gi alterations

Acid-peptic disorders are primarily driven by the overproduction of — or

of hydrochloric acid (HCl) or the breakdown of the mucosal barrier.

PUD involves what

the ulceration of the gastric or duodenal mucosa.

• Mechanism of PUD

• : Gastric acid (HCl) and pepsin (a proteolytic enzyme) break down the GI mucosa. Pepsinogen, secreted by chief cells, is converted to pepsin in the presence of HCl produced by parietal cells.

primary causative agent for PUD

• Helicobacter pylori: This bacterium is a primary causative agent for PUD.

whats the treatment for PUD

• H. pylori Triple Therapy: A standard 14-day regimen includes a Proton Pump Inhibitor (PPI), two antibiotics (Tetracycline and Metronidazole), and bismuth (which coats the mucosa). Adherence to the full 14-day course is critical for eradication.

—are two different ways the stomach lining gets damaged by acid and pepsin

Peptic Ulcer Disease (PUD) and Stress-Related Mucosal Damage (SRMD)

GERD is characterized by the

backflow of acidic stomach contents into the esophagus, leading to erosion and hyperacidity.

what is the LES and how does it relate to GERD

The LES is a smooth muscle ring located at the bottom of the esophagus that serves as the primary defense mechanism preventing stomach acid from flowing backward. Lower Esophageal Sphincter (LES) Dysfunction:

• Transient LES Relaxation: Involuntary, spontaneous relaxations unlinked to swallowing.

• Hypotensive LES: Permanently low baseline pressure in the LES muscle.

• Anatomic Disruption: The upper stomach slides above the diaphragm, reducing the LES pressure barrier.

• Impaired Acid Clearance:

• Reduced peristalsis or insufficient salivary bicarbonate (which normally neutralizes trace acids) increases acid contact time.

• Delayed Gastric Emptying:

• Food sitting in the stomach too long increases intragastric pressure, eventually overriding the LES.

famotidine class MOA Adverse, NI

H2 Receptor Antagonist , Blocks H2 receptors on parietal cells, reducing both basal and stimulated acid secretion , Confusion in elderly/renally impaired, Give before meals. Monitor renal function. Avoid irritants (alcohol, caffeine, spicy foods).

Omeprazole

Proton Pump Inhibitor (PPI), Irreversibly binds to H+/K+ ATPase pump in parietal cells, blocking the final step of acid production, Headache, GI upset. Long-term risks: fractures (calcium malabsorption), B12 deficiency, C. diff, pneumonia, Give before meals (usually breakfast). Do not crush/chew extended-release forms. Monitor magnesium/B12 in long-term use.

Aluminum, Magnesium, or Calcium Salts, class, MOA, Adverse, NI

Antacids, Directly neutralizes existing stomach acid; raises gastric pH. Does not reduce acid production. , Aluminum: Constipation. Magnesium: Diarrhea. Calcium: Constipation, milk-alkali syndrome., Separate from other oral meds by 1–2 hours (antacids bind drugs). Contraindicated in Renal Failure (risk of hypermagnesemia).

Sucralfate / Misoprostol class, MOA, Adverse, NI

Cytoprotective Agents, Sucralfate: Forms sticky gel barrier over ulcers. Misoprostol: Increases mucus/bicarbonate.

Misoprostol: GI distress.Misoprostol is contraindicated in pregnancy (prostaglandin analog).

Constipation is the

abnormally infrequent or difficult passage of feces. It is a symptom of an underlying issue rather than a disease itself.

causes of constipation

Lifestyle, Diet, Metabolic/Endocrine, Neurogenic, Drugs

Diarrhea is characterized by

an increase in the frequency, fluidity, and weight of stools.

• Acute Diarrhea: example

• Sudden onset, lasting 3 days to 2 weeks. Causes include bacteria, viruses, drug effects, and nutrition.

• Chronic Diarrhea:

• Lasts longer than 3–4 weeks. Causes include IBS, AIDS, tumors, and endocrine disorders (Addison’s, hyperthyroidism).

• Clinical Risk: of diarrhea

• Severe diarrhea can lead to fluid volume depletion and electrolyte imbalances.

Psyllium class , MOA, Implications, Education

Bulk-Forming, Absorbs water to increase stool volume and softness; stimulates peristalsis.Must be taken with at least 8 oz of fluid to prevent esophageal/bowel obstruction. Slower onset (12–72 hours).

Docusate Sodium class, moa, implications

Emollient (Stool Softener), Lowers surface tension, allowing water/fat to penetrate and soften stool ,Prophylactic use (e.g., post-op, heart patients) to prevent straining. Does not cause immediate urgency.

Bisacodyl class, MOA, indications

Stimulant, Irritates intestinal wall nerves to increase peristalsis, Short-term use only (risk of dependence). Do not take within 1 hour of antacids or milk.

Milk of Magnesia (Magnesium Hydroxide)

Osmotic (Saline), Draws water into the lumen via osmosis to increase bulk and peristalsis., Use cautiously in renal impairment (magnesium toxicity risk). Onset 30 mins to 6 hours.

Polyethylene Glycol (PEG)

Osmotic (Gentle), Holds water in stool through osmosis without significantly altering electrolytes., Mix powder in 4–8 oz of liquid. Onset is typically 1–3 days.

Diphenoxylate w/ Atropine

Antidiarrheal (Opioid), Slows GI motility and peristalsis. Atropine added to discourage abuse., Do not use for infectious diarrhea (e.g., C. diff, E. coli) as it traps toxins, risking toxic megacolon.

Loperamide

Antidiarrheal (Opioid-OTC), Binds GI opioid receptors to slow peristalsis; does not cross blood-brain barrier.,Stop and seek care if diarrhea persists >48 hours or fever develops.

Lactobacillus

Probiotic , Restores normal gut flora to outcompete pathogens and support the mucosal barrier., Often used post-antibiotics. Space doses apart from antibiotics by a couple of hours.

Describe the nursing plan of care for a client experiencing constipation.

Before giving any kind of bowel affecting medication → obtain a thorough patient history

and assess bowel movement patterns, general health status, recent illness history, GI concerns

and any recent dietary changes

Perform physical assessment of auscultation of bowel sounds in all four quadrants after

inspection and before any kind of percussion/palpatation (note tenderness/ridgidity, contour,

bulges, color. Assess bowel movements for any changes in frequency, color, texture, odor,

and document

Assess vital signs, weights, I/O, and fluid volume depletion, if any, and document any

findings in the patient chart

Educate the patient that the drugs (if they are given any) must be taken exactly as prescribed

with strict adherence to any recommended dosages