4A. GERD Management Flashcards
Erosin v. ulcer
* H1 receptor blockers > good for preventing nausea from motion sickness due to \_\_\_\_ effects * H2 blockers > used for gastric \_\_\_\_ for GI ulcers, GERD and minor heartburn
GI ulcers
• Less intense version = ____
○ Crater is in ____ membrane
○ No symptoms because the mucosa isn’t that well innervated
• When get into the ____ = ulceration
○ A lot more ____ are involved > substernal pain
§ Temporarily relieved with ____, but comes back
○ People may be asymptomatic unless have major ____
○ Life threatening when nicking an artery or vein
○ Can develop when a patient is anemic
anticholinergic hyperacidity erosion mucosa submucosa nerves antacid bleed
SOME RISK FACTORS
• Being a ____ carrier
• Smoking
• ____ (ibuprofen, naproxen, diclofenac)
• SSRIs –____ (Prozac®), paroxitene (Paxil®), ____ (Lexapro®)
• Stress - ____!!!!!
• Hot spicy foods – while may ____ an ulcer - ____!!!!!!!
• Good at surviving in high acidic environments by releasing ammonia > neutralizes acid and can survive ○ Found in people with GI cancers ○ Type of ulcers: \_\_\_\_ and duodenal • Smoking ○ Not bc of the smoke irritating the stomach ○ Hits nicotinic cholinergic receptors > \_\_\_\_ receptors > stimulates \_\_\_\_ cells, not directly on the end-organ though • NSAIDs ○ \_\_\_\_ is prescription ○ Block synthesis of \_\_\_\_ in the stomach ○ If get an ulcer and start bleeding > these drugs have \_\_\_\_ activity ○ If on drugs to 6 mo to a year on ibuprofen/diclo > 1% § With naproxen > \_\_\_\_% a year □ More selective at blocking \_\_\_\_ than it is at blocking COX-2 • SSRIs ○ Used to treat anxiety ○ SSRI and NSAID together > \_\_\_\_ effect on risk of getting a GI ulcer • Stress ○ Never been proven to cause GI ulcers • Hot spicy food ○ Never been proven to cause GI ulcers ○ May aggravate if you have one
H pylori NSAIDs fluoxitene S-citalopram NO aggravate NO
peptic
nicotinic N
parietal
diclofenac
PGs
antiplatelet
3
COX-1
additive and super-additive
Role of PGs
• Alerts of injury • PG involved in \_\_\_\_ and sensitize free-nerve endings to other mediators of \_\_\_\_ • One normal constitutive role > naturally produced in stomach > enhance amount of \_\_\_\_ ○ Slowing down effect on acid release also • Good guys in kidney > enhance \_\_\_\_ excretion bc they enhance renal blood flow
inflammation
pain
bicarb
water/sodium
Relative Risk of GI Bleed Compared to Non-Users Of Either Drug Class
* Compared to people who aren't on chronic NSAIDs > \_\_\_\_x more likely to develop an ulcer if on chronic NSAIDs * People on SSRIs > \_\_\_\_x greater risk than general population * NSAID and SSRI > \_\_\_\_x greater risk of developing a GI bleed
4
2.5
15-16
• Develop an ulcer from an NSAID > the NSAID will block ____ in a platelet (aspirin irreversibly binds COX it never lets go - the platelet will be finished bc it has no nucleus and cannot develop more COX) > can cause the ____ to continue
Serotonin also makes platelet ____; platelets suck it up from the blood stream > SSRIs block this function
COX-1
bleeding
aggregate
Treatment of NSAID Inducved GI symptoms and ulcers
ACH
- ____
- ____
H2
- ____
- ____
- ____
PG
- ____
- ____
Antacids
Antibiotics
- ____
- ____
atropine
pirenzipine
cimetidine
ranitidine
famotidine
misoprostol
diclofenac/misoprostol
clarithromycin
amoxicillin
Treatment of NSAID Induced GI Symptoms and ulcers
• + on a receptor > stimulates HCl secretion through the pump ○ Things with a + > want to use an antagonist ○ Things with a - > want to use an agonist • Atropine ○ Muscarinic cholinergic antagonist ○ Good at causing \_\_\_\_, constipation ○ Must be on 6-8 weeks > 80% of patients ulcers heal ○ Can be a problem with \_\_\_\_; or pupils dialated
• Pirenzipine ○ Not approved in the US ○ Selective \_\_\_\_ receptor blocker § More on \_\_\_\_ cells or salivary glands/heart □ If on heart > would increase HR ○ Being developed for \_\_\_\_ neuropathy
• Cimetidine, Ranitidine, Famotidine ○ -tidine ○ Can get all OTC for short-term \_\_\_\_ etc. ○ No more for \_\_\_\_ days use - not said it's used for GERD or GI ulcers § Lay person cannot diagnose if they have a GI ulcer Better \_\_\_\_ than the musc chol antagonists
xerostomia glaucoma M1 parietal peripheral heartburn 14 tolerated
Treatment of NSAID Induced GI Symptoms and Ulcers
• Misoprostol ○ \_\_\_\_ analog ○ Can be combined with NSAID ○ Not to treat GI ulcers but to \_\_\_\_ them ○ Most stays in \_\_\_\_, some can go systemic > contract smooth muscle > increased \_\_\_\_ > diarrhea; will also contract the uterus > early labor > \_\_\_\_ agent (can be combined with mithoprestone to induce abortions) • -azoles ○ More powerful and efficacious ○ \_\_\_\_ bind HCl pump > shut down the HCl pumps until new pumps are synthesized, so its action lasts far longer than its \_\_\_\_ ○ Esomeprazole § \_\_\_\_-isomer of omeprazole □ For activity > S-isomer has most beneficial activity > \_\_\_\_-dose and less \_\_\_\_ • Antibiotics ○ Dental infections > don't want to combine static and cidal; but here they'll do it > peptobismol is an \_\_\_\_, but bismith kills H pylori sometimes considered antimicrobial; sometimes metronidazole is included ○ Prevents a lot of ulcer \_\_\_\_ > most people recur; but antibiotics greatly reduces the chance of recurrence ○ Alone can help heal an ulcer § Will be on other drugs in addition; H2 blocker, etc. • Antacids ○ \_\_\_\_ hydroxize, mag hydoxide, \_\_\_\_ carbonate to neutralize the HCl ○ Would have to drink a lot of this to heal the ulcer ○ Used OTC; but can be used for breakthrough \_\_\_\_ from GI ulcers
PG prevent stomach peristalsis abortive covalently half-life S half SE antacid recurrence alumin ca++ pain
• Histamine hits all the receptors • Drugs that are therapeutically used either block the \_\_\_\_ (seasonal allergies, hay-fever, motion sickness) and \_\_\_\_ (hyperacidity gastric conditions); nothing at H3 or H4 receptor • 2 methyl histamine ○ Specific \_\_\_\_ receptor antagonist • 4 methyl histamine ○ Selective for \_\_\_\_ receptor • R-alpha methyl histamine ○ Selective for \_\_\_\_ receptor > may function as \_\_\_\_ in the brain; may be a brake on histamine release • Totally laboratory made
H1 H2 H1 H2 H3 autoreceptor
• What stimulation does
○ H1
§ ____ type reactions; sensi free nerve endings to pain; ____ to allergies; histamine subQ under skin > firey red area > raised like welt that’s white and then on the outside > pink area > triple response due to ____ inflammation
§ In brain, histamine is excitatory > why H1 blockers cause sedation; almost all have ____ effects > acetylcholine is excitatory
○ H2
§ Gastric mucosa, but also on ____ muscle
□ Diff second ____
§ Stimulation causes HCl release on ____ cells
□ Endochromaffin cells release ____
○ H3/H4
§ Not optimized for drugs
§ H4 > stimulation is by 4 methyl histamine (lab-made for H2) > ____ phases of allergic reactions/asthma
§ Brake on NT in brain > ____ receptors
allergic
diarrhea
neurogenic
anti-chol
cardiac messengers parietal histamine late H3
• Structures of H2 blockers
○ All have ____ nucleus
○ Similar to naloxon for opiod > make them bulkier > makes them ____
• What’s not on market? [LOOK IT UP]
histamine
antagonist
H-1 Receptor Blocker General Structure
* Used for \_\_\_\_, \_\_\_\_ sickness (must cross BBB) * Looks like \_\_\_\_
allergy
motion
lidocaine
Local Anesthetics
• In people with allergies to amide anesthetics (no esther anesthetic in cartridges - only good for premolar to premolar in max arch and snorted in nose) > the drug of choice is \_\_\_\_ at 1% concentration > local anesthetic activity > some \_\_\_\_ to tissues, and not available in dental \_\_\_\_
benedryl
irriation
cartridges
• Sucralfate
○ “Crater filler”
○ Used in GI ulcers > huge molecule with a lot of ____ in it > ____ is a major SE
○ Hits acid > forms purple ooze > and ____ the ulcer (similar to canker sore medicines) and protects from stomach acid
○ May enhance production of ____
○ Used for those who can’t tolerate the other ____ used
aluminum constipation protects PGs drugs
