pharm week 2

GERD (gastroesophageal reflux disease) occurs when stomach contents reflux upward into the esophagus, usually because the lower esophageal sphincter (LES) is weakened and does not close tightly. Acid irritates the esophageal mucosa and causes heartburn. Long-term complications can include esophagitis, esophageal ulcers, strictures, and Barrett's esophagus.

GERD — What is it?

Elevate the head of the bed; avoid fatty or acidic foods and known triggers; eat smaller meals; avoid eating close to bedtime; eliminate tobacco and alcohol; weight loss may improve symptoms when obesity contributes to GERD.

What lifestyle modifications help GERD?

A change/damage in the lining of the esophagus associated with chronic GERD. It is important because it is associated with an increased risk of esophageal cancer.

What is Barrett's esophagus?

An upper GI disorder involving erosion of the GI wall. It develops when aggressive factors overwhelm the protective defenses of the gastric/duodenal mucosa.

What is peptic ulcer disease (PUD)?

Mucus secretion, bicarbonate that neutralizes H⁺ ions, adequate blood flow, and prostaglandins. Prostaglandins help stimulate the protective mechanisms.

What are the major protective defenses of the gastric mucosa?

H. pylori, NSAIDs, gastric acid, pepsin, and smoking. NSAIDs contribute by inhibiting prostaglandin biosynthesis.

What are the major aggressive factors contributing to PUD?

→ pain is generally WORSE with food/eating and better with fasting. Duodenal ulcer → pain is generally BETTER with food and worse with fasting; nighttime pain is common.

Gastric ulcer vs. duodenal ulcer pain with food Gastric ulcer

H. pylori is a gram-negative bacterium that attacks the stomach and is thought to degrade the protective mucus layer. It can remain active for life if untreated and is strongly associated with PUD.

What is H. pylori?

Acid-reducing drugs have little or no effect on the H. pylori organism itself. Antibiotics are required to eradicate the bacterium. Eradication increases ulcer healing and decreases recurrence.

Why must antibiotics be used for H. pylori?

1. More than one antibiotic is used to reduce development of antibiotic resistance. 2. An acid-reducing medication such as a PPI or H2 blocker is included. 3. Treatment must continue long enough to eradicate the infection. You do NOT need to memorize the exact regimens from the PPT.

What are the 3 BIG rules to remember about H. pylori treatment?

Amoxicillin (Amoxil), bismuth (Pepto-Bismol), and metronidazole (Flagyl). The PPT also lists clarithromycin, tetracycline, and tinidazole, but those are not starred on this slide.

⭐ Which H. pylori drugs are starred in the PPT?

Bismuth can inhibit bacterial growth and prevent H. pylori from adhering to the gastric mucosa; the PPT also describes it as helping disrupt the cell wall of H. pylori.

What is the purpose of bismuth in H. pylori treatment?

Antibiotics for H. pylori; antisecretory agents including PPIs and H2-receptor antagonists; mucosal protectants; antisecretory drugs that enhance mucosal defenses; and antacids/buffers.

What are the major classes of antiulcer medications?

They inhibit gastric acid secretion by blocking histamine's effects at H2 receptors. H2 receptors in the stomach promote acid secretion, so blocking them decreases the volume and acidity of parietal-cell secretions.

What do H2-receptor antagonists/H2 blockers do?

H1 = allergies/inflammation. H2 = GI/gastric acid secretion. The PPT specifically says: “H1 = allergies; H2 = GI distress.”

Easy way to remember H1 vs. H2 receptors

H. pylori multidrug therapy, decreasing painful PUD symptoms and complications, NSAID-ulcer prophylaxis, heartburn/GERD, and hypersecretory conditions such as Zollinger-Ellison syndrome.

What are the uses of H2 blockers?

Cimetidine (Tagamet), ranitidine (Zantac), and famotidine (Pepcid)* are starred. Nizatidine (Axid) is listed but not starred. Know both the CLASS and the STARRED drugs.

⭐ Which H2 blockers must I know?

Confusion.

What important adverse effect is associated with cimetidine in older adults?

Cimetidine inhibits cytochrome P450, which can decrease the clearance of many other medications and therefore cause important drug interactions.

What important drug interaction occurs with cimetidine?

Antacids can diminish absorption of the H2-receptor antagonist. The PPT says to avoid antacids for about 1 hour before the H2 blocker.

Why should antacids NOT be taken at the same time as an H2 blocker?

The PPT notes blood dyscrasias and some risk of pneumonia. Reduced gastric acidity can increase colonization of the stomach and respiratory tract.

What other cautions are associated with H2 blockers?

Omeprazole (Prilosec)*. Other PPIs listed are esomeprazole, lansoprazole, rabeprazole, and pantoprazole. Know the PPI CLASS and starred omeprazole.

⭐ What PPI does the professor specifically want us to know?

PPIs suppress gastric acid secretion by irreversibly binding to H⁺/K⁺-ATPase, the proton pump responsible for releasing H⁺/acid onto the GI mucosal surface. They suppress acid more strongly and for longer than H2 blockers.

What is the mechanism of action of PPIs?

Food activates the proton pumps. Therefore, PPIs should be administered about 20–30 minutes before the first major meal of the day so the medication is present when the pumps become activated.

Why are PPIs given BEFORE eating?

Active PUD, erosive esophagitis, GERD, prophylactic treatment of PUD, and prevention of NSAID-induced ulcers.

What are the major uses of PPIs?

Headache, abdominal pain, diarrhea, nausea, and vomiting are among the commonly reported effects.

What are common adverse effects of PPIs?

The PPT emphasizes fracture/osteoporosis risk, pneumonia, intestinal infection, acid rebound, hypomagnesemia/hypocalcemia, and vitamin B12 deficiency with prolonged therapy.

What are important risks of LONG-TERM PPI therapy?

Use the lowest effective dose for the shortest necessary duration. Long-term therapy may require monitoring such as magnesium/B12 levels or bone density depending on the situation. Abrupt discontinuation may cause rebound acid hypersecretion.

What is an important principle for long-term PPI use?

Sucralfate (Carafate)*.

⭐ What mucosal protectant must I know?

Sucralfate is a local cytoprotective/mucosal protectant. It forms a thick protective barrier that adheres to the mucosal/ulcer surface, protecting it from further injury and promoting healing.

What is the action of sucralfate?

NO. Sucralfate protects the ulcer surface but does NOT neutralize acid and does NOT suppress gastric acid secretion. Think: sucralfate = SHIELD, not acid stopper.

CRITICAL: Does sucralfate decrease or neutralize stomach acid?

Short-term treatment of duodenal and gastric ulcers, prevention of stress ulcers, and relief of pain from oral/mucosal ulcers.

What are uses of sucralfate?

Constipation is a notable adverse effect. Because very little drug is absorbed from the GI tract, systemic adverse effects are relatively limited.

What adverse effect is associated with sucralfate?

It may harden with enteral feedings; there is a risk of aluminum toxicity; and the PPT instructs giving non-aluminum-based antacids 30 minutes before or after sucralfate. A disadvantage is that sucralfate must be taken four times daily.

What important nursing considerations apply to sucralfate?

Antacids are alkaline substances that neutralize existing gastric acid. They provide relatively rapid symptomatic relief but do not eradicate H. pylori and are no longer the primary treatment for PUD.

How do antacids work?

Sodium bicarbonate is classified as systemic and may cause electrolyte imbalance; the PPT states it is inappropriate for PUD treatment. Calcium carbonate, magnesium hydroxide, and aluminum hydroxide are classified as nonsystemic/local antacids.

What is the difference between systemic and nonsystemic antacids in the PPT?

Magnesium hydroxide (Milk of Magnesia), aluminum hydroxide (Amphojel), and calcium carbonate (Tums)*.

⭐ Which antacids must I know?

Magnesium = diarrhea/defecation. Magnesium hydroxide has high acid-neutralizing capacity and promotes defecation/diarrhea. It is often combined with aluminum to reduce diarrhea.

MAGNESIUM antacid = what bowel effect?

Aluminum = constipation. Aluminum hydroxide has relatively low acid-neutralizing capacity and can delay gastric emptying.

ALUMINUM antacid = what bowel effect?

Calcium can cause constipation. Calcium carbonate has high acid-neutralizing capacity and may cause acid rebound.

CALCIUM antacid = what bowel effect?

Easy antacid memory trick MAGnesium = makes you GO. ALuminum = ALways stops you up. Calcium = constipation too. The PPT specifically identifies diarrhea with magnesium and constipation with calcium/aluminum.

Liquid suspensions are the most effective. Chewable tablets must be thoroughly chewed and followed with a glass of water.

Which antacid formulation is most effective?

1. Fiber/bulk-forming supplements, 2. stool softeners, 3. osmotic agents, 4. lubricants, and 5. stimulants. Fiber supplements and stool softeners are often used to PREVENT constipation; the other categories are generally used to TREAT constipation.

What are the 5 major categories of laxatives in Chapter 7?

Bulk-forming laxative prototype + mechanism Psyllium (Metamucil). It adds bulk to the stool, facilitating passage through the rectum.

Mix each dose with at least 8 oz of water/fluid and drink promptly. Taking it without enough liquid can cause choking.

What is the BIG safety teaching for psyllium?

It can affect medication absorption. Chapter 7 says administer it at least 2 hours before or 2 hours after other medications.

Why should psyllium be separated from other medications?

Usually produces a bowel movement within 12–72 hours. It may cause bloating and cramping.

How quickly does psyllium work?

. It facilitates movement of water and fats into the stool, softening the stool and making it easier to pass.

Stool softener prototype + mechanism Docusate (Colace)

Usually within 12–72 hours. Potential effects include abdominal cramping; stool softeners can also cause diarrhea, nausea/vomiting, and electrolyte imbalance in some clients.

How quickly does docusate work?

they should not be used in individuals with intestinal blockages.

When should stool softeners NOT be used?

Osmotic agents retain water with the stool, which softens stool and increases bowel movements.

Osmotic laxative prototypes + mechanism Milk of Magnesia and polyethylene glycol (PEG) 3350/MiraLAX.

Important adverse effects of osmotic laxatives Diarrhea, abdominal cramping, electrolyte imbalance, dehydration, and possible allergic reactions.

Lubricants coat the stool and help seal water into it, making passage easier.

Lubricant laxative prototype + mechanism Mineral oil enema.

Stimulants cause intestinal contractions that move stool through the colon.

Stimulant laxative prototype + mechanism Bisacodyl (Dulcolax).

Adequate dietary fiber, plenty of water/fluids, regular physical activity, and trying to have a bowel movement at approximately the same time each day.

What nonpharmacologic measures should nurses teach to prevent constipation?

Complete absence of bowel sounds, worsening abdominal distention/pain, stool smearing, or other findings suggesting paralytic ileus or intestinal blockage.

What constipation findings require immediate provider notification?

In the medulla of the brain. Multiple neurotransmitters participate in nausea/vomiting, which is why different antiemetic classes target different receptors.

Where is the vomiting center located?

Know this antiemetic receptor map M1/ACh → scopolamine; H1/histamine → meclizine; DA2/dopamine → prochlorperazine; DA2 + M1 → metoclopramide; 5-HT/serotonin → ondansetron; NK1/substance P → aprepitant; CB1 → dronabinol/THC.

Blocks acetylcholine receptors in the vestibular system/brain, preventing nausea-inducing stimuli from reaching the CTZ and vomiting center. Used primarily for motion sickness and postoperative nausea/vomiting.

Scopolamine — class + mechanism + use Anticholinergic.

Scopolamine — major contraindication Glaucoma.

important adverse effects Anticholinergic effects including decreased GI motility and urinary retention; it can also cause drowsiness, confusion, and sedation and may exacerbate psychosis or induce seizures.

Scopolamine —

Scopolamine patch nursing teaching Apply to hairless/intact skin behind the ear; do not cut the patch; wash and dry hands thoroughly after application; remove before MRI.

Meclizine — class + use Antihistamine/H1 blocker used to prevent or reduce nausea and vomiting from motion sickness. It should be started about 1 hour before travel and may cause drowsiness.

important contraindications Glaucoma or an enlarged prostate gland.

Meclizine

Blocks dopamine in the chemoreceptor trigger zone (CTZ) and may also block acetylcholine.

Prochlorperazine — class + mechanism Dopamine antagonist.

It blocks dopamine in the CTZ while stimulating acetylcholine in the GI tract.

Metoclopramide — class + mechanism Prokinetic antiemetic.

Tardive dyskinesia and neuroleptic malignant syndrome are serious reactions identified in Chapter 7 and require discontinuation/urgent evaluation.

What SERIOUS reactions should be watched for with metoclopramide?

It blocks serotonin in the GI tract, CTZ, and vomiting center.

Ondansetron — class + mechanism Serotonin/5-HT antagonist.

Prevention/treatment of severe nausea and vomiting associated with surgery and chemotherapy; Chapter 7 also lists hyperemesis in pregnancy.

Ondansetron — major uses

Cause of nausea/vomiting; frequency and amount of emesis; appetite/fluid intake; and dehydration indicators such as decreased BP with tachycardia, decreased skin turgor, decreased urine output, and dark/concentrated urine. Ordered labs may include hemoglobin, hematocrit, and serum sodium.

What should the nurse assess in a patient receiving antiemetics?

Take frequent sips of clear fluids if liquids are difficult to tolerate; eat bland foods; avoid spicy, fatty, or salty foods; eat smaller meals more often; and avoid strong smells that trigger nausea.

What non-drug teaching can reduce nausea?

Gather → Document → Compare → Decide → Communicate. Gather a complete list of current prescriptions, OTC medications, vitamins, and herbals; document newly ordered medications; compare the lists; decide how discrepancies should be resolved; communicate the final updated list to the patient/caregiver and healthcare team.

What are the 5 steps of medication reconciliation?

Prescription medications, OTC drugs, vitamins, and herbal supplements—not just prescription medications.

What medications/substances must be included during medication reconciliation?

Drug name and therapeutic category, dose, schedule, route and administration technique, expected therapeutic response and when it should occur, duration, storage, major drug-drug and drug-food interactions, nondrug measures, what to do for adverse/allergic reactions, and whom to contact if treatment fails.

What should medication patient/family teaching include?

It can simplify the medication regimen and provide a clear schedule the patient can carry and follow, particularly when several medications are involved.

Why can a medication schedule/grid help a patient?

To detect, evaluate, prevent, and mitigate adverse events associated with medications that have the potential to cause serious adverse reactions.

What is the goal of FDA drug risk-management programs?

Patient package inserts, medication guides, restricted-access programs, classification of drugs as controlled substances, and Risk Minimization Action Plans (RiskMAPs).

What were examples of earlier FDA risk-management approaches?

The product's benefits and risks, a strategy for minimizing those risks, and information on how to use the medication safely and effectively. Healthcare providers and patients should be educated about the strategy.

What should a drug risk-minimization plan identify?

A structured database used to track and monitor patients taking certain medications, especially high-risk medications with serious adverse effects or strict safety requirements.

What is a drug registry?

Monitor patient safety/adverse effects, ensure REMS compliance, collect real-world information about medication effectiveness, and support research and post-marketing surveillance.

What are the major purposes of drug registries?

Drug registries specifically monitor the real-world effects of medications in patients and add long-term information beyond clinical-trial data.

How are drug registries different from general patient registries?

iPLEDGE for isotretinoin, thalidomide REMS, opioid REMS, and pregnancy registries that monitor medications and vaccines.

What are examples of registries/REMS programs from the PPT?

Educate patients about the registry and required monitoring; verify compliance before administering/dispensing medications when applicable; and help patients adhere by coordinating laboratory testing and follow-up care.

What are nursing responsibilities involving drug registries?

REMS may require regular laboratory testing, pregnancy monitoring, or restricted pharmacy dispensing. Transportation and financial limitations can make these requirements difficult. Family, caregivers, or case managers may be needed to support adherence.

How can social factors interfere with REMS requirements?

Pregnancy increases kidney clearance, which can affect drug dosing.

How does pregnancy affect renal handling of drugs?

The PPT states that liver metabolism increases during pregnancy, which can affect drug dosing.

How does pregnancy affect hepatic drug handling?

The PPT states that GI tone decreases during pregnancy.

How does pregnancy affect the GI tract?

The PPT instructs you to assume all drugs cross the placenta to some extent.

Do medications cross the placenta?

Lipid-soluble drugs cross more easily.

What types of drugs cross the placenta more easily?

Ionized drugs, highly polar drugs, and protein-bound drugs cross with greater difficulty. However, the PPT emphasizes assuming all drugs cross to some extent.

What characteristics make placental transfer more difficult?

A drug bound to a blood protein such as albumin forms a drug-protein complex that may not readily permeate. The unbound/free drug particles are the ones available for processes such as metabolism and transfer.

Why does protein binding reduce placental drug transfer?

The PPT identifies teratogenesis/birth defects, uterine stimulation, uterine suppression, drug-dependent infants, and neonatal respiratory suppression from CNS medications.

What types of adverse drug effects can occur during pregnancy?