiency

results from liver disease and bile obstructions; leads to poor intestinal absorption of lipids → fatty stools, diarrhea, loss of fat soluble vitamins

adenocarcinoma

type of esophageal cancer; mostly arises from Barett’s esophagus; occurs over extended period through stepwise acquisition of genetic and epigenetic changes

squamous cell carcinoma

type of esophageal cancer; occurs in upper and middle thirds of esophagus; risk factors include alcohol and tobacco use, achalasia, frequent consumption of very hot drinks

gastric carcinoma

mainly adenocarcinomas occuring in pyloric region or adjacent to antrum; one of leading causes of cancer-related death worldwide

gastric carcinoma etiology

causes including dietary factors such as excessive nitrates; gastric acid supression → inc bacteria; post-gastrectomy pts with persistent inflammation; genetics

gastric carcinoma pathophysiology

nitrates react with amino acids to form compounds that damage DNA → reduced HCl production allows bacteria to colonize → infections and gastritis

colorectal cancer

mainly adenocarcinomas occuring in colon and rectum; among top three cancers; caused by environmental risk factors, predisposing conditions, genetics

colorectal cancer pathophysiology

begins as adenomatous polyps → usually starts in mucosal glands → slow growth and spread → frequently metastasizes