13.2 GI Pharmacotherapy and Nutrition

The current FNP-BC Test Content Outline lists gastrointestinal among the official drug-agent classes. Domain III Planning asks whether the regimen matches the diagnosis in Section 13.1. Domain IV Implementation asks whether the dose, duration, interaction, and counseling are safe. Domain V Evaluation asks whether you stop what is no longer indicated. This is the prescribing-and-nutrition chapter, not another differential list.

PPI, H2RA, and antacids: appropriate use and de-escalation

A proton-pump inhibitor is the strongest routine acid suppressor. Appropriate FNP uses include a time-limited empiric trial (typically 4–8 weeks) for typical GERD without alarms, healing of erosive esophagitis, Barrett esophagus maintenance when GI has set that plan, NSAID gastroprotection in high-risk patients who must stay on an NSAID, and the acid-suppression piece of an H. pylori regimen. Zollinger–Ellison and severe erosive disease are specialty-led long-term indications — not a reason to put every 30-year-old with once-weekly heartburn on omeprazole forever.

De-escalation is the Evaluation skill. If uncomplicated GERD responded to a standard course, attempt step-down: on-demand PPI, a switch to an H2-receptor antagonist (famotidine is the usual adult example), or a stop-and-watch plan with lifestyle measures. Document why a patient remains on a daily PPI at every periodic visit. Associated risks — C. difficile, hypomagnesemia, B12 deficiency, and fracture signals in long-term observational data — do not mean you withhold a PPI that is truly indicated. They do mean you do not refill it on autopilot.

H2RAs are weaker acid suppressors useful for milder or nocturnal symptoms and as a step-down landing spot. They are not equivalent to a PPI for severe erosive disease. Antacids (calcium carbonate, magnesium/aluminum combinations) treat breakthrough symptoms in minutes. Separate them from drugs whose absorption they bind or change — levothyroxine, fluoroquinolones, tetracyclines, iron. Counsel patients that antacids are not a diagnostic test: relief does not exclude cardiac pain or ulcer bleeding.

Lifestyle counseling is part of the prescription: elevate the head of the bed for nocturnal regurgitation, avoid late large meals, reduce trigger foods the individual actually reacts to (not a 20-item ban list), treat obesity as a reflux driver, and stop tobacco. Lifestyle does not replace endoscopy when alarms are present.

H. pylori: current U.S. first-line thinking

Do not memorize a 2008 clarithromycin triple as if resistance never happened. Clarithromycin resistance is common in the United States, so legacy PPI–clarithromycin–amoxicillin triple therapy is often the wrong first choice unless susceptibility is known. Teach this conceptual rule: use a current U.S. first-line regimen, often 14-day bismuth quadruple therapy — a PPI plus bismuth plus tetracycline plus metronidazole. Counsel dark stool and dark tongue from bismuth so the patient does not present to urgent care with “melena.” Tetracycline is not for pregnancy or young children. If a patient cannot use a component, choose another current guideline first-line option (some regions use rifabutin- or potassium-competitive acid blocker–based regimens); do not invent a two-drug cocktail.

Confirm eradication in everyone you treat — especially ulcer disease, persistent dyspepsia, MALT lymphoma, and resected early gastric cancer, and as routine good practice after any treatment. Use a urea breath test or stool antigen at least 4 weeks after antibiotics, with the PPI held about 1–2 weeks. Serology is not a test of cure. Symptom improvement is not proof of eradication. A failed first regimen needs a different second-line combination, preferably with susceptibility data, not a repeat of the same four pills.

Stop NSAIDs when PUD is the story, add PPI gastroprotection if an NSAID is unavoidable, and test for H. pylori in the ulcer patient even if NSAIDs look like the whole explanation — dual risk is common.

Antiemetics: QT, tardive dyskinesia, and short courses

Ondansetron is a 5-HT3 antagonist useful for acute gastroenteritis vomiting and many medication-related nauseas. It prolongs the QT interval. Avoid stacking it with other QT-prolonging drugs when you can, and be cautious in congenital long-QT, bradycardia, and electrolyte depletion. It is not a daily “upset stomach” vitamin.

Metoclopramide is a dopamine antagonist with prokinetic effect. It carries an FDA boxed warning for tardive dyskinesia, which can be irreversible. Do not write open-ended daily metoclopramide for “chronic nausea.” If gastroparesis truly needs a prokinetic, use the lowest dose for the shortest time (labeling warns against use beyond 12 weeks) and comanage with GI. Counsel patients to report new involuntary movements immediately.

Promethazine sedates and has anticholinergic and extrapyramidal effects; it is a poor first-line pediatric reflux drug and a fall risk in older adults. Vestibular nausea is a different pathway (meclizine or similar), not a reason to escalate ondansetron. Pregnancy nausea has its own first-line pair (doxylamine–pyridoxine) in Section 13.3 — do not jump to ondansetron before the indicated pregnancy sequence unless an obstetric plan already says so.

Loperamide is not for febrile or bloody diarrhea

Loperamide slows motility. It is reasonable for non-inflammatory, afebrile traveler’s or viral diarrhea in a reliable adult who can hydrate, after you have considered the differential. Do not use it when there is high fever, bloody stools, severe abdominal pain, suspected C. difficile, or a suspected IBD flare — you can worsen toxic megacolon and delay the right workup. High-dose loperamide abuse is a QT/QRS and dysrhythmia problem; that is not an FNP “just take more until it stops” instruction.

Hydration is the actual disease-modifying step in most acute gastroenteritis. Oral rehydration solution (ORS) with the right glucose–sodium pairing beats free water, juice, or sports drink in kids and in older adults at risk of hyponatremia. Antiemetics can enable ORS; they do not replace it. Antibiotics for watery community gastroenteritis are the exception, not the rule.

Laxative ladder

Treat constipation as a ladder, not a random drawer of bottles.

1. Fiber and hydration and activity. Increase dietary fiber gradually. A bulk agent (psyllium) needs adequate water or it becomes a plug. This is first-line for many chronic functional cases.
2. Osmotic laxative. Polyethylene glycol (PEG 3350) is the usual FNP first pharmacologic step — daily, titrated to soft stool, safe for longer use than stimulant cathartics. Lactulose is an alternative, including when hepatic encephalopathy is the other indication.
3. Stimulant (senna, bisacodyl) for rescue, opioid-induced constipation adjuncts, or short courses when the vault is full. Chronic daily stimulant-only therapy without a bowel regimen review is a failure of planning.
4. Secretagogues and specialized agents (linaclotide, lubiprostone, prucalopride, peripherally acting mu-opioid antagonists) are next-step or specialty tools after the ladder and after you have excluded obstruction and overflow.

Opioid-induced constipation needs a stimulant or a targeted agent from the start; fiber alone is not enough and can worsen a packed vault. Overflow diarrhea is treated by disimpaction, not by loperamide (Section 13.1).

5-ASA is GI-specialty IBD therapy

Mesalamine and other 5-aminosalicylates treat mild-to-moderate ulcerative colitis and have a limited Crohn role depending on location. The FNP recognizes the class, watches renal function, asks about paradoxical worsening or allergy, and does not start 5-ASA as a guess for “bloody diarrhea that might be IBS.” New suspected IBD is stool infection studies, labs, and GI referral. Thiopurines, methotrexate, biologics, and JAK inhibitors are specialty prescribing with infection and cancer-surveillance baggage — know that they exist and that live vaccines and untreated infection are problems; do not construct an induction regimen from a study-guide table.

Nutrition that actually changes outcomes

Oral rehydration is the nutrition intervention for gastroenteritis. Breastfed infants keep breastfeeding; formula-fed infants use ORS and resume formula. The “BRAT diet only for a week” instruction starves children and is outdated. Early return to an age-appropriate diet after ORS is the teaching point.

For IBS, a time-limited low-FODMAP trial with a dietitian can reduce fermentable-carbohydrate triggers. The trial is typically a few weeks, then structured reintroduction so the patient does not live on three foods and become deficient. Do not hand a 40-item “never eat” list and call it nutrition counseling. Soluble fiber (psyllium) helps many IBS-C and mixed patients; insoluble bran can worsen bloating.

A gluten-free diet is disease-modifying for celiac disease, necessary for wheat allergy, and sometimes used after non-celiac gluten sensitivity is diagnosed with celiac disease excluded. It is not a default wellness plan. Gluten-free packaged food is not automatically healthier, is expensive, and can be low in fiber and B vitamins. If celiac is confirmed, the diet is strict and lifelong, with dietitian teaching about hidden gluten and follow-up serology as GI directs.

Alcohol counseling belongs in every hepatitis, pancreatitis, and reflux visit. For chronic liver disease, skip herbal “liver cleanses.” For older adults, protein-energy intake and fiber plus water prevent the constipation–impaction cycle that Section 13.3 will treat as a geriatric emergency when it is ignored.

FNP vignette trap: the patient who “finished H. pylori triple therapy in 2014 and still has pain” needs a current regimen and a test of cure, not another clarithromycin script. The patient on omeprazole since a 2019 urgent-care visit with no Barrett’s and no ulcers needs a de-escalation conversation. The patient with bloody febrile diarrhea who wants “the diarrhea pill” needs stool testing and hydration, not loperamide.