26 - GI Flashcards
_ occurs when stomach acid used for digestion repeatedly backs up, or refluxes, into the esophagus
gastroesophageal reflux disease - GERD
heart burn/ chest pain - symptom
can lead to tooth erosion
normal reflux is normal but not repeated episodes
low pH in stomach is okay - why?
esophagus not okay
secretion from mucous cells create a mucous layer with trapped bicarbonate that serves as a buffer
Paritetal cells - HCl acid
Mucous secreting cells - trap Bicarb
Immediate enviroment where cells are - pH is higher
Inner - lower pH
GERD is caused by _ acid reflux- the backup of stomach acid or bile into the esophagus
_ most important factor/mechanism for preventing reflux
frequent, repeated
lower esophageal sphincter (LES)
esophagus - muscular tube - LES is a specialized ring of muscle that surrounds the most distal end of esophagus where it joins the stomach
active most of the time - contracting and closing off the passage
Major causes GERD
Hiatal hernia - LES lines up with diaphragm and stomach -No longer at the level of the diaphragm - pressures no longer addictive - so reflux more easily
abnormalities in LES fxn - weak contraction, or relaxation (most common after meals), laxity of LES (opens more than should)
defects in esophageal contractions - swallows should eliminate acid (peristalsis down)
minor causes of GERD
defects in emptying of stomach
excess production of acid - least likely cause
Least likely reason for heart burn - too much acid - THE LOWER ESOPHAGEAL SPHINCTER - major cause
symptoms of GERD are treated with drugs that either _ intragastric acidity or _ gastrointestinal mucosal defense
reduce intragastric acidity or
promote gastrointestinal mucosal defense
pharm intervention for GERD symptoms
gastrin’s role
directly and indriectly
the most important pharm intervention for GERD
gastrin stims parietal cells secrete H+ via H/K ATPase
indirectly via binding onto CCK2/gastrin receptors on ECL cells in the stomach , hich then responds by releasing histamine - which stims more HCL secretion
not as important pharm for GERD but here
stims parietal cells secrete H+ via H/K ATPase
_ via parasympathetic innervation
Acetylcholine
not important
_ stims parietal cells secrete H+ via H/K ATPase
acting on H2 receptor
histamine
H2 antagonist
Doesn’t work for Ulcers (bc ulcers are usually an infection)
Affects interaction with LIDOCAINE
Inhibits metabolism of lidocaine - might make it stick around longer
pharm intervention to lower intragastric acid levels
3
gastrin -major - 2 path - most important PPI proton pump inhibitors - irreversible
histamine - major
acetylcholine - minor
Peptic Ulcer disease - results from Helicobacter Pylori infection
Can give _ and it is treated
antibiotics
drugs used to treat gastric acid and treat peptic ulcer disease
H+/K+ ATPase inhibitors - most effective
H2 antagonists
proglumide - gastrin antagonist = Less important- has effects + on opioids
antacids - neutralizes the stomach acid into water and salt - can’t reallt get above 4-5pH with these
CNS - brainstem _ center coordinates motor activities after input from the chemoreceptor trigger zone
vomiting brainstem center
drugs used to treat _ and _
receptor antagonists on the higher order areas - cerebral cortex, peripheral
D2 receptors, 5-HT3, neurokinin 1, opioid for _
mAcCH receptors, H1 receptors
vomiting and nausea
cancer chemother for d2 serotonin opi
motion sickness for H1
cannabis - acts on medulla
_ laxative
act on enteric nervous system and colonic electrolyte and fluid secretion
anthraquinone derivatives - Aloe, senna, and Cascara - occur naturally in plants - porrly absrobed
6-12 hrs when given oral
2hr rectally
chronic used leads to brown pigmentation of colon known as melanosis coli
stimulant laxatives
increase peristalsis via intestinal nerve stimulation and most important cause accumulation of water and electrolytes in lumen by altering the absorptve and secretory activity of the muscoal cells
_ laxatives
act like detergents for stool
anionic detergents reduce surface tension
allow intestinal fluids and fatty substances to penetrate the decal mass
decal softeners and lubricants
lubes like mineral oil coat the intestinal contents - preventing the abs of fecal water
_ laxatives
increase water retention, which increases intraluminal pressure and stimulates peristalsis
osmotic laxatives
saline cathartics - salts that are poorly absorbed
non-saline cathartics - glycerol, sorbitol, polyethylene glycol
_ laxatives
are not digested by absorb water and expand, increasing the bulk and moisture content of stool: peristalsis increases, and absorbed water softens the stool
bulk forming laxatives
synthetic fibers and natural plant products
polyethylene glycol moity used to treat _
does not cross BBB
opioid induced constipation
antidiarrheal agents work in 1 of 3 ways
soak up excess water - increase viscosity
anti-secretory in gut
decrease intestinal motility - give body more time to absorb luminal water)
Kaolin - an absorbent 0 complex clay like compount - not used in humans
antidiarrheal agent
_ antidiarrheal
inhibits PGs and Cl secretion (salicylate part)
also protects mucosa (coatings)
antisecretory, anti-inflammatoy, binds and absorbs bacterial and viral enteropathogens
mismuth subsalicylate
peptobismol
_ antidiarrheal
inhibits peristalsis, reduces fecal volume and loss of fluid and electrolytes
adverse effects 0 dry mouth, and pain, constipation, dizziniss/drowsiness
opioids
Diphenoxylate - antidirrheal opioid
abuse potential diminished by adding _
atropine
ioperamide - imodium - different drug - stays in GI tract non in brain
no evidence of damage or diseas
a group of symptoms treated with diet and bulking agents
anti cholinergics for cramps
no great tx’s
Irritable Bowel Syndrome - IBS
increase fiber,
