cellular protection of the stomach
- mucous and bicarb secretion
- prostaglandin E (inhibits acid, stimulates bicarb and mucus, maintains blood flow to mucosa)
- alkaline bile and pancreatic juices
cell destruction of the stomachy
gastric acid and pepsin (proteolytic enzyme)
cholinergic stimulation
rest and digest
- acetlycholine is a cholinergic neurotransmitter
- stimulates muscarinic receptors
- increases GI motility and digestion
- in the GI tract, acetylcholine stimulates the vagus nerve to release histamine via histamine type 2 receptors in parietal cells to increase HCL production
gastritis
inflammation of the gastric mucosa which may be due to alcohol, NSAIDS, and aspirin
PUD
peptic ulcer disease occurs when cell destructive properties are greater than cell-protective qualities
- chronic NSAID use inhibits prostaglandins
- stress ulcers are seen in patients with severe illnesses like trauma, sepsis, or acute respiratory distress syndrome
- ZES
- H. pylori
ZES
Zollinger-Ellison syndrome is a rare gastric condition in which there is a gastrin secreting tumor in the duodenum or pancreas leading to a severe peptic ulcer or erosive esophagitis. s/s: diarrhea, abdominal pain, and reoccurring ulcers
-usually ages 20-50 with a greater occurrence in males than females
Helicobacter pylori infection
an infection of a gram-negative bacteria
- found in gastric ulcers, duodenal rulers, and gastric cancers
- secretes urease to buffer the acidity of its own environment. it produces continuous inflammation that leads to atrophy and ulcer. increases the ph of the environment
ulcerogenic factors
- gastric acid
- H. pylori
- pepsin
- NSAIDS
gastric ulcers
more common in the 60s and 70s
s/s: asymptomatic bleeding (the first symptom is low h/h), bloating, indigestion, heartburn, nausea, dull achy pain right after eating but not right before
duodenal ulcer
can be with any age but there is an increased risk with cigarette smoking
s/s: heartburn, burning, severe stomach pain which is worse when the stomach is empty, at night, or right before food
GERD
reflux of stomach acid or bile due to the incompetent lower esophageal sphincter. More common in pregnancy and those greater than 40.
- aggravated by foods that are fatty and chocolates, fluids such as alcohol and caffeinated beverages, medications such as beta-blockers, beta-adrenergic, nitrates, gastric distension, smoking, recumbency, and H. Pylori.
- causes painful swallowing usually due to esophagitis or esophageal ulcer
- when the lining thickens and becomes reddened its called barret’s esophagus
what are the four categories of medications used for PUD and GERD
- antacids
- histamine 2 receptor blockers
- proton pump inhibitors
- others
post marketing recall of ranitidine drugs (Zantac)
the FDA withdrew all rx and OTC drugs of this time because a contaminant known as NDMA was found int he medications. it was found that the impurity in these drugs increase over time and when stored at higher than room temp. it is a potential human carcinogen
H. Pylori eradication
quadruple therapy is used(with bismuth)ex: PPI + bismuth substrate + tetracycline + metronidazole (an antifungal)
triple therapy: PPI + clarithromycin + amoxicillin
peptobismol
can turn the stool gray and should not be given to children with viral illness or fever because it contains salicylates
Irritable bowel syndrome
cause: unknown
the clinical diagnosis is based on the frequency and intensity of symptoms: recurrent abdominal pain for more than 3 days and month for more than 3 months as well as changes in bowel movements(constipation and diarrhea or alternation)
-treated with cognitive behavioral therapy and anti-anxiety medication
-symptomatic treatment for constipation or diarrhea
inflammatory bowel disease
- there are genetic risk factors
- it is the chronic inflammation of the bowel
- there are 2 types: ulcerative colitis (continuous inflammation along the large intestine) and Crohn’s disease ( spotty inflammation anywhere from the mouth to the anus)
- treated with anti-inflammatory medications, steroids, and immunomodulators (TNF- alpha inhibitors). TNF is a cytokine for inflammation
- there is also the symptomatic treatment of constipation and diarrhea.
ulcerative colitis
ages 15-35 and 60-80
- 2% have a family history
- risk factors: high fat diet
- begins in the rectum and may process backward to the sigmoid colon but it confided the large intestine. mucosal and submucosal damage may be given a steroid enema.
crohn’s disease
ages 15-35
- 10% have a family history
- risk factors: smoking, high fat diet, low vitamin D-discontinuous pattern of lesions in the small intestine, colon, mouth, and esophagus
- transmucosal damage (to the muscle layer) increases the risk for abscesses, fistulas, and peritonitis.
agents used for constipation
laxatives, cathartics, and others
age related medication concerns
- changes in pharmacokinetics and pharmacodynamics
- polypharmacy
- anticholinergic burden
- high alert medicines
- increased risk for adverse drug interaction
geriatric absorption
- CHF may result in reduced blood flow to the GI tract
- achlorhydria (absence of hydrochloric acid in the gastric secretions) may change absorption of some drugs
geriatric distribution
- decrease in the total % of body water. this increases plasma concentration for lithium, digoxin and increases the risk for dehydration with diuretic therapy
- increase fat content: lean muscle mass ratio. increases the volume of distribution for lipophilic drugs such as diazepam, resulting in markedly prolonged 1/2 life.
geriatrics metabolism
- decrease in phase I metabolism leads to a prolonged half-life for some medications.
- decreases in first-pass metabolism leads to increase the serum concentration of oral nitrates, beta-blockers, calcium channel blockers, and estrogens
