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disorders involving alterations in the integrity of the gastrointestinal tract wall
gastritis
gastroenteritis
peptic ulcer disease
gastritis
inflammation of the stomach lining
acute gastritis
caused by
ingestion of irritating substances (alcohol; aspirin; tobacco; NSAIDs)
infections (viral; bacterial)
autoimmune diseases
chronic (superficial) gastritis
caused by Heliocobacter pylori
mode of transmission of H. pylori
person to person (primary)
fecal-oral route
reservoir in water sources
clinical manifestations of gastritis
asymptomatic
anorexia
nausea/vomiting
postprandial (post eating) discomfort
hematemesis (vomiting up blood)
treatment for gastritis
remove offending agent
manage & treat causative infection
complications of gastritis
peptic ulcer disease
atrophic gastritis
gastric adenocarcinoma
mucosa-associated lymphoid tissue lymphoma
decreased acid & intrinsic factor (= pernicious anemia)
gastroenteritis
inflammation of stomach & small intestine (usually resolves on its own)
acute gastroenteritis
caused by:
direct infection of GI tract lining by pathogenic bacteria
bacterial toxin
imbalance in normal bacterial flora of GI tract
chronic gastroenteritis
usually the result of another (inflammatory) GI disorder (ex: Crohn’s disease)
clinical manifestation of (acute) gastroenteritis
(secretory) diarrhea
abdominal discomfort & pain
nausea
vomiting
fever
malaise
treatment for gastroenteritis
replace fluid & electrolytes (especially elderly & children) ex: oral rehydration solution or gatorade (SOLELY WATER = WORSE)
peptic ulcer disease (PUD) refers to disorders of
the upper GI tract caused by action of acid & pepsin
peptic ulcer disease (PUD)
characterized by injury to the mucosa of the esophagus, stomach or duodenum
may range from slight mucosal injury to severe ulceration
complications of peptic ulcer disease
perforation; bleeding
gastric PUD
caused by breakdown of protective mucous layer that normally prevents diffusion of acids into gastric epithelia b/c of chronic irritations
duodenal PUD
inappropriate excess secretion of acid
increased basal activity of vagus nerve
result of increased activity of vagus nerve in duodenal PUD
stimulation of pyloric antrum cells to release gastric to act on gastric parietal cells to release HCl
high level of HCl
causes of PUD
key role: H. pylori
NSAIDs
stress (glucocorticoids)
smoking
genetics
H. pylori relation in promoting gastric & duodenal ulcer formation
thrives in acidic conditions
slows rate of ulcer healing
high rate of recurrence
clinical manifestations of gastroenteritis
epigastric burning pain
pain of gastric ulcers on empty stomach or after meal
pain of duodenal ulcer 2-3 hrs after meal which is relieved by ingesting more food
diagnosis of gastroenteritis
endoscopy (tube insertion)
testing for H. pylori (breath test, fecal Ag test, serology test)
treatment of gastroenteritis
H. pylori antibiotics; H2 antagonists; proton pump inhibitors; sucralfate; smoking cessation; avoidance of ASA & NSAIDs; stress reduction; avoiding irritating foods
inflammatory bowel disease (IBD) refers to
the two separate disease entities of UC & CD
IBD risks
onsets in childhood or young adulthood
possible 2nd peak btwn 50-80 yrs
CD: more females
UC: more males
Jewish & white
western diet
IBD is typically characterized by
exacerbations (sudden worsening) & remissions (significant reduction)
causes of IBD not confirmed but factors involved are
genetic, environmental, & immunologic
ulcerative colitis (UC)
inflammatory disease of the mucosa of the rectum & colon
UC characterization & risks
inflammation @ base of crypts of Lieberkuhn
large ulcerations in epithelium
7-10+ yrs = associated w/ increased cancer risks
hallmark clinical manifestations of UC
bloody (exudative) diarrhea
lower abdominal pain
rectal bleeding
treatment for UC
mainstay for acute: corticosteroids
antibiotics
salicylate
immunomodulating agents
cut out infected parts
crohn disease (aka regional enteritis or granulomatous colitis)
inflammation of the GI tract that extends through all layers of the intestinal wall
characterization of crohn disease
affects proximal portion of colon or terminal ileum
transmural
blockage & inflammation of lymphatic vessels
RLQ mass
clinical manifestations of CD
ulcerations
strictures
fibrosis
fistulas (abnormal openings)
constant abdominal pain
possibly bloody stool
treatment of CD
no cure
can’t cut out infected parts
smoking cessation
drugs similar to UC
enterocolitis (appendicitis)
inflammation of the vermiform appendix b/c of obstruction by lumps of feces
clinical manifestations of appendicitis
periumbilical pain
RLQ pain & tenderness (McBurney’s point)
nausea/vomiting
fever
systemic signs of inflammation
treatment for appendicitis
immediate surgical removal (best)
antibiotics w/ fluid & electrolyte replacement
localized abscesses may be managed w/ tube drainage
untreated appendicitis may result in
rupture of the appendix & subsequent peritonitis
irritable bowel syndrome (aka spastic colitis; irritable colon syndrome) [motility disorder]
alternating diarrhea & constipation
abdominal cramping
no identifiable pathologic process
mucus in stool
nausea
causes of irritable bowel syndrome
unclear but slow wave activity of bowel is increased
treatment of irritable bowel syndrome
antidiarrheal agents
antispasmodic meds
high fiber diet
support groups
therapies
malabsorption disorders of GI
failure of small intestine to absorb or normally digest one or more dietary constituents
causes of malabsorption disorders in GI system
enzyme abnormalities
infection
radiation enteritis
mucosal dysfunction (crohn, celiac, tropical sprue)
post surgical intervention (dumping, short-bowel)
clinical manifestations of malabsorption disorder
diarrhea; passage of inappropriately processed intestinal contents; abdominal pain
celiac disease (malabsorption disorder)
aka celiac sprue
characterized by intolerance of gluten (protein in wheat (products))
celiac disease leads to
inflammation & atrophy of the intestinal villi
decrease in the activity & amt of surface epithelial enzymes
malabsorption of ingested nutrients = malnutrition
treatment for celiac disease
gluten-free diet
supplemental iron, folate, B12, fat-soluble vitamins
oral corticosteroids or other agents for refractory
colon cancer
second cause of cancer deaths; risks:
increases after age 40
high-fat, low-fiber diet
polyps
chronic irritation or inflammation
hereditary
clinical manifestations of right side colon cancer
black, tarry stools
clinical manifestations of left side colon cancer
intermittent abdominal cramping & fullness
ribbon or pencil shaped stools
blood or mucus in stool
clinical manifestations of rectum colon cancer
constipation & diarrhea
sensation of rectal fullness
dull ache in rectum/sacral region
treatment for colon cancer
surgical removal; colostomy; chemotherapy, radiation or both