strointestinal disorders
includes GERD, peptic ulcer disease, duodenal ulcer, nausea, emesis, IBS, diarrhea,
constipation.
preepithelial layer
layer of stomach that is composed of mucus, bicarbonate, and surface active
phospholipids.
epithelial layer
layer of stomach that has cellular resistance, restitution, growth factors, prostaglandins,
and cell proliferation. Secretion of hydrogen ions.
subepithelial layer
layer of stomach that consists of blood flow and leukocytes.
chief cell
cell in gastric gland that secretes pepsinogen. Stimulated by Epi and NE, ACh, gastrin,
CCK, VIP, and secretin.
parietal cell
cell in gastric gland that secretes HCl, which converts pepsinogen to pepsin. Stimulated
from variety of sources include ACh (vagus nerve), histamine (ECL cell), gastrin (G cell).
This release is inhibited by somatostatin (D cell).
gastric mucosal barrier
surface mucosa cells here secrete thick, alkaline-rich mucus that protects epithelium of
stomach and duodenum from harsh acid conditions of the lumen. Cells here are
stimulated by mechanical (eating food) and chemical irritation and parasympathetic
inputs. This can be damaged by bacterial and viral infection, certain drugs, and aspirin.
gastroesophageal reflux disease (GERD)
backflow of stomach acid into esophagus. Esophagus isn't equipped to handle stomach
acid leading to scarring. Usual symptom is heartburn. More severe symptoms include
difficulty swallowing and chest pain. May cause sore throat if acid gets there.
Complications include esophageal erosions, esophageal ulcer, narrowing of the
esophagus (stricture). In some patients, Barrett's epithelium may replace damaged layer
and can lead to cancer. Caused by food (fatty food, alcohol, caffeine), smoking, obesity,
and pregnancy. Usually chronic relapsing course.
peptic ulcer disease (PUD)
when the acid in the stomach creates pits or erosions. Malignant when it is excessive
and there is overstimulation of the parietal cells. Benign is when normal gastric acid
production occurs but the mucosal barrier is unusually weak. Malignant is when
excessive secretion of gastric acid overwhelms the mucosal barrier. Usually caused by
helicobacter pylori bacteria or NSAIDs.
treatment of heartburn, GERD, and PUD
includes antacids, H2 receptor blockers, mucosal protective agents, proton pump
inhibitors, anticholinergics, prostaglandin analogs, and anti-microbial agents.
antacids
treatment option of heartburn, GERD, and PUD. Includes systemic and nonsystemic.
These change the pH of the blood and what's in the GI tract.
systemic antacid
includes sodium bicarbonate. This can be given IV to change the blood pH.
nonsystemic antacid
includes aluminum hydroxide and magnesium hydroxide combinations. Contraindicated
in patients with impaired renal function. Magnesium in this can sometimes cause
diarrhea. This doesn't cross into the blood so changes pH in GI tract. Also includes
calcium carbonate, or Tums. The calcium in this can cause constipation.
histamine H2 receptor blockers
treatment option of heartburn, GERD, and PUD. Inhibit the secretion of gastric acid
through competitive inhibition of histamine H2 receptors (which normally stimulate
parietal cells to release acid). Prevention and treatment of PUD, esophagitis, GI
bleeding, stress ulcers, and Zollinger-Ellison syndrome. May alter the effects of other
drugs through interactions with CYP450 (especially cimetidine). Very few side effects
(except for cimetidine which inhibits the metabolism of estrogen). Suppresses 24 hour
gastric secretion by 70%. Include cimetidine, famotidine, ranitidine, and nizatidine.
proton pump inhibitors
treatment option of heartburn, GERD, and PUD. Strong inhibitors of gastric acid
secretion through irreversible inhibition of proton pump, preventing "pumping" or release
of gastric acid (24 hour action). Indicated in PUD, gastritis, GERD, and Zollinger-Ellison
syndrome. Faster relief and healing than H2 receptor blockers. Decreases acid
secretion by up to 95% for up to 48 hours. 4-8 week course of treatment.
Contraindicated in patients taking clopidrogel since these can reduce it's efficacy.
Includes omeprazole, esomeprazole, rebeprazole, lansoprazole, pantoprazole.
Lansoprazole may cause higher incidence of mortality.
prostaglandins
treatment option of heartburn, GERD, and PUD. Includes misoprostol. These are for
treatment of NSAID induced injury - since COX activity is inhibited by the NSAIDS,
these drugs help to increase COX activity. Side effects include diarrhea, pain, and
cramps (30%). Do not give to women of childbearing years unless reliable method of
birth control can be documented. Can cause birth defects and premature birth.
anticholinergics (M1 antagonists)
treatment option of heartburn, GERD, and PUD. Includes pirenzipine. Blocks gastric
acid secretions. About as effective as H2 blockers. Rarely used, primarily as adjunct
therapy. Side effects include anorexia, blurry vision, constipation, dry mouth, and
sedation. Only used if the patient has an allergy to another drug.
sucralfate (carafate)
mucosal protective agent. Can be used to prevent and treat PUD. Requires an acid pH
to activate. Forms sticky polymer in acidic environment and adheres to ulcer site,
forming a barrier. May bind with other drugs and interfere with absorption. Give
approximately 2 hours before or after other drugs. Take on empty stomach before
meals. Can interfere with drug and nutrient absorption.
chelated bismuth
mucosal protective agent. Protects ulcer crater and allows healing. Some activity
against H. pylori. Should not be used repeatedly of for more than 2 months at a time.
Can cause black stools and constipation. No antacid properties.
anti-helicobacter pylori therapy
includes combinations including bismuth, clarithromycin, amoxicillin, tetracycline, and
metronidazone. Basically need to disrupt bacterial cell wall and inhibit protein synthesis.
Triple therapy includes 7 day treatment (effective 80-85%) of proton pump inhibitor +
amoxicillin/tetracycline + metranidazone/clarithromycin. Quadruple therapy is the same
thing but 3 days (and as efficacious) but Bismuth is added.
inflammatory bowel disease
includes ulcerative colitis and Crohn's disease. Both are autoimmune diseases.
Treatment includes resolving acute episodes and prolonging remission. Treatment
includes aminosalicylates (mild symptoms), corticosteroids (moderate symptoms),
thiopurines (active and chronic symptoms), methotrexate (active and chronic
symptoms), cyclosporin (for active and chronic symptoms refractory to corticosteroids),
and infliximab (antibody infusion).
ulcerative colitis
diffuse mucosal inflammation limited to the colon. Can lead to bloody diarrhea, colicky
pain, urgency, and tenesmus.
Crohn's disease
patchy transmural inflammation. May affect any part of the GI tract. Can lead to
abdominal pain, diarrhea, weight loss, and intestinal obstruction. Surgical resection may
be necessary in extreme cases.
constipation
usually effectively treated with dietary modification. Only if this fails should laxatives be
used. But then again, number 1 cause of this is laxative abuse. Therapy includes
bulking agents, osmotic laxatives, stimulant drugs, and stool softeners.
laxatives
treatment for constipation; the mechanism of action for this is to increase the diameter
of the intestine (usually by increasing the size of da poop), which stimulates
mechanical/stretch receptors, which then activate reflex contraction or peristalsis and
propel the stool down.
bulk laxatives
include psyllium, bran, and methylcellulose. These are insoluble and nonabsorbable,
non digestible. Must be taken with lots of water or it will make the constipation worse!
Takes several days to work.
saline and osmotic laxatives
these are effective in 1-3 hours. Used to purge intestine in situations like surgery or
poisoning. Fluid is drawn into the bowel by osmotic force, increasing volume and
triggering peristalsis. These include nondigestible sugars and alcohols (lactulose and
prunes which have sorbital) and salts which include milk of magnesia, epsom salt,
glauber's salt, sodium phosphates (enema), and sodium citrates (enema). Also include
polyethylene glycol.
stool softeners (emollients)
include docusate sodium (surfactant and stimulant), liquid paraffin (oral solution) and
glycerin suppositories (mainly used in children).
irratant/stimulant laxatives (cathartics)
increases intestinal motility, irritate GI mucosa and pull water into the lumen. Indicated
for severe constipation where more rapid effect is required (6-8 hours). Include castor
oil, senna, bisacodyl, and lubiprostone (PGE1 derivative that stimulates chloride
channels, producing chloride rich secretions). Overnight kind of therapy.
diarrhea
caused by toxins, microorganisms (shigella, salmonella, E. coli, campylobacter, c. diff),
and antibiotic associated colitis. more than 2-3 days for treatment, can be severe in
elderly and small children. Can be caused by chronic inflammatory disease.
anti-diarrheal agents
Or, anti-motility agents. Reduce peristalsis by stimulating opioid receptors in the bowel.
Allow time for more water to be absorbed from the gut. Include morphine, codeine,
diphenoxylate, and loperamide. Contraindicated with toxic materials, microorganisms
(salmonella, E. coli), and if the diarrhea is antibiotic associated. Sometimes will be
combined with antimuscarinic like atropine to prevent overdose.
loperamide
opioid receptor agonist that is used as anti-diarrheal agent. 40-50x more potent than
morphine, has poor CNS penetration. Increases transit time and sphincter tone.
Antisecretory against cholera toxin and some E. coli toxin. Half life of 11 hours. 4 mg
dose folows by 2 mg doses (16mg/d max). Overdose leads to paralytic ileus and CNS
depression. Caution is to be taken in IBD, can lead to toxic megacolon.
clostridium difficile
major cause of diarrhea and colitis in patients exposed to antibiotics (20%). Fecal/oral
route of transmission. Usually caused by alteration of normal fecal flora, colonic
colonization of C. difficile, growth and production of toxins, and infection that can lead to
formation of colitis and toxic megacolon. Can cause permanent scarring. Treated with
discontinuation of offending antibiotic. Also metronidazole (contraindicated in patients
with liver or renal impairment) and vancomycin (contraindicated in patients with renal
impairment).
antiflatulants
used to relieve the painful symptoms associated with gas. Includes simethicone (a
detergent). This alters elasticity of mucus-coated bubbles, causing them to pass easier.
Used often but limited data regarding effectiveness. May only alleviate painful gas due
to diarrhea in combo with loperamide.
emesis
can be stimulated from seeing something repulsive (cortex), motion sickness (vestibular
apparatus), or ingesting a toxin in the stomach. The CTZ receives these inputs and
sends ACh to stimulate this. Dopamine pathways.
syrup of ipecac emetic
prepared from the root of ipecacuanha plant. Induces emesis. Side effects include
drowsiness, diarrhea, and stomach ache. Acceptable for use when there are no
contraindications, there is substantial risk of serious toxicity to the victim, there is no
alternative therapy available or effective to decrease GI absorption, there will be a delay
of greater than 1 hour before patient will arrive at medical facility, and that administration
of this will not adversely effect more definitive treatment at hospital. Not really
recommended anymore.
antiemetic therapeutics
this includes scopolamine, phenothiazines, ondansetron, and granisetron.
scopolamine
antiemetic therapeutic that is a muscarinic M1 receptor antagonist. The side effects are
dry mouth, dizziness, restlessness, dilated pupils, delirium at high doses, and allergic
reactions. Patch behind the ear is easy.
phenothiazines
antiemetic therapeutic that is histamine H1/dopamine D2 receptor antagonist. Includes
promethazine and prochlorperazine. Side effects include neuroleptic effects, blurred
vision, dry mouth, dizziness, restlessness, seizures, and tardive dyskinesia. Initially
developed as antihistamine.
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