Test 2: lecture 29 +30 GI part 2 Flashcards
sucralfate (sucramal) causes what things
- forms paste to protect gastic epithelial cells
- binds and inactivates bile salts and pepsin
- Stimulates prostaglandin synthesis
- increases Mucosal blood flow
chemical diffusion barriers:
sucralfate (sucramal)
Bismuth subsalicylate (pepto-bismol)
montmorillonite (diarsanyl)
montmorillonite (diarsanyl)
smectite clay forms protective layer in stomach
absorbs toxins, bacteria, viruses, enzymes and free radicals
used for diarrhea in dogs and cats by coating intestinal mucosa
chemical diffusion barriers:
sucralfate (sucramal)
Bismuth subsalicylate (pepto-bismol)
montmorillonite (diarsanyl)
— is a chemical diffusion barrier drug that is used to treat diarrhea in dogs
montmorillonite (diarsanyl)
smectite clay forms protective layer
absorb toxins, bacteria, viruses, enzymes and free radicals
chemical diffusion barriers:
sucralfate (sucramal)
Bismuth subsalicylate (pepto-bismol)
montmorillonite (diarsanyl)
how does bismuth subsalicylate (Pepto-Bismol) work
Bismuth:
* Coats ulcerated mucosal surfaces
* Absorbs toxins
* Mild antibacterial action (H pylori)
Salicylate (aspirin)
* Anti-inflammatory action
can’t be metabolized by cat
chemical diffusion barriers:
sucralfate (sucramal)
Bismuth subsalicylate (pepto-bismol)
montmorillonite (diarsanyl)
GI is under — control what happens when you give atropine?
PARA
blocks ACh (muscarinic) receptors
cause dry, mouth, tachycardia, decrease secretions, bronchioconstriction, large pupils ect.
pirenzepine
M1-selective blocker
but causes decreased gastric acid somehow even though there are M3 receptors on parietal cells?
H1 receptors
Located on smooth muscle and endothelium and in CNS and promotes vasodilation, bronchoconstriction, smooth muscle activation, and CNS activation
make you sleepy
H2 receptors are found where and cause what?
Located on parietal cells and regulates histamine-mediated gastric acid secretion
what are the H2 receptor blockers
cimetidine (Tagamet)
ranitidine (Zantac)
famotidine (Pepcid)
Pepcid Complete (Life cycle management)
nizatidine (Axid)
cimetidine (Tagamet)
1st gen H2 blocker
decreases gastric acid without causing sleepiness (H1 blockage)
- inhibits CYP → toxic levels of drugs from decreased metabolism
- many drug interactions
- decreases liver blood flow→ decreased clearance of propranolol and lidocaine
H2 receptor blockers:
cimetidine (Tagamet)
ranitidine (Zantac)
famotidine (Pepcid)
Pepcid Complete (Life cycle management)
nizatidine (Axid)
ranitidine (Zantac)
2nd gen H2 blocker
fewer side effects that cimetidine → less drug interactions, less CYP inhibition
longer lasting
10x more potent
H2 receptor blockers:
cimetidine (Tagamet)
ranitidine (Zantac)
famotidine (Pepcid)
Pepcid Complete (Life cycle management)
nizatidine (Axid)
famotidine (Pepcid)
3rd gen H2 receptor blocker
poor bioavilability
30x more potent than cimetidine
no CYP inhibition
increases motility of stomach
H2 receptor blockers:
cimetidine (Tagamet)
ranitidine (Zantac)
famotidine (Pepcid)
Pepcid Complete (Life cycle management)
nizatidine (Axid)
Pepcid Complete (Life cycle management) is a combo of what drugs
famotidine H2 antagonist (10 mg)
calcium carbonate antacid (800 mg) (constipation)
magnesium hydroxide antacid (165 mg) (diarrhea)
Ca and Mg balance each other out
Antacids act quickly and H2 blocker act slowly
H2 receptor blockers:
cimetidine (Tagamet)
ranitidine (Zantac)
famotidine (Pepcid)
Pepcid Complete (Life cycle management)
nizatidine (Axid)
nizatidine (Axid)
H2 receptor blocker
no CYP inhibition
excreted unchanged in urine
increases motility of stomach
H2 receptor blockers:
cimetidine (Tagamet)
ranitidine (Zantac)
famotidine (Pepcid)
Pepcid Complete (Life cycle management)
nizatidine (Axid)
which H2 blockers do not cause CYP inhibition
famotidine (pepcid)
nizatidine (axid)
H2 receptor blockers:
cimetidine (Tagamet)
ranitidine (Zantac)
famotidine (Pepcid)
Pepcid Complete (Life cycle management)
nizatidine (Axid)
— is an experimental gastrin blocker
netazepide (YF476)
CCKB receptor blocker
— are proton pump inhibitors
omeprazole (Prilosec)
lansoprazole (Prevacid)
esomeprazole (Nexium)
rabeprazole (Aciphex)
how does omeprazole (Prilosec) work
weak base that is absorbed and then protonated
will irreversibly covalently bind and inhibit proton pump inhibitors
lasts 2-3 days
proton pump inhibitors:
omeprazole (Prilosec)
lansoprazole (Prevacid)
esomeprazole (Nexium)
rabeprazole (Aciphex)
— covalently and irreversibly binds and blocks proton pumps
omeprazole (prilosec)
lasts 2-3 days
proton pump inhibitors:
omeprazole (Prilosec)
lansoprazole (Prevacid)
esomeprazole (Nexium)
rabeprazole (Aciphex)
what happens with prolonged use of omeprazole (prilosec)
Prolonged decrease in gastric acid production will cause increase in stomach pH
this can cause bacterial overgrowth → pneumonia
stomach will try to bring pH back to 4 by increasing acid → increased gastrin levels and parietal cell hyperplasia
omeprazole: irreversibly and covalently bind to proton pump
proton pump inhibitors:
omeprazole (Prilosec)
lansoprazole (Prevacid)
esomeprazole (Nexium)
rabeprazole (Aciphex)
how does prostaglandin help with gastric mucosal integrity
(1) Inhibit gastric acid secretion
(2) Stimulate bicarb secretion
(3) Stimulate mucous secretion
(4) Increase mucosal blood flow
(5) anti-inflammatory
how does misoprostol (Cytotec) work
prostaglandin
Binds to Prostaglandin receptor on parietal cell and ↓ intracellular cAMP levels leading to a ↓ in proton pump activity
(1) Increase mucous production in gastric ulcers
(2) Co-administered with NSAIDs to prevent ulceration
off label uses of misoprostol (Cytotec)
prostaglandin
Primary Indications:
* Increase mucous production in gastric ulcers
* Co-administered with NSAIDs to prevent ulceration
Off label Uses:
* induce labor by causing smooth muscle contraction
* Abortion in conjunction with RU-486
* Erectile dysfunction
the — plexus of the ENS controls gut motility
myenteric
the — plexus of the ENS controls secretions and absorption
Submucosal plexus
Promote elimination of soft formed stools
laxatives
Result in elimination of more liquid stools
cathartics
bisacodyl (Correctol, Fleet)
Stimulant Laxative
↑ water and electrolytes in colon lumen and/or stimulate intestinal muscle motility
slow onset of action (6 hrs)
docusate
Surfactant Laxative
detergent-like action that act as stool-wetting and stool softening agents allowing the efficient mixing of water
↑ intestinal water secretion to soften stools
mineral oil
soften and lubricate fecal mass make it easier to expel
Indigestible, takes 2-3 days to soften stools
Anal leakage and irritation can be a problem and chronic use can also lead to malabsorption of fat soluble vitamins and drugs
dietary fiber
bulk forming laxative
Material absorbs water and increases bulk which stimulates bowl peristalsis
Concentration of solute in the medication is GREATER than in intestinal cells
hypertonic
causes water to come toward it
Concentration of solute in the medication is THE SAME as in intestinal cells
isotonic
water does NOT move
what is osmosis
Movement of water across a semi permeable membrane from an area of low concentration of solute to an area of high concentration of solute
hypertonic laxatives such as — will cause water to —
Solutions of Mg2+, tartrate, Na+ salts, or solutions of lactulose, glycerin, sorbitol, mannitol, or polyethylene glycol (miralax)
pulls water from intestinal cells into poop
Need to be careful to avoid dehydration due to movement of water into colon
— is used to clean out colon before a colonoscopy
isotonic agent (cathartics)
colyte
no movement of water- does NOT cause dehydration
loperamide (Imodium)
opioid agonist→ antidiarrheal
acts on μ and δ opioid receptors in the myenteric plexus decreasing motility of the large intestine. This permits more time for water resorption. Also increases anal sphincter tone
muscarinic antagonist is added to prevent abuse/addiction to this drug
loperamide (Imodium)
diphenoxylate (Lomotil)
Kaolin-pectin Suspensions (Kao-Pec)
antidiarrheal
Kaolinite is a clay mineral → absorbs water in the intestine to decrease fluidity of fecal material
DOES NOT decrease diarrhea-induced water loss
Why can’t you give cat pepto bismol (bismuth subsalicylate)
salicylates (aspirin) is toxic in cats
cant break it down
what are some humorally mediated causes of emesis
Kidney failure
Liver Disease
Endotoxinemia
apomorphine
digoxin toxicity
humorally = blood bourne
what are some neurally mediated causes of emesis
- Gastrointestinal infection
- Gastrointestinal toxicity
- Gastrointestinal inflammation
- Malignancy
emetic center receives input from what 4 sources
(1) Chemotrigger zone (CRTZ)
(2) Vestibular system (ear)
(3) Peripheral sensory receptors (stomach, intestine)
(4) Higher central nervous system (CNS) centers
what happens with excessive vomiting
dehydration
low potassium, chlorine, sodium
high blood pH
chlorpromazine and acepromazine work on what receptor
- α2/1 adrenergic blocker
- Weak dopamine, histamine and cholinergic receptor blocker
Blocks vomiting reflex at Emetic Center and CRTZ
cause mild sedation from H1 block and hypotension from ⍺1 block
chlorpromazine and acepromazine will block vomiting by —
Blocks vomiting reflex at Emetic Center (⍺2)
CRTZ (D2, H1, M1)
will cause hypotension(⍺1 block) and mild sedation (H1 block)
metoclopramide (Reglan)
D2 Dopamine Antagonists
Anti-emetic action due to blockade of D2 dopamine receptors in the CRTZ
high dose can block serotonin 5-HT3 receptor
increases peristalsis in jejunum and duodenum from some muscarinic activity, D2 antagonism, and 5-HT4 receptor agonism
side effects: hyperactivity, tremors and constipation
what are some side effects of metoclopramide (reglan)
D2 Dopamine Antagonists
hyperactivity, tremors and constipation
Anti-emetic → blocks D2 dopamine receptors in the CRTZ and at high dose→ blocks serotonin 3 receptor
increases peristalsis in jejunum and duodenum) due to some muscarinic activity, D2 antagonism, and 5-HT4 receptor agonism
ondansteron (Zofran)
5-HT3 Serotonin Antagonists
Anti-emetic action due to blockade of 5-HT3 serotonin receptors in the CRTZ and in the gastrointestinal tract
Side effects include transient headache, constipation and dizziness
ondansteron (Zofran)
granisteron (Kytril)
butorphanol (Torbugesic)
Opioid Antagonists
Anti-emetic activity due to blockade of opiate receptors in the emetic center and higher
CNS centers
Sedation is a common side effect
butorphanol (Torbugesic)
Opioid Antagonists
Anti-emetic activity due to blockade of opiate receptors in the emetic center and higher
CNS centers
Sedation is a common side effect
5-HT3 Serotonin Antagonists
ondansteron (Zofran)
granisteron (Kytril)
Anti-emetic action due to blockade of 5-HT3 serotonin receptors in the CRTZ and in the gastrointestinal tract
Side effects include transient headache, constipation and dizziness
D2 Dopamine Antagonists
metoclopramide (Reglan)
Anti-emetic action due to blockade of D2 dopamine receptors in the CRTZ
At higher doses it blocks 5-HT3 receptors which also may contribute to its anti-emetic properties
increases peristalsis in jejunum and duodenum) due to some muscarinic activity, D2 antagonism, and 5-HT4 receptor agonism
Side effects include hyperactivity, tremors and constipation
α2 Adrenrgic Antagonists
acepromazine
chlorpromazine
also blocks dopamine, histamine and ACh receptors
Blocks vomiting reflex at **Emetic Center and CRTZ **
Side effects include mild sedation due to histamine receptor blockade and hypotension due to α1 receptor blockade
dimenhydrinate (Gravol, Dramamine)
Antihistamines
block motion sickness
Anti-emetic activity due to blockade of H1 Histamine receptors in CRTZ by diphenhydramine
sedation →H1 receptors in CNS
why doesn’t dimenhydrinate (Gravol, Dramamine) stop motion sickness in cats
dramamine works on H1
receptors in the CRTZ
anti-motion sickness
cats: Vestibular nucleus impulses pass directly to the emetic center
dogs: Vestibular nucleus impulses pass through CRTZ to the emetic center
anti-emesis
antihistamine
dimenhydrinate (Gravol, Dramamine)
anti motion sickness in dogs by H1 receptor in CRTZ
not in cats which vestibular skips the CRTZ and goes right to emetic center
meclizine (Dramamine II)
Anti-emetic activity due to blockade of H1 histamine receptors in CRTZ
less sedation then dramanine cause less BBB cross ?
Used to treat vertigo as a result of inner ear infections
Anticholinergics Anti-Emetics
scopolamine (Hyoscine)
propantheline isopropamide
darbazine
scopolamine (Hyoscine)
Anticholinergics- anti-emetics
blockade of muscarinic receptors in Emetic Center
Blocks muscarinic receptor activation in the emetic center
activated by vagal afferent pathways from stomach and gut
use for travel sickness
propantheline isopropamide
Anticholinergics
anti- emetic
not as effective alone, should be combined with other meds
Anticholinergics combined with phenothiazines
Anti- ACh Anti- vomiting:
scopolamine (Hyoscine)
propantheline
isopropamide
darbazine
darbazine
anti- ACh
anti-vomiting
Side Effects: due antimuscarinic effects Tachycardia, loss of visual accommodation, urine retention, constipation, xerostomia
maropitant (Cerenia)
Neurokinin1 (NK-1) Antagonists
anti-vomiting and motion sickness
Blockade of NK-1 activation in CRTZ reduces vomiting
THC
Cannabinoids
anti-vomiting
Binds to CB1 and CB2 (GPCR) receptors in many areas of CNS
centrally acting emetics
apomorphine
xylazine
apomorphine
Nonselective dopamine AGONIST
Stimulates CRTZ
centrally acting emetics:
apomorphine
xylazine
xyalzine
centrally acting emetic
α2 adrenergic AGONIST induces vomiting in cats then mild sedation.
centrally acting emetic:
apomorphine
xylazine
peripherally acting emetics
Sodium Chloride
Hydrogen Peroxide (H2O2)
Syrup of Ipecac
Ayahuasca (a-ya-wa-ska)
