patho ch 42 GI disorders

4 cardinal signs & symptoms

pain, altered ingestion, altered mobility, bleeding

digestive pathway

food & liquids enter the mouth—>mastication & addition of salivary enzymes—>voluntary transport of food & liquids (positioned at back of throat for esophageal entry)—>involuntary transit to the stomach

common manifestations of esophageal defects

pain, alteration in ingestion, bleeding

dysphagia

difficulty swallowing

causes of dysphagia

neurological deficit, muscular disorder, mechanical obstruction

presentations of dysphagia

pain w/ swallowing, inability to swallow larger pieces of solid material, difficulty swallowing liquids

dysphagia caused by fibrosis

scar tissue causes contraction of esophagus

dysphagia caused by compression

cyst/mass/tumor causes narrowing of the esophagus

diverticulum

fold in the esophagus where food gets accumulated; bad breath is a symptom

esophageal atresia

born w/ walls of esophagus closed

indications of esophageal atresia

baby is always hungry but always throwing up

congenital tracheoesophageal fistula

connection between esophagus & trachea

achalasia

walls of esophagus don’t contract properly, food gets stuck

neurologic causes of dysphagia

damage to cranial nerves that control mastication or swallowing can affect digestion

esophageal web & rings

thin membranes or folds that narrow the esophagus

causes of esophageal web & rings

iron deficiency anemia, autoimmune disease, gastroesophageal reflux

esophageal web & rings treatment

dietary restrictions (soft food), endoscopic dilation therapy

esophageal cancer

primary squamous cell carcinoma (most common distal esophagus), significant dysphagia in later stages, poor prognosis due to late manifestation

esophageal cancer is associated w/ chronic irritation due to

chronic esophagitis, achalasia, hiatal hernia, alcohol abuse & smoking

hernia

a condition where an organ or tissue protrudes through a weak spot in the muscle or CT that surround it

hiatal hernia

part of the stomach protrudes into the thoracic cavity

sliding hiatal hernia

paraesophageal (rolling) hiatal hernia

etiology of hiatal hernia

multifactorial, may involve genetic link

pathogenesis of hiatal hernia

herniation of stomach through esophageal hiatus of the diaphragm, lower esophageal sphincter permits reflux of gastric contents

manifestations of hiatal hernia

may be asymptomatic; frequently involves symptoms of gastroesophageal reflux

type IV paraesophageal hernia

may produce dyspnea, reduced exercise tolerance, syncope, may cause chronic esophagitis

signs of hiatal hernia

heartburn/pyrosis, frequent belching, increased discomfort when laying down, substernal pain that may radiate to the shoulder & jaw

treatment for hiatal hernia

medications for symptomatic gastric reflux, surgery may be indicated

etiology of eosinophilic esophagitis

cause unknown, many associated factors

etiology of radiation esophagitis

treatment of thoracic cancers, exacerbated by chemotherapeutic agents

etiology of corrosive esophagitis

ingestion of strong alkaline or acid substances

etiology of pull esophagitis

Swallowed pill lodges transversely in esophageal lumen and causes inflammation

pathogenesis of esophagitis

irritation to & inflammation of esophageal tissues lead to esophageal damage

treatment of esophagitis

varies based on etiology, thorough history & physical exam is required

most common cause of esophageal diverticula

impaired esophageal mobility

etiology of esophageal diverticula

acquired condition, may be caused by traction on esophagus due to inflammatory disease of mediastinum such as tuberculosis

pathogenesis of esophageal diverticula

increasing pressure on esophageal lumen, esophageal mucosa protrudes through weakened esophageal wall & produces outpouching

manifestations of esophageal diverticula

most often asymptomatic, vary based on location, may produce dysphagia & heartburn

treatment of esophageal diverticula

depends on size & location, surgical intervention may be needed if it is too large

main categories of stomach disorders

disorders of secretion, disorders of mobility

associated cardinal GI symptoms of stomach disorders

pain, altered ingestion, altered digestion, GIT bleeding

peptic ulcer disease

Inflammatory process that damages epithelial lining of stomach and body is not able to replace the injured area—critical injury

stomach perforation

very bad complication; full thickness tear in stomach wall, fluid of stomach leaks to surrounding organs

most common causes of peptic ulcer disease

H. pylori infection and NSAID use

contributing factors of peptic ulcer disease

smoking, excessive alcohol use, drug use, emotional stress, psychosocial components

pathogenesis of peptic ulcer disease

increased gastric acid secretion or a weakened mucosal barrier leads to mucosal erosion or ulceration of GIT

manifestations of peptic ulcer disease

epigastric pain, dyspepsia (upset stomach)

common complications of peptic ulcer disease

bleeding, perforation, obstruction

treatment of peptic ulcer disease caused by H. pylori

triple or quadruple therapy

treatment of peptic ulcer disease caused by NSAID use

H2 receptor antagonist & cease NSAID use

gastritis

inflammation of stomach wall

common etiology of gastritis

infection induced (H. pylori), NSAID use

etiology of acute gastritis

drug induced (NSAIDs, steroids, some chemotherapeutic drugs, alcohol, iron supplements), ulcerohermorrhagic—physiologic stress & ischemic changes caused by shock, hypotension

pathogenesis of acute gastritis

acute imbalance between mucosal injury & repair mechanisms, development of mucosal hyperemia & erosive changes w/ histologic presence of inflammation

etiology of chronic gastritis

chemical & caustic agents (NSAIDs, excessive alcohol ingestion, radiation exposure), autoimmune disease (Crohn, Wegener granulomatosis, sarcoidosis)

pathogenesis of chronic gastritis

begins w/ superficial gastritis—>progresses to atrophic gastritis—>advances to gastric atrophy—>gastric glandular structures are lost and/or metaplasia

what is gastric atrophy a precursor to?

gastric cancer

manifestations of gastritis

most often asymptomatic or report mild dyspepsia; may have abd pain/upset, burning sensation in chest or upper abd, feeling of fullness, bloating, belching, reflux

more severe symptoms of gastritis

nausea, vomiting, GI bleeding, fever, weight loss

common treatments of gastritis

elimination of causative/exacerbating factors, eradication

etiology of gastric outlet obstruction

malignancies of digestive organs, surgical & interventional induced obstructions, metastatic cancer

pathogenesis of gastric outlet obstruction

mechanical obstruction in the pyloric region

manifestations of gastric outlet obstruction

abd pain/distention/bloating, vomiting, dehydration, weight loss, possibly early satiety & nausea

treatment of benign gastric outlet obstruction

nasogastric tube suction, medications to suppress gastric acid production, IV fluid & electrolyte replacement, nutritional supplementation, trial liquid diet, endoscopic balloon dilation or surgery

treatment of malignant gastric outlet obstruction

based on underlying cause; may include stenting, chemotherapy, endoscopic balloon dilation or surgery

treatment of gastric outlet obstruction in advanced cancers

palliative procedures may be preferred

stomach cancer risk factors

H. pylori infection, cigarette smoking, high alcohol ingestion, excessive dietary salt, inadequate fruit & vegetable consumption, pernicious anemia, high nitrate diet

pathogenesis of stomach cancer

tumors or neoplasms in the stomach arise from gastric mucosa

most common stomach cancer

adenocarcinoma (about 85% of case)

what are clinical manifestations of stomach cancer known as

alarm features

most common clinical manifestations of stomach cancer

weight loss & abdominal pain

other clinical manifestations of stomach cancer

dysphagia, nausea, early satiety, occult GI bleeding, palpable abd mass

stomach cancer treatment

depends on staging, endoscopic resection, radiation, chemotherapy, and/or surgical resection

absorption in lower GIT

chyme enters small bowel via duodenum

what is primarily absorbed in the small bowel

nutrients & vitamins, electrolytes, water

what can impaired motility cause?

malabsorption, malnutrition, dehydration

inflammatory bowel disease (IBD)

chronic inflammatory disorder involving GIT

two major IBD disorders

ulcerative colitis (UC) & Crohn disease (CD)

ulcerative colitis (UC)

chronic inflammatory condition limited to mucosal layers of colon and characterized by relapsing & remitting episodes of inflammation; develops as a continuous lesion

Crohn disease (CD)

chronic inflammatory condition that may involve any portion of GIT and is characterized by transmural inflammation of the bowel; most commonly affects ileum & proximal colon, lesions are not always continuous (skip lesions)

manifestations of IBD (including UC & CD)

active: fever, loss of appetite, weight loss, fatigue, night sweats

remission: symptoms may decrease & even disappear

etiology of UC & CD

not completely understood; appears to involve environmental factors, microbial imbalance in the gut, genetic susceptibility, & inappropriate immune response

pathogenesis of UC

inflammation of mucosal & submucosal layers of colon, continuous lesion of inflammation may extend into the proximal colon or may affect the whole colon (pancolitis), bowel changes include epithelial damage, inflammation, crypt abscesses, loss of goblet cells

manifestations of UC

bloody and/or mucoid, diarrhea, dehydration, anemia, crampy abd pain, pain w/ defecation, tenesmus; involvement of rectum may lead to constipation

tenesmus

sense of urgency and a feeling of incomplete bowel evacuation

pathogenesis of CD

inflammation & destruction of the bowel

manifestations of CD

nausea, vomiting, diarrhea w/ or w/o blood, abd pain, pain w/ defecation due to anorectal fissures

complications of CD

bowel strictures, obstructions, perforations in the bowel & intra-abd abscesses

treatment guidelines for IBD

optimize quality of life by treating acute processes, induce & maintain remission, decrease use of corticosteroids, wholesome nutrition & healthy lifestyle habits, anti-inflammatory agents, immunosuppressants, anti-tumor necrosis factor agents, antibiotics, probiotics, surgery if indicated

appendicitis etiology

not fully understood, believed to be due to appendiceal obstruction

pathogenesis of appendicitis

obstruction is thought to lead to bacterial overgrowth & luminal distention, increased intraluminal pressure and/or excessive inflammation can inhibit blood flow causing vascular compromise to affected tissue, appendix may become gangrenous & can rupture

manifestations of appendicitis

cramping abd pain, tenderness w/ palpation of the RLQ, nausea or vomiting, increased WBC, low-grade fever

appendicitis treatment

gold standard is laparoscopic surgery

etiology of bowel obstruction

75% due to adhesions; other causes are hernia, adhesion neoplasm/tumor, gallstone ileus, intussusception, volvulus (small intestine twists)

pathogenesis of bowel obstruction

intestinal tract blockage develops due to various etiologies, up to 80% can be small bowel obstructions, obstruction can be partial or complete

complications of bowel obstruction

strangulation & bowel necrosis; may lead to bowel perforation, sepsis, & death

bowel obstruction manifestations

abd pain, nausea, vomiting, abd distention, inability to satisfactorily pass gas or stool, hyperactive high pitched bowel sounds

when will bowel sounds be absent (in bowel obstruction)

if ileus develops

treatment of bowel obstruction

gastric decompression, IV fluids, serial physical & serum tests, surgery if other methods fail