- hypersecretion of acid - ineffective mucus/HCO3- production - poor cellular repair

- gnawing/buring pain - discomfort 1 - 3 hours after meals - discomfort worse w/ empty stomach - risk of bleeding (bright red blood in emesis; dark stools)

- dysphagia - dyspepsia - heartburn - belching - nausea

Monica - Final Exam: Acid-controlling/Anti-emetic drugs Flashcards by Erin Nelson

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

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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

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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).

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Parietal cells secrete ____, which activates ______, and secrete _____, which promotes the absorption of _____.

HCl - pepsinogen

intrinsic factor - B12

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How is pepsinogen converted to pepsin?

acidity

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How are mucus neck cells cytoprotective?

Mucus and HCO3- neutralize acid and form a protective layer over the gastric lining to prevent damage.

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Parietal cells can secrete _ - _ liters of HCl per day.

1 - 3 liters/day

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What is the function of prostaglandins in the stomach?

stimulate secretion of mucus and HCO3

- inflammatory response: promotes repair and blood flow

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GI diagnostic studies (4)

EGD
Upper GI series w/ barium swallow
Lower GI series w/ barium enema
Colonoscopy

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EGD and colonoscopy

esophagogastroduodenoscopy: scope of esophagus, stomach, and dueodenum
colonoscopy: scope of the entire colon

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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

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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

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What is PUD?

Peptic ulcer disease: lesion or erosion in the stomach or duodenum

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PUD: causes

hypersecretion of acid
ineffective mucus/HCO3- production
poor cellular repair

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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

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How do corticosteroids increase the risk of PUD?

inhibit the inflammatory response - less blood flow and repair of damaged cells…

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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,

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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)

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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.

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GERD

Gastroesophageal reflux disease:

- stomach acid enters the esophagus (heartburn) d/t weakening of the LES

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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

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GERD: symptoms

dysphagia
dyspepsia
heartburn
belching
nausea

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Heartburn can feel like a:

cardiac event.

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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

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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:

1. proton-pump inhibitors 2. H2-receptor antagonists/blockers 3. 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:

1. magnesium 2. aluminum 3. aluminum + magnesium 4. 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)

1. promethazine 2. prochlorperazine 3. metoclopramide 4. 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

Monica - Final Exam: Acid-controlling/Anti-emetic drugs Flashcards

(85 cards)