Monica - Final Exam: Acid-controlling/Anti-emetic drugs Flashcards
Describe the mechanical functions of the GI tract (from opening of stomach to the duodenum):
- Lower esophageal sphincter - ring of smooth muscle that prevents backflow of stomach contents
- food is churned into chyme (pulpy acidic fluid)
- peristalsis moves chyme to the pylorus
- pyloric sphincter provides entry into the duodenum
List the cells and chemicals that function within the stomach:
- parietal cells: HCl, intrinsic factor
- chief cells: pepsinogen
- mucus neck cells: mucus, HCO3-
- prostaglandins: stiumulate mucus, HCO3- secretion; promote repair and blood flow
Disruption in any of the chemical functions of the stomach can lead to an imbalance that increases the risk of:
damage to the lining of the stomach (peptic ulcer disease).
Parietal cells secrete ____, which activates ______, and secrete _____, which promotes the absorption of _____.
HCl - pepsinogen
intrinsic factor - B12
How is pepsinogen converted to pepsin?
acidity
How are mucus neck cells cytoprotective?
Mucus and HCO3- neutralize acid and form a protective layer over the gastric lining to prevent damage.
Parietal cells can secrete _ - _ liters of HCl per day.
1 - 3 liters/day
What is the function of prostaglandins in the stomach?
- stimulate secretion of mucus and HCO3
- inflammatory response: promotes repair and blood flow
GI diagnostic studies (4)
- EGD
- Upper GI series w/ barium swallow
- Lower GI series w/ barium enema
- Colonoscopy
EGD and colonoscopy
esophagogastroduodenoscopy: scope of esophagus, stomach, and dueodenum
colonoscopy: scope of the entire colon
Upper GI series w/ barium swallow
fluoroscopic x-ray using oral contrast to see the movement through the upper GI tract
ex. dx aspiration pneumonia
Lower GI series w/ barium enema
fluoroscopic x-ray using rectal contrast to visualize movement through lower GI tract
ex. polyps, obstructions, diverticuli, strictures caused by colon cancer
What is PUD?
Peptic ulcer disease: lesion or erosion in the stomach or duodenum
PUD: causes
- hypersecretion of acid
- ineffective mucus/HCO3- production
- poor cellular repair
PUD: risk factors (6)
- family hx
- meds: corticosteroids, NSAIDs, platelet inhibitors
- smoking
- alcohol
- caffeine intake - acidic
- H. pylori - corkscrew-shaped bacteria that screws into stomach lining
How do corticosteroids increase the risk of PUD?
inhibit the inflammatory response - less blood flow and repair of damaged cells…
How do NSAIDs increase the risk of PUD?
aspirin and ibuprofen inhibit COX-1 and COX-2 enzymes: - COX-1 protects stomach mucosal lining - COX-2 promotes prostaglandins Thus,
PUD: symptoms
- gnawing/buring pain
- discomfort 1 - 3 hours after meals
- discomfort worse w/ empty stomach
- risk of bleeding (bright red blood in emesis; dark stools)
For people with PUD, why might gastic discomfort lessen after eating?
Food acts as a protective barrier and the LES closes preventing acid backflow into the esophagus.
GERD
Gastroesophageal reflux disease:
- stomach acid enters the esophagus (heartburn) d/t weakening of the LES
GERD increases the risk of:
esophageal lining erosion, that could lead to ulceration and possibly over time:
- respiratory problems: chronic cough, aspiration pneumonia
- lifestyle changes: inablility to lay flat; sleep upright
GERD: symptoms
- dysphagia
- dyspepsia
- heartburn
- belching
- nausea
Heartburn can feel like a:
cardiac event.
If a patient presents to the ER with chest pain, the physician will want to rule out _______ first.
R/O a cardiac event FIRST! Then determine if there is a GERD issue.
*sometimes given meds for GERD to relieve those possible symptoms and distinguish them from cardiac symptoms
Factors that worsen GERD:
- large meals
- acidic food and drinks
- spicy foods
- smoking, alcohol
- obesity
- NSAIDs, corticosteroids
How does obesity worsen GERD?
Increased weight places pressure on the LES.
How does a large meal worsen GERD?
All that food doesn’t fit in the tum tum placing pressure on the LES and backing into the esophagus.
acidic food and drinks to avoid:
citrus, tomato-based, coffee
How do NSAIDs and corticosteroids worsen GERD?
especially long-term use
Lifestyle changes to help manage GERD:
- elevate HOB
- smaller meals
- lose weight
- smoking/alcohol cessation
- if taking aspirin or corticosteroids long-term, also take preventative meds
Pharmacotherapy, along with ________, are needed to relieve symptoms, promote healing, and prevent reoccurances of ulcers.
lifestyle modifications
3 drug classes for suppressing or neutralizing gastic acid:
- proton-pump inhibitors
- H2-receptor antagonists/blockers
- antacids
**may affect absorption of other drugs/nutrients
Gastric acid is essential in the absorptions of (vitamins/minerals):
B12, vit C, folic acid, iron
proton pump inhibitor: drug
pantoprazole (Protonix)
pantoprazole: classification
proton pump inhibitor
PPIs: indication
- ulcer management
- GERD
PPIs: action and effect
A: blocks H+-K+ ATPase pump located on parietal cells
E: decreased acid production
PPIs: form/route, implementation
IV, PO (capsule, sprinkles); 1xday
- swallowed whole
- sprinkled on food
- give 30 min before meals
- *most designed to last ALL day
Why does pantoprazole need to be given before meals?
b/c the hydrogen-potassium pump is activated by food
PPIs block __% of acid.
95% - is it TOO effective??
There is a positive correlation between PPIs and _______ because:
C. dificile - 65% risk of acquiring C. dif-diarrhea
- b/c bacteria that is normally killed by the acidic environment of the stomach survives and overgrows
PPIs: adverse effects
- C. dif-associated diarrhea
- respiratory infections
- osteoporosis
Are PPIs too effective?
- benefits w/in 3-5 days
- 95% of acid blocked
- heal 90% of ulcer w/in 4-9 weeks
How do PPIs cause osteoporosis?
The interfere with the absorption/metabolism of calcium.
With both PPIs and H2 blockers, avoid concurrent use with:
antacids - b/c both need acid for absorption
H2 blockers: drug
ranitidine (Zantac)
ranitidine: classification
Histamine receptor antagonist (H2 blocker)
H2 blockers: action and effect
A: interferes with acid production by blocking histamine-2 receptors
E: decreased secretion of gastric acid
H2 blockers: indication
- short-term tx of duodenal and gastric ulcers
- maintenance therapy after healing
- GERD and dyspepsia
H2 blockers: implementation
- avoid concurrent use w/ antacids
- administer w/ meals and bedtime: 3-4 x per day to be effective
Antacids are indicated for prevention or healing of ulcers.
FALSE!! **only for neurtralizing stomach acid and providing temporary relief from heartbur and indigestion
antacids: action
- stimulate prostaglandin production
- increase mucus and HCO3 secretion
Antacids can contain the following minerals:
- magnesium
- aluminum
- aluminum + magnesium
- calcium
Magnesium-containing antacid:
Milk of magnesia (laxative)
Adverse effect of MOM
diarrhea
Aluminum-containing antacid:
Amphogel
Adverse effect of Amphogel
constipation
Amphogel may inhibit absorption of:
iron
Aluminum-containing w/ magnesim antacid:
Maalox, Mylanta
Adverse effect of Maalox, Mylanta
constipation, diarrhea
Why should CKD patients avoid Maalox/Mylanta?
d/t increased risk of calcium loss
- hyperphosphatemia
Mylanta/Maalox increase the risk of ___ loss.
calcium loss - leading to osteoporosis
calcium-containing antacid:
Tums
Adverse effects of Tums
constipation, kidney stones
If a patient has a bottle of Tums at their bedside what should the RN do?
Question why they are taking it and how much they are taking. It could impact their health.
MOM contains:
Magnesium
Amphogel contains:
aluminum
Mylanta and Maalox contain:
aluminum + magnesium
Tums contains:
calcium
Simethicone is an __________, sometimes added to _____ preparations.
anti-flatulent; antacids (Mylanta…)
simethicone: indication
relief of excess gas
simethicone: action and effect
A: coalescence of gas bubbles for easier expulsion and relief of distention/discomfort
E: passage of gas thru belching or flatus
Sucralfate is a _____ ______ that prevents:
gatrointestinal protectant (mucosal protectant) that prevents further ulcer erosion.
Sucralfate has nothing to do with gastric acid.
TRUE - action: aluminum salt of sulfated sucrose reacts with gastric acid to form a thick paste, which adheres to the ulcer surface.
sucralfate: indication
short-term therapy of ulcers - up to 8 wks
sucralfate: AE
constipation
sucralfate: implementation
- give 1 hour before a meal and at bedtime (4xday)
- not given concurently w/ antacids, H2-blockers, PPIs b/c needs HCl to be activated
vomiting
forcible emptying or expulsion of gastric acid
vomiting pathway
*vomiting center in the lower medulla initiates and controls the act of emesis. It receives signals from digestive tract, inner ear, and chemoreceptor trigger zone (CTZ)
anti-emetic drugs (4)
- promethazine
- prochlorperazine
- metoclopramide
- ondansetron
promethazine: action
blocks the effects of histamine receptors and CTZ
prochlorperazine: action
alters the effects of dopamine receptors and depresses CTZ
metoclopramide: action
- blocks dopamine receptors in CTZ
- accelerates gastric emptying
ondansetron: action
blocks effects of serotonin receptors in CTZ
anti-emetics: adverse effects
extrapyramidal reactions, constipation, dry mouth, sedation, drowsiness, HA
