GI medications

GI medication items ask whether you stop the vomiting safely, move the bowel without blowing a surgical belly, or recognize a drug-induced dystonia. Acid reducers, ulcer coating, and bleed priorities live in GI bleeding and obstruction. This chapter owns antiemetics and bowel motility agents.

Antiemetics: mechanism and bedside traps

Nausea pathways converge on the chemoreceptor trigger zone and vomiting center. Ondansetron (a 5-HT3 antagonist) blocks serotonin receptors that chemo and surgery light up - that is why it appears so often on oncology and PACU stems. It is usually well tolerated; the exam still cares about QT prolongation when the client is already on other QT-prolonging drugs or has electrolyte chaos. Teach that it treats nausea, not the underlying obstruction or raised ICP that may be causing it - always ask why the client is vomiting.

Metoclopramide is a prokinetic and dopamine antagonist. It helps gastroparesis and some nausea by increasing upper GI motility and raising lower esophageal sphincter tone. Because it blocks dopamine, it can produce extrapyramidal symptoms: acute dystonia (torticollis, oculogyric crisis, facial spasm), akathisia, and - with long exposure - tardive dyskinesia. Restlessness and muscle tightness after a dose are not “anxiety” to ignore. Hold the drug, protect the airway if needed, and expect ordered anticholinergic or antihistamine rescue per protocol. Elderly clients and prolonged courses raise risk.

Anticholinergic side effects show up across several GI symptom drugs: dry mouth, blurred vision, constipation, and urinary retention. On exams, stacking anticholinergic load onto BPH or glaucoma stems is intentional. Sedating antiemetics add fall risk. At the bedside, assess hydration after prolonged vomiting, check for abdominal distention that might mean obstruction rather than simple gastroenteritis, and clarify before giving a prokinetic into a suspected complete obstruction.

• Report dystonia, tongue thrusting, or severe restlessness after metoclopramide immediately.
• Do not assume every vomit needs an antiemetic - surgical belly and ICP have other first moves.
• Document response and sedation level after PRN doses.

Laxatives versus antidiarrheals

Constipation and diarrhea look opposite, but both fail exams when you pick the wrong direction of motility. Bulk-forming agents (psyllium) need adequate fluid or they can worsen obstruction-like bulk. Osmotics pull water into the lumen - useful for cleanouts and opioid constipation when ordered, with electrolyte watch on aggressive regimens. Stimulants increase peristalsis; softeners (docusate) ease passage by wetting stool and are common for strain prevention after surgery or MI when ordered. Match the agent to the goal: soften versus evacuate versus daily fiber habit.

Antidiarrheals such as loperamide slow gut transit so more water is absorbed. That is helpful for noninfectious functional diarrhea and dangerous when the bowel needs to clear invasive organisms or toxins. Bloody diarrhea, high fever, or suspected C. difficile patterns on stems usually mean hydrate, isolate as indicated, and avoid antimotility drugs unless the provider explicitly orders them. The distractor is “stop the diarrhea at all costs” while the toxin sits longer against the mucosa.

1. Assess last stool, abdomen, and surgical history before any laxative.
2. Teach opioid users that softeners/stimulants may be ordered prophylactically - constipation is expected pharmacology.
3. Rehydrate first in diarrhea; drugs are secondary to volume status.

When NOT to give a laxative

A laxative is contraindicated when increasing pressure or motility could perforate or worsen a closed-loop problem. Undiagnosed acute abdominal pain - especially with rebound, rigidity, fever, or bilious vomiting - is an obstruction or appendicitis pathway until cleared. Fecal impaction with overflow sometimes needs disimpaction rather than blind stimulants. Severe inflammatory bowel flares and post-op anastomoses follow surgeon orders, not PRN senna from the med cart. If the stem shows RLQ pain migrating from the umbilicus, the answer is NPO and surgical evaluation, not “relieve constipation.”

Prokinetics share the same logic: do not whip a bowel that may be ischemic or completely blocked. Clarify orders when imaging or surgical consult is pending. Acid suppression for ulcer and GI bleed risk is a different toolkit - see GI bleeding and obstruction for PPI and H2 teaching rather than expanding it here.

Lactulose and pancreatic enzymes

Lactulose is not “just another laxative” on hepatic encephalopathy stems. It acidifies gut contents so ammonia converts to ammonium and stays trapped, then drives evacuation so ammonia leaves in stool. Success is judged by mentation improving toward the ordered stool pattern (often soft, several stools daily) - not by watery dehydration. If the client is volume-depleted from overshoot diarrhea, hold and clarify rather than chasing more syrup. Mental status and ammonia trends belong with the liver chapter; here, own the drug purpose and titration logic.

Pancrelipase and related enzyme products replace lipase, protease, and amylase when the pancreas cannot. Take them with meals and snacks so enzymes meet food in the gut. Swallow delayed-release capsules whole or open onto soft food only if the label allows - crushing enteric-coated beads ruins the delivery system. Calcium carbonate or magnesium hydroxide antacids can interfere; separate as taught. Abdominal cramping can occur; steatorrhea that continues means the dose or timing needs a provider look, not a silent double dose.

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