Term
| What 3 effects can GI drugs have? |
|
Definition
*Gastric pH
*Gastric volume
*Gastric Motility |
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Term
| What patients are at risk of aspiration pneumonitis? |
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Definition
*Full Stomach
*Pregnant
*Obses
*Diabetics (with gastroparesis)
*hiatal hernia
*Gastro-Esophageal Reflux Disease (GERD) |
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Term
| The more ______ gastric fluid is, the more ______ it does to the pulmonary epithelium. |
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Definition
*Acidic
*harm
*The problem encountered is often the result of the degree of acidity and the type of particulate in the aspirate. |
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Term
| What is the composition of gastric acid secretions? |
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Definition
*Hydrochloric acid
*Sodium
*Potassium
*HCO3
*Pepsinogen
*Glycoprotein
*Intrinsic factors
*Mucous |
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Term
| Aspiration of gastric contents >_____mL in volume, with a pH <________ can cause pulmonary complications. |
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Definition
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Term
| What is another name for aspriation pneumonitis? |
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Definition
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Term
What are the functions of normal gastric secretions?
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Definition
*Protect normal bacterial flora
*Digestion
*Absorption of B12 and iron
*Protection of gastric mucosa
*Total daily secretion is 2L
*Normal pH of 2-3.5 |
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Term
| What are the major pathways controlling gastric secretion? |
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Definition
*Vagal stimulation via acetylcholine. Major extrinsic control of gastric acid secretion. Stimulation of the vagus or a vaso-vagal reaction results in profuse acid secretory response. The magnitude of the response is dependent on the strength of the stimulus.
*Stress- a major stimulus to gastric acid secretion
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Term
| What are some surgical treatments for excessive gastric acid? |
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Definition
*Vagotomy-surgical procedure to denervate the gastric mucosa
*Truncal Vagotomy- cut the major branches of teh vagus
*Highly selective vagotomy- cut specific branches of the vagus that innervate the acid secreting mucosa |
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Term
| What control does the endocrine system have over acid secretion? |
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Definition
*Mediated by gastrin from antral G-cells: controls release of gastric fluid
*Gastrin- produced in pyloric glands located in distal antrum ****It is the major hormonal regulator of gastric acid secretion**** |
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Term
| What facilitates or accelerates the release of gastrin? |
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Definition
*cAMP
*Presence of food and elevated pH in the antrum |
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Term
| What is released from enterochromaffin cells? What else stimulates the hormone released from enterochromaffin cells? |
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Definition
*Local release of histamine from paracrine cells
*Located at the basolateral membranes of the parietal cells.
*Gastrin secretion
* |
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Term
| Where does histamine act and what does it trigger in the GIT. |
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Definition
*Acts on H2 receptors of parietal cells
*Major trigger to the production and secretion of gastric acid. |
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Term
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Definition
*Mediates histamine induced contraction of the smooth muscles in the GIT and bronchi.
*Stimulation of H1 receptors produces bronchoconstriction and intestinal contraction, nasal congestion, sneezing. |
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Term
| What do H2 receptors mediate? |
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Definition
*Major role is related to acid production by the parietal cells. Mediates histamine-induced secretion of gastric hydrogen ions.
*Occupation of H2 receptors by histamine activates adenylate cyclase thus increasing intracellular concentration of cAMP.
*The increased level of cAMP activates the parietal cells to secrete hydrogen ions. |
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Term
| What is the primary regulator of acid secretion by the parietal cells. It is a potent stimulus to gastric acid secretion from parietal cells in the distal third of stomach mucosa? |
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Definition
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Term
| Where else other than the GIT are histamine receptors located? What effects do they have? |
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Definition
| *Present in myocardium and cardiac conduction tissues-causes positive inotropic and chronotropic effects and negative dromotropic effect |
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Term
| What effects do H1 receptors have on the heart? |
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Definition
| *The only cardiac effect of H2 receptor stimulation is delay of AV conduction- negative dromotropic effect |
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Term
| What effect do H2 receptors have on the heart? |
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Definition
| *Positive inotropic and chronotropic effects of histamine are H2 receptor mediated effects (Can be blocked by H2 antagonists like Cimetidine) |
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Term
| Why are H2 Antagonists used? |
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Definition
*Reduction of acid secretion
*Treatment of duodenal and gastric ulcers
*Prevent PUD associated with NSAID/ASA use
*Reduce severity of stress ulcers in severely ill patients (in the past) |
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Term
| What are the properties of H2 blockers? |
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Definition
*H2 antagonists are selective and competitive blockers of the parietal H2 receptors
*They reduce gastric acid secretion by blocking the ability of histamine to induce the secretion of gastric fluid
*****Technically reduces gastric volume*******
*******The gastric pH is increased******* |
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Term
| What are incidence of adverse effects with H2 blockers? |
|
Definition
*Low and side effects are usually transient.
*SE include: diarrhea, headache, fatigue, drowsiness and constipation. |
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Term
| What are disadvantages of H2 blockers? |
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Definition
*Does not affect fluid already present in the stomach
*Has no significant effect on gastric emptying, LES tone and pancreatic secretion |
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Term
| What are H2 Blocker Pharmacokinetics? |
|
Definition
*Rapid absorption
*Extensive 1st pass
*Bioavailbility 50%
*Hepatic Metabolism
*Renal Clearance
*Cross BBB and Placenta w/o fetal effects |
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Term
| What drug is the prototype of all the H2 antagonists, it blocks histamine induced secretion of H+ by the gastric parietal cells? |
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Definition
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Term
| What is the Peak, Dose, duration, and time given of Cimetidine prior to surgery? |
|
Definition
*Peak: 60-90 Minutes
*Dose: 150-300mg Oral or 3-4mg/kg IV
*Duration: 6 hours
*Given PO 1-2 hours before surgery |
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Term
| What is a major side effect of cimetidine? |
|
Definition
*Inhibits cytochrome p450.
*Can have prolonged effect in renal patients
*Rapid IV infusion associated with life threatening dysrhythmia, hypotension, cardiac arrest
*CNS Depression- increased in elderly
*<1% thrombocytopenia, gynecomastia or glactorrhea |
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Term
| What drugs have a major interaction with Cimetidine? |
|
Definition
*Dilantin
*Propranolol
*Lidocaine
*Theophylline
*Phenobarbitol
*TCA
*Coumadin
*Labetolol
*Diazepam |
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Term
| What drug is more selective and 5-8 times more potent than Cimetidine? |
|
Definition
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Term
| What is the dose, duration, and AME of Zantac? |
|
Definition
*Dose: 50-200mg oral, 50-100mg IV (Give slow)
*Duration: 8-12 hours
*Absorbed in GIT 30-60 minutes
*Excreted by kidneys 30-50%, 30% by liver
*Same effectiveness as Cimetidine but fewer side effects
*Weakly bind with Cytochrome p450
*Minimally crosses placental/BBB |
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Term
| Which H2 blocker has no effect on cytochrome p450, is the most potent and longest acting with virtually no CNS effects? |
|
Definition
|
|
Term
|
Definition
*Omeprazole (Prilosec)
*Pantoprazole (Protonix)
*Lansoprazole (prevacid)
*Rabeprazole (Aciphex) |
|
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Term
| Which class of drugs are the best inhibitors of HCl secretion by interfering with the H+ pump? |
|
Definition
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|
Term
| Unlike H2s- PPIs affect all three known stimulators of acid production: _____, _____, _______. |
|
Definition
*Gastrin
*Acetylcholine
*Histamine |
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Term
| What is the specific MOA of PPIs? |
|
Definition
| *Specifically binds non-competitively to H+/K+ ATPase enzyme (proton pump) located on the surface of gastric parietal cells, thus inhibiting the secretion of H+ ions into the gastric lumen. |
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Term
| What effect do PPIs have on the stomach? |
|
Definition
*Decrase Gastric Volume
*Increase Gastric pH
*NO effect on motility |
|
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Term
| What syndromes are PPIs superior for? |
|
Definition
*GERD
*PUD
*Esophagitis
*Zollinger-Ellison Syndrome |
|
|
Term
| What PPI can cause thrombocytopenia? |
|
Definition
|
|
Term
| What drugs are the quickest and best way to increase gastric pH? |
|
Definition
|
|
Term
|
Definition
*Bases that interact with gastric acid to form salt and H2O
*Used to neutralize the acids in gastric contents
*Raise stomach pH
*Decrease acid load delivered to duodenum
*Reduce activity of pepsin |
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Term
| What are particulate antacids? What components make up particulate antacids? |
|
Definition
*Particulate antacids are colloid antacid suspension that contain aluminum or magnesium hydroxide as their base substance. Most are a combination of Al and Mg to achieve rapid and sustained neutralization of acid and to balance their effects on bowel function.
*Aluminum: Slow and constipating
*Magnesium: Fast and laxative
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|
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Term
| What is the advantage and disadvantage of particulate antacids? |
|
Definition
*Advantage: Most effective in increasing pH
*Disadvantage: Harmful if aspirated |
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Term
| What are different types of non-particulate antacids? |
|
Definition
*Usually NaHCO3 preparations
*Sodium Citrate (Bicitra)
*Alka Seltzer Gold
*Not harmful if aspirated |
|
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Term
| What are the advantages of antacids? |
|
Definition
*Single dose given 15-30 minutes prior to induction is almost 100% effective in increasing pH >2.5
*No lag time-starts working immediately
*Effective on fluid already present in stomach |
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|
Term
| What are the disadvantages of Antacids? |
|
Definition
*Will increase overall gastric volume
*May actually slow gastric emptying
*Chronic use alkalinization of GIT and urine |
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Term
| What drug is made of sucrose and aluminum hydroxide and adheres to ulcer forming a cytoprotective barrier against pepsin? |
|
Definition
*Sucralfate (Carafate)
*Decrases stress ulcer is long term vent patients
*Not really better than H2 blockers |
|
|
Term
| How do gastrokinetic agents act? What are they good for? |
|
Definition
*Act through smooth muscles (M2 muscarinic cholinergic receptor) of the GIT directly or indirectly. These agents will increase the strength of propulsive contractions and enhance the rate of gastric emptying
*Therefore they are effective in reducing the overall gastric volume |
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|
Term
| What patients are gastrokinetic agents good for? |
|
Definition
*Full stomach
*Parturient
*Obese
*Stressed patients (trauma)
*GERD
*Diabetics
*Ileus |
|
|
Term
| What drug is a prototype agent with a benzene ring with amide linkages also known as Benzamides? |
|
Definition
*Metoclopramide (Reglan)
*They are related to procanamide but lack the LA or antiarrhythmic actions |
|
|
Term
| Reglan is a _________. Requires background _________________ function to increase motility. |
|
Definition
*D2 antagonist
*ACH/cholinergic |
|
|
Term
| Where are dopamine receptors found in the GIT? What occurs when they are stimulated? |
|
Definition
*Found in the esophagus, stomach, small intestine.
*When stimulated: Enhancement of GI secretions and diminish intestinal motility |
|
|
Term
| What does reglan do the the GIT? |
|
Definition
*Stimulates upper GI motility
*Increases GE sphincter tone
*Relaxes pylorus and duodenum thus facilitates propulsion of gastric contents into the small intestine
*Some anti-emetic properties
*NO known effect on acid secretion and gastric fluid pH |
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|
Term
| How is reglan dosed or given? |
|
Definition
*IV 5-20mg, give 15-30 minutes prior to induction
*Give slow to avoid cramping
*Oral 10-20mg onset 30-60 minutes
*Crosses placenta/BBB
*30% excreted unchanged in urine- remainder undergoes glucuronic conjugation |
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|
Term
| What are the side effects of Metoclopramide? |
|
Definition
*Extrapyramidal symptoms- involuntary movements, parkinsonism like movements, tardive dyskinesia, motor restlessness
*Akathisia (young and elderly)
*Anxiety
*Depression d/t dopamine blockade
*May prolong action of Succinylcholine and ester LA
*May have mild sedative effects
*Its effects may be offset by narcotics and anticholinergics
*It works best in combination with an H2 blocker |
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|
Term
| What disease should Reglan be avoided in? |
|
Definition
|
|
Term
| What should EPS be treated with? |
|
Definition
|
|
Term
| What drug is a benzamide but lacks the anti-emetic properties and the D2 receptor activity seen with Metoclopramide with the same affect on GI motility as Metoclopramide? |
|
Definition
|
|
Term
| How does Cisapride (Propulsid) work? |
|
Definition
*By enhancing the rate of release of Ach from myenteric plexus
*Dose oral only
*10-20mg
*onset 30-60 minutes |
|
|
Term
| How do anticholinergics exert their effects on the GIT? |
|
Definition
*Antagonize Ach at muscarinic receptors in GIT
*Weak antagonism of H+ ions by parietal cells
*High doses inhibit motility and decrease LES tone |
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