Professional Documents
Culture Documents
GI A&P
GI Disorders
Effects of gastric suctioning on Acid-Base balance and Fluid & Electrolytes: hypokalemia,
metabolic alkalosis from Na, Cl, and H+ ion loss
Abdominal Pain:
o Parietal: from the parietal peritoneum (lines abdominal walls), sharp- localized and intense,
tends to be on 1 side of the other due to nervous system innervation
o Visceral: pain from abdominal organ, radiates, diffuse, vague since nerve endings sparse
Referred: visceral pain felt at distant location, well localized there, areas share same
pathway
Diarrhea/Constipation
o Constipation Dietary recommendations: drink more fluids, increase fiber intake
o Diarrhea Dietary Recommendations: restoration of fluid and electrolyte balance
Anorexia: lack of desire to eat despite physiologic stimuli that would normally produce hunger
o Causes: side effects of drugs and disorder of other organ systems including cancer, heart
disease, and renal disease
o S&S: nausea, abdominal pain, diarrhea, psychologic stress
Dysphagia: difficulty swallowing
o Causes: mechanical obstruction of esophagus or functional disorder that impairs
esophageal motility via neural or muscular disorders
o S&S: distention and spasm of esophageal muscles during eating or dirnking may cause mild
or severe stabbing pain at level of obstruction, discomfort 2-4 seconds after swallowingupper esophageal obstruction, 10-15 secs after swallowing- lower esophagus obstruction,
regurgitation of undigested food, unpleasant taste sensation, vomiting, aspiration, weight
loss, aspiration could lead to pneumonia
Hematochezia: bloody stools, bright red stools
o Causes: frank bleeding from rectum or lower GI tract
o S&S: fresh, bright red blood passed from rectum
Hematemesis: bloody vomitus
Hiatal hernia: protrusion of the upper part of the stomach through the diaphragm (esophageal
hiatus) into the thorax
o Causes:
Sliding/direct: congenitally short esophagus, trauma, weakening of the diaphragmatic
muscles at GE junction, slides into hernia while lying down, stomach slides back into
abdomen when standing, exacerbated by factors that increase intra-abdominal
pressure
Paraesophageal/indirect: through not norm diaphragm hole, GE junction not affected
and remains below the diaphragm, NO REFLUX
o S&S: GER, dysphagia, heartburn, epigastric pain, regurgitation and substernal discomfort
after eating are common
GERD: reflux of gastric contents (chyme- acid and pepsin) into esophagus
o Causes: incompetent lower esophageal sphincter- cause unknown, irritant effects of
refluxate, abnormal esophageal clearance ,hiatal hernia present, delayed gastric emptying
potentiates (gastroparesis, partial gastric outlet obstruction)
o S&S: heartburn, dysphagia, chronic cough, asthma, upper abdominal pain within 1 hr of
eating, if chronic and severe-strictures
Intestinal/Bowel Obstruction: something that prevents stools from moving through the
intestines
o Causes: hernia, mesenteric occlusion, torsion/volvulus, intusscesception, diverticulosis,
tumor/neoplasm, adhesions, paralytic ileus
Paralytic Ileus: from surgery, peritonitis, hypokalemia, ischemic bowel, spinal
trauma, or drugs
o S&S: colicky abdominal pain, vomiting, diarrhea, abdominal distention, bowel sounds,
dehydration, hypotension- shock (decreased venous return, intestinal edema, large amt of
peritoneal fluid sequestered, bacterial translocation-sepsis)
Ulcers: break in protective mucosal lining of lower esophagus, stomach, or duodenum, exposes
muscle layers to damage from autodigestion from gastric acids
o Duodenal Ulcers: caused by hypersecretion of acid and pepsin, H pylori, or NSAIDs, most
common
S&S: epigastric pain- visceral or referred, chronic, intermittent, 2-3 hrs after eating,
empty stomach, may occur at night then gone in am, pain-food-relief pattern,
remission- exacerbation, hemorrhage may be first sx, perforation
o Gastric Ulcers: NSAIDs, H pylori, increased mucosa permeability to H+ ions, often preceded
by chronic gastritis since reduces mucosal barrier
S&S: pain immediately after eating, chronic (no remissions/exacerbations), more
N&V and weight loss
o Stress Ulcers: acute form of peptic ulcer caused by severe stress, decreased mucosal
blood flow major factor
Ischemic ulcer: within hrs of trauma, critical illness
Cushing Ulcer: severe head injury or brain surgery causes overstimulation of vagus
nerve= increased acid production
o What blood in the vomit or stool can indicate about ulcer location (also shade of
blood: bright red vs. dark or brown):
Upper GI bleed: esophagus- bright red blood, stomach- coffee grounds (bc interacts
with H in stomach which oxidizes the iron in hemoglobin), duodenum
Lower GI bleed: jejunum on, hemorrhoids- bright red blood, farther up- occult, black,
tarry
Gastritis: inflammation of gastric mucosa, acute or chronic, affects fundus and/or antrum
o Causes:
Acute Gastritis: alcohol, NSAIDs, Chemicals/toxins [urea]
Chronic Fundal Gastritis-Type A: most severe, have antibodies to parietal, gastric
cells, and intrinsic factor (so cant maintain mucosal lining), associated with other
auto-immune diseases, gastric atrophy, loss of chief and parietal cells, pernicious
anemia, risk for gastric cancer
o S&S: bleeding, anorexia, N&V, fullness, epigastric pain
Pancreatitis: norm secretes trypsins/proteolytic enzymes to break down proteins into duodenum
in inactive form but leads to autodigestion
o Causes: activation of trypsins while still in pancreas- biliary obstruction like gallstones,
activated proteases (trypsins), autodigestion
Alcohol: causes sphincter of Odi to swell which obstructs pancreatic enzyme release
into the duodenum
o S&S: pain, fever, N&V, abdominal distention, 3rd spacing of fluid-peritoneal edema, acute
renal failure (protein breakdowns go into circulation and clog glomerulus), increased WBCneutrophils, increased amylase and lipase in bloodstream
Chronic pancreatitis: chronic pain, pancreatic enzyme deficiency, glucose control
issues
Inflammatory Bowel Disease: ulcerative colitis and crohns disease
o Compare/Contrast Ulcerative Colitis versus Crohns disease
o Ulcerative Colitis: chronic inflammatory disease usually of rectum and sigmoid colon (but
can affect entire large bowel) causing ulcer formation
Cause: anticolon antibodies T lymphocyte cytotoxic reaction, genetic, infectious, or
unknown
S&S: ulcerations, skip lesions, pseudopolyps, cramping abdominal pain, bloody
diarrhea, remissions and exacerbations, increased colon cancer risk, severe- fever,
anemia, weight loss, 10-20 stools/day
o Crohns Disease: AKA regional enteritis/granulomatous colitic
Cause: inflammatory process by activated neutrophils and macrophages- immune,
genetic, infectious, unknown, stress may exacerbate but doesnt cause, no increased
colon cancer risk
Affects ascending and transverse colon
S&S: thickening of wall, cobble stoning, diarrhea, fever, abdominal pain, weight loss
Cholelithiasis: gallstones
o Causes: chronically elevated rate of bilirubin excretion (binds with calcium, associated with
chronic liver disease), supersaturated cholesterol bile- crystal aggregation
o S&S: RUQ pain that radiates to scapular and associated with N&V secondary to/stimulated
by fatty meals
Liver Disorders: Definitions, Causes, Clinical Manifestations, lab changes/assessment
findings
Cirrhosis: irreversible inflammatory disease in liver that disrupts liver structure and
function
Stages:
Fatty liver (reversible)
Alcoholic hepatitis (scar tissue remains but can recover, hepatocytes necrosis)
Cirrhosis (alcohol changed to toxin that irreversible damage all liver functions,
CT growth, and nodules)
Types:
Alcoholic (hepatocyte damage)
Biliary (canaliculi or bile duct damage)
o Primary: viral or autoimmune anti-mitochondrial antibodies [transplant]
o Secondary: obstruction of bile ducts
S&S: damage to all cell processes, altered metabolism of nutrients, liver
inflammation- pain and fever, N&V, anorexia, fatigue, liver fibrosis and scarring lead
to portal hypertension, ascites, edema, splenomegaly (anemia and
thrombocytopenia), and varices (esophageal, hemorrhoids, caput medusa- abdominal
veins superficial), fatty infiltrates, liver necrosis (hyperbilirubinemia, jaundice, clay
colored stools, bleeding, dark urine, hypoglycermia, ascites and edema,
gynecomastia, loss of body hair, menstrual dysfunction, palmar erythema, increased
ADH and aldosterone to try to compensate for hypovolemia)
Liver Failure
Most common causes: acetaminophen toxicity or overdose [alcohol gets rid of the
liver enzyme (glucothionate) thats needed to break down the toxic metabolite made
from Tylenol metabolism]
GI Disorders in Children
GI Pharmacology
Hepatic drug metabolizing enzymes and how they affect drug inactivation: enzymes can
inactivate
Acetaminophen and liver toxicity: CYP2E1- NAPQI- protein adducts, lipid peroxidation- liver
failure, hepatocyte necrosis
Drugs for ulcer disease (reduce acids/neutralize acids) and how they should be taken
together