• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/60

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

60 Cards in this Set

  • Front
  • Back
classes of drugs to prevent and treat vomiting?
anticholinergic
antidopaminergic
5-HT3 antagonists
H1 antihistamines
cannabinoids
corticosteroids
benzodiazepines
stimuli that trigger vomiting?
stimulation of sensory nerve endings in gi tract and pharynx;
endogenous emetic substances produces as result of radiation damage or disease;
disturbance of vestibular apparatus;
stimuli to the sensory nerves of the heart and viscera;
endocrine factors;
rise in intracranial pressure;
nauseating smells;
repulsive sights;
disgusting experience
chemoreceptor trigger zone?
area postrema on floor of IV ventricle;
sensitive to chemical stimuli due to poorly developed bbb
vomiting center?
dorsolateral border of reticular formation of medulla;
consists of N. tractus solitarius, parvicellular reticular formation, and visceral and somatic motor nuclei coordinating the act of vomiting;
integrates the emetic response
where does VC receive excitatory inputs from?
vagal sensory from gi
labyrinths via vestibular nuclei
higher cortex centers
CTZ
intracranial pressure receptors
drugs that can cause emesis via action on CTZ?
apomorphine
L-dopa
cardiac glycosides
emetine
estrogens
ergot alkaloids
opiates
cancer chemotherapeutic agents
mechanism of drugs causing emesis by acting locally on gi?
activate enterochromaffin cells in mucosa --> release of 5-HT --> stimulation of 5-HT3 receptors --> excite N. tractus solitarius --> activates VC;
aka 'local irritants'
drugs causing emesis via action locally in gi?
ipecac
copper sulfate
zinc salts
antimony salts
when might drugs causing emesis be useful?
ingesting harmful substance;
patient must be conscious;
must be within certain time so substance has not passed the stomach
most highly emetogenic agent?
cisplatin
hyoscine?
M antagonist
prevention of motion sickness
ineffective against substances acting in CTZ
H1 antihistamines?
cinnarizine
cyclizine
promethazine
use of antihistamines?
motion sickness
ineffective against substances acting in CTZ
why are newer antihistamines not useful in prevention of emesis?
do not cross the bbb
antidopaminergics?
metoclopramide
domperidone
metoclopramide?
D2 blocker at CTZ
psychotic side effects
domperidone?
D2 blocker at CTZ
does not cross bbb so no cns side effects
preferred vs metoclopramide
benzodiazepines use as antiemetics?
anticipatory n/v before cancer therapy
useful for vestibular disorders
PONV?
post operative nausea and vomiting
corticosteroids use as antiemetics?
prevention of PONV
reportedly as effective as ondansetron
nabilone?
synthetic cannabinoid derivative
not well accepted
5-HT3 antagonists?
ondansetron
granisetron
5-HT3 antagonist use?
prevention of n/v due to cancer chemotherapy and causes little toxicity;
given in combo with dexamethasone (synergistic);
widely used for PONV but less effective;
sublingual preps available
complications of peptic disease?
hemorrhage
obstruction
perforation
factors that influence peptic ulcer disease?
lifestyle
smoking
alcohol
stress
how does smoking affect peptic ulcer disease?
slows healing of existing ulcers
increased chances of getting an ulcer
how does caffeine affect ulcers?
stimulate acid secretion in stomach, aggravating pain of existing ulcer
how does stress affect ulcers?
emotional stress increases pain
physical stress increases risk of developing ulcers
ulcer presentation?
gnawing or burning pain in epigastrium
n/v
loss of appetite
bleeding
anemia (due to prolonged bleeding)
gold standard treatment for peptic ulcer disease?
H2 blockers
H2 blockers characteristics?
competitive antagonist to block acid release;
promote healing;
useful for hypersecretory states (zollinger-ellison);
prophylaxis for at risk patients;
useful for reflux esophagitis, bile reflux gastritis, prevention of aspiration pneumonitis
cimetidine?
H2 blocker
reduces acid secretion by 70% for 4-5 hrs so patient compliance can be problematic as taking high dose often
side effects of cimetidine?
gi upset
headache
confusion
gynecomastia (androgen receptor antagonist)
increased prolactin release
impotence
inhibitor of microsomal enzymes
decreased bioavailability with antacids
ranitidine?
H2 blocker
more potent than cimetidine
none of side effects of cimetidine
does not bind to testosterone receptors
low incidence of headache and rash
H2 blockers?
cimetidine
ranitidine
nizatidine
famotidine
roxatidine
effect of anticholinergics?
decreased ACh stimulated secretion and motility;
rare systemic anticholinergic effects;
rarely used alone
antacids characteristics?
weak bases to partially neutralize gastric acid, reduce pain associated with ulcers, and promote healing;
danger of over-neutralizing resulting in alkalosis
calcium carbonate?
antacid
overuse can lead to hypercalcemia
contraindicated with renal disease
rebound acid production due to stimulated gastrin release
magnesium hydroxide?
antacid
can cause diarrhea and lead to hypotension
aluminum hydroxide?
antacid
can cause constipation
binds bile acids
stimulates mucus secretion
which antacid stimulates mucus secretion?
aluminum hydroxide
sodium bicarbonate?
antacid
not for long term therapy
contraindicated with HTN due to Na content
drug interactions with antacids?
altered bioavailability of drugs due to change in pH;
chelation of drugs to prevent absorption (digoxin and tetracyclines)
omeprazole?
proton pump inhibitor
inhibits parietal cell proton pump by covalent modification
side effect of omeprazole?
hypertrophy of gastrin producing cells;
inhibits microsomal enzymes;
tumors in animals at high doses
proton pump inhibitors?
omeprazole
urogastrone
enterogastrone
sulcralfate?
protective agent;
complex polysaccharide complexed with aluminum hydroxide;
crosslinks in gastric pH with affinity for exposed proteins in peptic ulcers
sulcralfate side effect?
nausea
constipation
requires acidic gastric pH to be activated?
sulcralfate
complications of untreated GERD?
severe chest pain
esophageal stricture
bleeding
barrett's esophagus
important features of h. pylori?
potent producer of urease
2/3 world infected
unknown transmission
unknown reason for symptomatic presentations
most never suffer symptoms
associate with gastric cancer
confirmation of h. pylori presence?
IgG
breath test
upper esophgogastroduodenal endoscopy
agents that increase fecal bulk?
psyllium
carboxymethylcellulose
dietary fiber
polycarbophil
calcium polycarbophil
salt containing osmotic agents?
magnesium sulfate
magnesium citrate
magnesium hydroxide
sodium phosphates
mineral waters
use of salt containing osmotic agents?
bowel evacuation prior to surgery
elimination of parasites after therapy
non salt containing osmotic agents?
glycerine
lactulose
polyethylene glycol
irritant agents
wetting agents
coating agents
antidiarrheals?
adsorbents
glucocorticoids
bismuth subsalicylate
loperamide
anticholinergics
adsorbents?
kaolin
pectin (donnagel)
dietary fiber
use of opioid preparations?
high doses to control refractory diarrhea
opioid preparations?
opium tincture
camphorated opium tincture
codeine
diphenoxylate