GI Flashcards
Histamine Receptor Antagonists
MOA: selective, competetive blockade on basolateral side of parietal receptor cells - prevents stimulation of proton pump
what are some risk factors with H2RA
anti-adrogenic (gynecomastia, impotence), arrhytias, headache, dizziness, GI upset
major interactions with H2RA
caffeine (cimetidine)
St John’s Wart
PPI MOA
selective irreversible H/K?ATPase inhibition on luminal side of parietal cells.
- acid-labile: broken down in stomach acid which reduces their absorption.
- secretory activity returns 3-5 days after stopping
risk factors with PPIs
and interactions
Mg depletion, osteoporosis, c diff infections, CAP, HA, dizziness, GI
CYP - hepatic impairment
St John’s Wart and Grapefruit
Are PPIs or H2RAs better at immediate symptom relief and why?
H2RA are better for immediate relief because their onset is 30-45 minutes rather than 2-3 hours. PPIs also have a commuluative effect if they are taken multiple days in a row
What would you prescribe for GERD?
Antacids - acid buffer in lumen
H2RA - competitive antagonism of H2 receptors
PPI - Inhibit H/K/ ATPase pump
What site of action do PPIs and H2RAs have in common?
both act on the parietal cell
both inhibit proton pump (H2RA indirectly)
tachyphlaxis
rapidly diminishing response to successive doses of a drug, rendering it less effective. The effect is common with drugs acting on the nervous system
rx for gas
simethicone: siicone polymer
Alpha- galactosidase: beano
what can simethicone interact with?
thyroid medication - can decrease serum concentration
Simethicone
inert silicone polymer, de-foaming agent, reduces surface tension of gas bubbles
Alpha- galactosidase
mold-derived enzyme that cleaves oligosaccharides before reaching colonic bacteria.
A diabetic patient on medications wants a flatulene product, what would you recommend?
simethicone because
alpha-galactosidase is not recommended in diabetic patients and activated charcoal can impact absorption of medications.
Stimulant laxatives
senna (ex-lax): anthraquinone stimulates peristalsis by directly acting on mucosa nerve plexus
bisacodyl (dulcolax): irritates smooth muscle causes peristalsis
osmotic laxatives
plyethylene glycol 3350 (miralax): water retention in stool increases frequency
magnesium citrate: osmotic retention of fluid in bowel
stool softeners
docusate (colace): diocyl dosium sulfosuccinate reduces surface tension of oil water on stool and inhances incorporation of water and oil into stool
if a patient was taking senna, what else could you add for persistent constipation?
docusate stool softener
bulk laxatives
psyllium (metamucil): absorbs water in intestine and promotes peristalsis and reduces transit time
if you are a prescribing opiates, what is important to also give?
laxatives
antidiarrheal: opiate like
loperamide (immodium)
Diphnoxylate
Atropine
loperamide (immodium)
decreases GI motility acting on circular and longitudinal muscles. Reduces GI secretions
Diphnoxylate and Atropine
opiate receptro agonist inhibiting GI activity
also inhibits SLUD
what are the actions of antidiarrheal drugs?
act on smooth muscle or inhance chloride channel activity to increase fluid secrtion into intestinal lumen
lamotil and imodium have what similar mechanism of action?
decrease GI motility
pharmacology for IBD
Corticosteroids/Glucocorticoids
Aminsalicylates - most common
Immunosuppresants
Atibiotcs
MOA corticosteroids - Prednisone
modulates protein synthesis leading to reduced migration of plymophonuclear leukocytes and fibroblasts. Prevents/controls inflammation by reversing capilarry permeability
MOA Glucocorticoid: budesonide
same as prednisone
interacts with grapefruit and st johns wart
Aminosalicylates: Mesalamine MOA
modulates local chemical mediators of inflammatory response and supresses lukotriens, acts as free radical scavenger and inhibits tumor necrosis factor. Most *activity is topical, minimal absorption
Aminosalicylates: sulfasalazine MOA
prodrug of mesalamine and bond is cleaved by colonic bacteria.
- competetive inhibitor of folate
- take a away from meals
- sweat, urine, tears turns orange
where are azo drugs released?
closer to colon
Antimetabolites (immunosuppresants)
azathioprine:
- inhibits most rapidly proliferating cells in body.
- purine analog/antimetabolite
- inhibits purine synthesis and DNA replication, resulting in an anti-proliferative effect and induction of apoptosis of T-cells
What is the major interaction with Azathioprine?
ETOH
Monoclonal Abs: Tumor necrosis factor (TNF alpha)
Inhibits TNF alpha which is responsibe for induction of proinflammatory cytokines which activate neutrophils and eosinophils adn induce acute phase reactants
what is recommended along with TNF alpha
premedication with antihistimines to preventand manage infusion related reactions
Anti-TNF alpha: Infliximab
chimeric IgGk that binds both free and membrane bound TNF a: different ab smashed together that contain zone that will attach to ag.
Anti-TNF a: Adalimumab (Humira)
human mAb (IgG1k) against TNFa more accepted in body because comes from human, not animal.
Explain cycle of inflammation that happens with IBD
- innate cells produce increased TNF a, interleukins and chemokines
- marked expansion of lamina propria with increased CD4 t cells (especially proinflammatory ones)
- These secrete increased levels of cytokines and chemokines wich results in more leukocytes
- cycle of inflammation
Rx for Nausea/Emesis
serotonin antagonists
dopamine antagonists
Serotonin Antagonists
Ondansetron: selectively antagonizes serotonin receptors
- hepatic metabolism
risk factors with Ondansetron
QT prolongation, HA, fatigue, malaise, diarrhea
interacts with grapefruite and St johns wart
If Serotonin antaginsts prevent nausea, what would SSRIs do
induce nausea
as well as decrease depression/anxiety
Dopamine antagonists
promethazine
metoclopramide
promethazine
blocks postsynaptic dopaminergic receptors in brain and depresses release of hormones (hypothalamic and hypophyseal)
- anti-muscarinic and anti histimine activity
- hepatic metabolism/CYP
Metoclopramide
antagonizes dopamine receptors and blocks serotonin receptors in CNS
- prokinetic: enhanced motility and increased gastric emptying
what receptors does metoclopramide effect?
D2
Seratonin
where is the emetic center
medulla
