comfort drugs and oxygenation

Somatic nociceptive pain

Tissue injury; sharp and localized.

Visceral nociceptive pain

Tissue injury in organs; dull, throbbing, or aching.

Neuropathic pain: helpful adjuvants

Antiseizure drugs and antidepressants; ordinary analgesics may work poorly.

Nonopioid analgesics: site/action

Act at the nociceptor level.

Opiate vs opioid

Opiates are natural opium-containing substances; opioids include natural or synthetic opiate-like drugs.

Pain-relevant opioid receptors

Mu and kappa are most important for analgesia; delta is another opioid receptor.

Mixed opioid agonist-antagonist

Activates one opioid receptor while blocking or having no effect at another; examples: buprenorphine, butorphanol.

Morphine: action

Binds mu and kappa receptors to produce profound analgesia.

Morphine: uses

Moderate to severe pain; vasodilation may be useful in acute MI or heart failure.

Morphine: adverse effects

Nausea, vomiting, constipation, itching, dysphoria, hallucinations, euphoria, and respiratory depression in overdose.

Morphine: other effects/risks

Miosis, tolerance, physical and psychological dependence, and abuse potential; epidural route has a black-box warning.

Naloxone: action/use

Blocks mu and kappa receptors; rapidly reverses opioid effects, including overdose-related respiratory depression.

Intranasal naloxone: onset and peak

Onset about 2–5 minutes; peak about 15–30 minutes.

Opioid use disorder: treatment options

Methadone; buprenorphine/naloxone; or naltrexone.

Aspirin: action

Inhibits prostaglandin synthesis and platelet aggregation.

Aspirin: uses

Pain, inflammation, fever, and MI/CVA prevention.

Aspirin: toxicity/adverse effect

High doses can cause tinnitus and GI bleeding.

Aspirin interactions

May potentiate oral hypoglycemics; garlic, ginger, ginkgo, and feverfew can increase bleeding risk.

Acetaminophen: actions

Analgesic and antipyretic; acts on the hypothalamus and promotes heat loss via peripheral vasodilation and sweating.

Acetaminophen: interactions

Potentiates warfarin; avoid alcohol and other hepatotoxic drugs.

Acetaminophen overdose antidote

IV acetylcysteine.

GERD: underlying problem

Weak or incompetent lower esophageal sphincter (LES) allows acidic stomach contents to reflux into the esophagus.

GERD: pH comparison

Esophageal/LES pH about 6–7; stomach pH about 1–2.

GERD: contributing factors in slides

Obesity, nasogastric tube, pyloric stenosis, and motility problems.

GERD: possible complications

Aspiration pneumonia, esophagitis, esophageal ulcers or strictures, and Barrett’s esophagus.

GERD: symptoms

Heartburn, dyspepsia, regurgitation, dysphagia, and odynophagia.

Odynophagia

Painful swallowing.

GERD lifestyle teaching

Small, frequent, low-fat meals; avoid irritants/triggers; lose weight if indicated; elevate HOB; no food for 2 hours before bedtime.

GERD triggers listed in slides

Caffeine, tobacco, alcohol, milk, chocolate, peppermint, and carbonated drinks.

GERD: medication classes

H2 blockers, PPIs, antacids, and prokinetics; fundoplication is a surgical option.

GERD H2 blocker examples

Famotidine and ranitidine.

GERD PPI examples

Omeprazole and pantoprazole; reduce gastric acid release.

GERD prokinetic example

Metoclopramide; accelerates gastric emptying.

Gastric acid: source

Parietal cells secrete hydrochloric acid.

Stomach pH

About 1.5–3.5; highly acidic to support chemical digestion.

Gastric mucosal protection

Thick mucus and bicarbonate protect the stomach lining from acid.

Gastric vs duodenal ulcer location

Gastric ulcers occur in the stomach; duodenal ulcers occur in the small intestine.

PUD: other risk factors

Family history, blood type O, smoking, caffeine, corticosteroids, platelet inhibitors, stress, Crohn’s disease, ulcerative colitis, excess acid, or inadequate mucus.

Gastric ulcer: associated findings

Delayed gastric emptying, poor appetite/malnourished appearance, vomiting may relieve pain, hematemesis; association with cancer.

Duodenal ulcer: typical pattern

More common at ages 30–50; right epigastric, gnawing/burning pain 1–3 hours after meals or at night.

Duodenal ulcer: food effect

Food often relieves pain; patient may appear well nourished.

PUD medication groups

PPIs, H2 blockers, and antibiotics when H. pylori is present.

H. pylori: typical regimen

14-day combination therapy with at least two antibiotics, often plus a PPI and bismuth.

H. pylori: why combine antibiotics?

Improves eradication and reduces resistance risk.

Bismuth in H. pylori therapy

Inhibits bacterial growth and interferes with H. pylori adherence to gastric mucosa.

H. pylori: why complete eradication matters

Untreated infection can persist for life; recurrence is high if not eradicated and infection raises gastric cancer risk.

Omeprazole: action

Reduces gastric acid secretion by inhibiting the H+/K+ pump.

Omeprazole: uses

Short-term, typically 4–8 weeks, for GERD or peptic ulcers.

Omeprazole: administration

Give 20–30 minutes before meals.

Omeprazole: common adverse effects

Headache, nausea, diarrhea, rash, and abdominal pain.

Long-term PPI risks in slides

Hypomagnesemia, osteoporosis, and increased gastric cancer risk.

PPI interaction concern

Higher gastric pH can alter absorption of drugs that require an acidic environment.

Famotidine: action

Blocks gastric H2 receptors to decrease acid production.

Famotidine: uses

PUD, GERD, gastric ulcers, and hypersecretory states.

Famotidine: cautions/adverse effects

Use caution in CKD; may reduce RBCs, WBCs, platelets, libido, and B12 absorption.

Antacid: aluminum hydroxide action

Neutralizes stomach acid by raising gastric pH.

Aluminum hydroxide: use/adverse effect

Relieves heartburn as adjunct therapy; high doses may cause constipation.

Antacid administration spacing

Give 2 hours before or after other medications because absorption may be affected.

IBS: defining feature

Functional bowel disorder: symptoms occur without detectable structural disease.

IBS: symptoms

Abdominal pain, bloating, gas, colicky cramps, constipation alternating with diarrhea, and mucus in stool.

IBS-C: lubiprostone/linaclotide

Options for constipation-predominant IBS; linaclotide increases intestinal water and transit and can reduce bloating/constipation.

IBS-D: loperamide/eluxadoline

Options for diarrhea-predominant IBS; loperamide slows transit, and eluxadoline acts on opioid receptors to slow contractions.

Dicyclomine for IBS

Anticholinergic that reduces bowel spasm.

Ondansetron for IBS-D

May reduce nausea and slow intestinal transit.

Amitriptyline/doxepin for IBS

Tricyclic antidepressants used off-label for pain.

Ulcerative colitis: location/depth

Inflammatory bowel disease limited to the large intestine lining; surgery can be curative.

Crohn’s disease: location/depth

Often affects terminal ileum but can occur anywhere; may involve all bowel-wall layers.

Crohn’s after surgery

Disease tends to recur.

IBD: contributing factors listed

Genetic immune dysregulation, smoking, NSAIDs, and stress.

UC: common manifestations

Cramping, frequent bowel movements, bloody diarrhea, fever, dehydration, and weight loss.

Crohn’s: common manifestations

Abdominal pain/cramps, diarrhea, and bloody stools.

IBD management: lifestyle

Low-fiber diet, avoid smoking, reduce stress, and avoid very hot or cold foods.

IBD medication groups

Antibiotics such as metronidazole, steroids, 5-ASA drugs, and immunosuppressants/biologics.

5-ASA drugs: action (sulfonamide sulfasalazine, olsalazine, mesalamine

Reduce colonic inflammation by inhibiting prostaglandins and leukotrienes.

5-ASA examples

Sulfasalazine, olsalazine, and mesalamine.

IBD corticosteroids

Potent anti-inflammatories; use the shortest course needed to achieve remission due to long-term risks.

IBD immunosuppressant examples

Azathioprine, methotrexate, and infliximab.

Sulfasalazine: uses

Mild to moderate UC symptoms; also used off-label for Crohn’s disease and rheumatoid arthritis.

Sulfasalazine: adverse effects

Nausea, vomiting, diarrhea, abdominal pain, rash, and Stevens–Johnson syndrome.

Sulfasalazine: contraindications

Sulfa allergy, aspirin allergy, or hepatic impairment.

Nausea

Subjective feeling that may include weakness, sweating, and increased salivation; may precede vomiting.

Vomiting: control centers

Medulla and chemoreceptor trigger zone (CTZ) in the cerebral cortex.

Ondansetron: action

Blocks serotonin receptors in the GI tract and CTZ to prevent nausea/vomiting.

Ondansetron: common adverse effects

Headache, drowsiness, and dizziness; relatively few adverse effects in slides.

Ondansetron oral timing

Onset about 30 minutes; peak about 2 hours; duration 2–7 hours.

Constipation: definition

Fewer than 3 bowel movements per week with hard/dry stool or incomplete evacuation.

Laxative vs cathartic

Laxatives promote bowel movement frequency/quality; cathartics produce stronger, more complete emptying.

Bulk-forming laxatives

Fiber absorbs water and increases stool bulk.

Saline cathartics

Osmotically pull water into the intestine.

Stimulant laxatives

Promote peristalsis.

Surfactant/stool softener laxatives

Increase water and fat in stool; commonly used for prevention.

Senna

Herbal stimulant that irritates the bowel and increases peristalsis.

Peripheral opioid antagonists for constipation

Block opioid receptors in the large intestine without crossing the blood-brain barrier.

Mineral oil

Lubricates stool and colonic mucosa.

Psyllium: action/use

Insoluble fiber swells in the colon, increasing fecal mass; used for constipation, fiber supplementation, and cholesterol reduction.

Psyllium: administration/safety

Mix with at least 8 oz water or juice; inadequate fluid may cause cramping.

Diarrhea: mechanism

Colon fails to reabsorb enough water, increasing stool frequency and fluidity.

Prolonged diarrhea: major risks

Fluid, electrolyte, and acid-base imbalance; monitor frequently.

Persistent diarrhea: concern

May be related to pseudomembranous colitis.

Mild diarrhea medication options

Loperamide, bismuth subsalicylate, psyllium, and probiotics.