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59 Cards in this Set

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  • Back
What is the primary regulator of gastric acid secretion int he parietal cell?
What are the enhancers of histamine and resulting gastric acid secretion by the parietal cells?
Ach and Gastrin
What type of acetylcholine receptor on the parietal cell enhances gastric acid secretion?
M3 receptor
What is the acetycholine receptor type on the vagus nerve?
M1 Receptor
Pirenzipine is a drug that is what?
Anticholinergic, M1 antagonist
Following the cephalic phase the vagus nerve stimulates what type of cells through what transmitter to cause histamine release?
ECL cell through acetylcholine
What cells are the primary site of histamine production for gastric activation?
ECL cells
What is the cascade for H+ release in the stomach starting with the histamine released from the ECL cells?
Histamine binds to the H2 receptor of the parietal cell causing a Gs signaling increasing cAMP which results in increased H+ ion. The H+ ion is pumpe out of the cell into the stomach by a H/K proton pump. Once in the stomach H+ combines with Cl- to form HCl
How does stimulation of the gastric phase/intrinsic stimulatory pathway function?
Mechanoreceptors in the stomach through distension releases ACh to both the muscarinic receptor on the ECL cell and the M3 receptor on the parietal cell to enhance gastric acid release.
What is the intrinsic activation system of the muscarinic receptor of the stomach?
M3 receptor is coupled to Gi protein causing through cascade an increase in intracellular Ca which boosts the histamine pathway (somehow somewhere)
How does alkaline pH assist in acid secretion?
alkaline pH is a stimulator of gastrin release. Gastrin binds to the CCK receptor on parietal cells coupled to a Gq receptor causing an increase in intracellular Ca also boosting the histamine pathway.
What are the primary counter regulatory mechanism mediators for inhibition of gastric acid secretion?
PGE2 and PGI2 prostaglandins bind to EP3 receptors to inhibit the cAMP dependent pathway on the parietal cells and increase the mucus and bicarb production on the superficial epithelial cells
How does activation of EP3 on the parietal cell work for Gastric acid inhibition?
EP3 is a Gi protein that inhibits adenylate cyclase thereby reducing calcium
What stomach enzyme assist gastric acid in the breakdown of food particles and requires HCl to be activated?
Pepsinogen to pepsin!
What controls mucosal barrier secretions?
Ach and Prostaglandins
What is the function of Cimetidine? huh? Huh?? answer me!
Histamine receptor agonist
How should GERD be treated and what is the possible underlying pathology associated with GERD?
GERD is thought to be caused by a dysfunction of the Lower Esophageal Sphincter. It can be treated with local anesthetics for immediate relief with behavioral modifications during flare-ups (in essence change in diet and sleeping methods) and it may finally be treaed with drugs such as cimetidine or proton pump inhibitors
What percentage of the population with a complaint of chest pain actually have GERD?
What is the etiology of Peptic Ulcer Disease?
It is thought to be due to disregulation of gastric acid secretion pathways
What is the most common form of peptic ulcer disease and what is the other form?
Benign - most common
Malignant - other
What are the possible causes of benign peptic ulcer disease?
Helicobacter pylori, Chronic NSAIDS use or Zollinger-Ellison syndrome (gastrin producing tumor)
What are the types of treatments for GERD, PUD, and Duodenal Ulcers?
Histamine 2 Receptor Agonists
H/K proton Pump Inhibitors
Anti-Pylori therapy
Mucosal Protective Agents
Prostaglandin Analogs
What type of systemic antacids are there?
Systemic Antacids: Sodium bicarbonate antacid (aka Baking SOda) - quick acting short duration acid neutralizer reactis with acid to form carbon dioxide SE excessive sodium and bicarb may cause systemic metabolic alkalosis
What type of antacids are there?
Systemic and Non-systemic... hahah
What type of non-systemic antacids are there?
Aluminum hydroxide and magnesium hydroxide combination (Maalox and Mylanta) - works locally to treat heartburn by neutralizing acid and increasing the pH. Aluminum hydroxide is slow acting while the magnesium hydroxide is potent and quick SE: no GI motility issues when in combination but alone aluminum (constipation) and magnesium (diarrhea)
Calcium Carbonate (tums, rolaides) good source of Calcium and treats heartburn locally SE: rebound acid production due to the Ca negating effects. ALso causes increased CO2 causing bloating and constipation
What are the various type of H2 receptor antagonists?
Cimetidine (tagamet) - Prototype
What is now the treatment of choice for PUD?
Proton Pump Inhibitors
How does Cimetidine work?
Reduces acid secretion and allows time for healing. Treatment time is 6 weeksIt is a competitive antagonists of H2 receptor SE: headache most common and anti-androgenic activity with long term use (You turn into a woman)
What is the utility of Ranitidine?
5-10x more potent than Cimetidine best for mild peptic ulcer disease
Competitive antagonist of the histamine H2 receptor
Does NOT inhibit the Cytochrome P450
What is the Utility of Famotidine?
160X more potent than Cimetidine and 20x more potent than Ranitidine
Competitive antagonist of H2 receptor
Does not inhibit the Cytochrome P450
What is the utility of Nizatidine?
Competitive antagonist of the H2 receptor
Does not inhibit the cytochrome P450
What are the H/K proton pump inhibitors (PPI)?
Omeprazole (Prilosec) - Prototype
Esomeprazole (Nexium), Lansoprazole (Prevacid), Rabeprazole (Aciphex)
What is the utility of Omeprazole?
GERD, PUD - #1 choice
Duodenal ulcers and Zollinger Ellison syndrome
Administered as a pro-drug
Protonated to its active metabolite by acid
Active form irreversibly binds to the proton pump
What are the therapy methods for H. Pylori?
Proton pump inhibitors are often used as part of a combination therapy
Dual Therapy - PPI+Antibiotic
Triple Therapy (Current Choice) - Acid suppressing drug (PPI or high does anti-H2) + antibiotic to eradicate the bug + broad spectrum antibiotic
Quadruple therapy (#1 current choice) - Triple therapy + Bismuth Subsalicylate
What is Bismuth Subsalicylate?
Pepto-Bismol! which also has anti-bacterial activity
What are the mucosal protective agents?
Sucralfate (Carafate)
Short term treatment of mild peptic ulcer disease. Can be bought over the counter
Sucrose-aluminum polymer that coats ulcerative areas of the epithelial linin
Constipation due to aluminum major side effect
What are the prostaglandin analogs?
Misoprostol (Cytotec) - Prophylaxis against NSAID-induced peptic ulcers
PGE2 analog. Binds EP3 and direct effect on parietal cells inhibiting secretion.
Not for preexisting PUD
What is the utility of Lansoprazole & Naproxen combination (Prevacid Napra PAC)
Most common combination for people who must be on NAIDS = PPI+Naproxen
Prophylaxis against peptic ulcers in arthritis patients
Naproxen is an anti-inflammatory which also has analgesic and anti-pyreic properties
What are the antimuscarinic drugs given in the treatment of GI disturbances?
Pirenzipine used to treat uclers and GI hypermotility problems. Adjunct with triple and quadruple therapy.
M1 antagonist - decreases gastric acid secretion and reduces smooth muscle motility
What are the 4 categories of laxatives that assist in constipation treatment?
Bulking agents
Saline and osmotic laxatives
Stimulant/Irritant Laxatives
Surfactant Laxatives
What are the Bulking agents in laxatives and how do they work?
Agar, methylcellulose, psyllium seds, bran, insoluble fiber, saline cathartics
They function by forming gels in the large intestine causing water retention, distending the colon and causing a reflexive increase in peristaltic activity.
Safest agents for constipation in the elderly
May promote fecal impaction
Containdications: if fecal impaction present these do nothing to loosen.
What are the saline and osmotic laxatives and how do they work?
Saline sodium phosphates, epsom salt, lactulose, polyethylene glycol
Combine with stool and promote osmotic flow of water used as a cathartic in emergency situiations involving stoo impaction. not to be used in those with electrolyte disturbances or CHF patients
What are the stimulant/irritant laxtives and how do they work?
Castor oil, senna, cascara, bisacodyl, lubiprostone
Stimulate or irritate local afferent nerves int he gut increasing intestinal motlity
Not for use in the elderly because of intrinsic nerve damage
What are the surfactant laxatives and how do they work?
Docusate sodium, mineral oil, glycerin suppositories
Lubricating coat around the stool facilitating passage and promote fluid and electrolyte secretion
What are the anti-diarrheal agents?
Opioid analogs (decrease intestinal motility and increase fluid adsorption)- Loperamide, diphenoxylate
Bismuth salicylate
How do the opioids loperamide and diphenoxylate work?
bind to 2 different opioid receptors in the gut decreasing motility and increasing adsorption:
mu opioid receptor - major effect on smooth muscle intestinal motility
delta opioid receptor - binding epithelial linin causing an increase in intestinal adsorption (presynaptic nerve terminals of acetylcholine - decreasing Ach)
Do not cross the BBB at therapeutic doses
No analgesic effects
Not for treatment of chronic, secretory diarrhea caused by IBD
How does Bismuth Salicylate (pepto bismol)?
acts as an adsorbant, decreasing the amount of free water int he intestinges. also has some antibacterial activity
Used in quadruple therapy for treatment of H. pylori
May turn patient's stool black
How does Octreotide work?
Analog of somatostatin, producing a general inhibitory action on the GI tract
What is the primary neurotransmitter responsible for relaying vomiting signals from the periphery to the Nucleus Tractus Solitarius?
Serotonin binding to the 5HT3 receptor
What are the vomiting receptors that are located in both the CTZ (chemoreceptor trigger zone) and the Nucleus solitary tract?
5HT3, D2, and M1 receptors
How can acetylcholine release cause vomiting?
Ach is released by the vestibular apparatus and stimulates the vomiting center. In addition M1 receptors are located at both the Nucleus Solitarius and CTZ
How does histamine play a role in vomiting?
Similar role to Ach in response to motion sickness. Also has H1 receptors located in the nucleus solitarus
What are the different potencies of antiemetics?
High: 5'HT antagonists and D2 antagonists
Moderate: Cannabinoids and Butyrophenones
Low: Histamine blockers and Muscarinic blockers
What are the strongest antiemetics and how do they work?
Serotonin antagonists: ondansetron, granisetron
Prevent both peripheral and central stimulation thorugh visceral afferent nerves in the GI tract, solitary tract nucleus and the CTZ
What are strong emetics but not the strongest and how do they work?
Dopamine antagonists: pprochlorazine and metoclopramide
Block the D2 receptor in the CTZ and the solitary tract nucleus. Metoclopramide also inhibits 5HT3 receptors in the gut and CNS
What does the moderate anti-emetic cannabinoids and how do they work?
Dronabinol and nabilone
Marijuana or tetrahydrocannabinol (THC) derivatives
Never 1st line treatment
Given only if patient has failed both strong antiemetic treatment therapies
Appetite stimulant for AIDS patients with ANorexia (get munchies)
What are the moderate anti-emetic butyrophenones and how doe they work?
domperidone, droperidol and haloperidol
They are all CNS drugs
What are the weak antiemetic H1 antagonist drugs and how do they work?
Diphenhydramine, promethazine, meclizine, and cyclizine
They block H1 receptors present in the nucleus of the solitary tract
No direct effect on inhibition of the chemotrigger zone
Also have antimuscarinic abilities
What are the weak antiemetic muscarinic receptor antagonists and how do they work?
Blocks muscarinic receptors prophylactically to prevent motion sickness