PPIs Β· H2 Blockers Β· Antiemetics Β· GI Protectant Β· GI Stimulant Β· Statins Β· Miscellaneous Antilipidemics
NG-203PHARM Β· GI + LIPIDSSeries: NCLEX Drug Review 5 of 8ADHD-friendly visual edition
Two systems, one page. The GI half is a tour of the stomach: turn acid off at the pump, turn it down at the receptor, coat what is already damaged, and move the contents along. The lipid half is about interrupting cholesterol in three different places β made in the liver, absorbed in the gut, or recycled through bile. Match each drug to its physical location and the side effects follow automatically.
π Brand β generic β the pairs NCLEX actually asks
Group
Brand
Generic
Proton pump inhibitors
Nexium
esomeprazole
Prilosec
omeprazole
Protonix
pantoprazole
H2 receptor antagonists
Pepcid
famotidine
Zantac
ranitidine see note
Antiemetics
Phenergan
promethazine
Zofran
ondansetron
GI protectant
Carafate
sucralfate
GI stimulant
Reglan
metoclopramide
Statins
Crestor
rosuvastatin
Lipitor
atorvastatin
Zocor
simvastatin
Cholesterol absorption inhibitor
Zetia
ezetimibe
Fibric acid derivatives
TriCor
fenofibrate
Lopid
gemfibrozil
Bile acid sequestrant
Questran
cholestyramine
β οΈ Note on ranitidine (Zantac). It appears on most older drug sheets, but ranitidine products were withdrawn from the United States market in 2020 after an impurity (NDMA) was found. Learn it as the classic H2-blocker example, and know that famotidine is the one you will actually give.
π½οΈ The map β where every GI drug on this page acts
π§ Off, down, coat, move. PPI turns acid off Β· H2 blocker turns it down Β· sucralfate coats the damage Β· metoclopramide moves the contents on.
βοΈ
ACTION β HOW EACH ONE WORKS
STEP 2 Β· MECHANISM
Acid, nausea, mucosal repair, motility β then the three interruption points for cholesterol.
π Proton pump inhibitors β "-prazole"
Action: block the final common step of gastric acid production β the HβΊ/KβΊ-ATPase proton pump on the parietal cell. Whatever the stimulus (histamine, gastrin, acetylcholine, food), the last door is shut.
π― Used for GERD, peptic and duodenal ulcers, as part of H. pylori regimens, and to protect a stressed stomach.
β° Most oral PPIs work best taken before a meal β commonly about 30 to 60 minutes before the first meal of the day.
π Delayed-release capsules and tablets are swallowed whole; do not crush or chew.
π§ "PRAZOLE = pump." Off at the source, so it is the strongest acid suppression on this page.
π¦ H2 receptor antagonists β "-tidine"
Action: competitively inhibit histamine at H2 receptor sites on the parietal cell β less acid secretion, especially the nocturnal and basal output.
π Weaker and shorter-acting than a PPI, but faster to start working.
π Often dosed with or after meals and at bedtime.
π§ Older adults with renal impairment can become confused on H2 blockers β dose is adjusted for kidney function.
π§ Dimmer switch vs off switch. H2 blocker = dimmer. PPI = off switch.
π€’ Antiemetics β the nausea pathway and where each drug plugs in
π§ "Setron stops serotonin; Phenergan parks dopamine." Different receptors is why they can be used together when one alone is not enough.
β οΈ Sucralfate needs an acid environment to form its paste and it binds other drugs. It is given on an empty stomach, typically about an hour before meals and at bedtime, and other oral medicines are separated from it β commonly by about two hours. Check the specific product and facility guidance.
β‘οΈ Metoclopramide β the prokinetic
Action: increases the resting tone of the lower esophageal sphincter and promotes gastric emptying and intestinal transit. It also blocks dopamine in the CTZ, so it works as an antiemetic.
π½οΈ Used for diabetic gastroparesis, GERD and nausea when the stomach is not emptying.
β° Usually given before meals and at bedtime.
β οΈ Boxed warning: tardive dyskinesia. Risk rises with duration and cumulative dose, and the movements can be irreversible. Treatment is generally kept short β commonly no more than about 12 weeks.
πͺ Statins β cutting cholesterol production at the top of the assembly line
π§ "Statins stop the START." HMG-CoA reductase is an early step, so blocking it shuts the whole line down.
𧬠The other three lipid drugs β three different addresses
π§ "Made, absorbed, recycled." Statins stop cholesterol being made; ezetimibe stops it being absorbed; cholestyramine stops bile acids being recycled; fibrates target triglycerides.
π Which lipid drug moves which number
π§ Statin for LDL, fibrate for triglycerides. That single sentence answers most lipid-drug selection questions.
π¦ Where acid drugs fit in H. pylori treatment
Ulcer disease is frequently caused by Helicobacter pylori. Acid suppression alone will not cure it β the organism must be treated with antibiotics as well.
π Regimens combine a PPI with two or more antibiotics, sometimes with bismuth. The exact combination varies by guideline and local resistance.
β³ Finish the entire course β stopping early is the main reason treatment fails.
π§ͺ Confirmation of eradication is done after therapy, per the prescriber's plan.
π§ Acid drugs heal the crater; antibiotics remove the cause. Ulcer questions often hinge on knowing you need both.
π§ Antacids are not on this page β and that matters
Antacids neutralize acid that already exists. The drugs on this page reduce or block acid production, or coat tissue. They are not interchangeable.
β οΈ Antacids also interfere with absorption of many drugs β including sucralfate, which is usually separated from an antacid by about 30 minutes. Check the specific instruction.
ποΈ Given per protocol as an intermittent infusion or continuous infusion, with a dedicated line or a documented compatibility check.
π§ͺ Monitor hemoglobin, hematocrit and hemodynamics β the drug does not replace resuscitation or endoscopy.
π§ Protonix is the PPI you are most likely to hang as an infusion.
π¨
WATCH β SAFETY & ADVERSE EFFECTS
STEP 3 Β· ASSESS
Three things on this page can seriously injure a patient: promethazine in a vein, metoclopramide over time, and a statin in a muscle.
π§ Body map β where this page's adverse effects appear
π¨ Promethazine IV β a tissue emergency
Promethazine is severely irritating to tissue. Extravasation or inadvertent intra-arterial injection can cause burning, blistering, tissue necrosis and gangrene, sometimes requiring amputation.
π Deep intramuscular injection into a large muscle is the preferred parenteral route.
π« Never give it subcutaneously or intra-arterially.
πΆ It carries a boxed warning against use in children under 2 years because of fatal respiratory depression.
π§ "Phenergan burns." Any complaint of pain at the site during administration means stop, not slow down.
π¨ Rhabdomyolysis β the statin emergency
Muscle breakdown releases myoglobin, which can injure the kidneys.
πͺ Unexplained muscle pain, tenderness or weakness β especially if widespread.
π½ Dark, tea- or cola-colored urine.
π§ͺ Creatine kinase rises; renal function is monitored.
π Teach patients to report muscle symptoms rather than wait for the next appointment.
β οΈ Risk increases with higher doses, with fibrates (gemfibrozil in particular), and with drugs that raise statin levels.
β οΈ Metoclopramide movement disorders
Because it blocks dopamine, metoclopramide can cause extrapyramidal symptoms β restlessness (akathisia), dystonic reactions, a Parkinson-like picture β and, with longer use, tardive dyskinesia.
π½οΈ Lifestyle teaching that goes with the GI half
ποΈ Elevate the head of the bed; avoid lying down for about 3 hours after eating.
π« Reduce known triggers β large fatty meals, chocolate, peppermint, caffeine, alcohol, citrus, tomato.
π Smoking cessation matters: nicotine lowers esophageal sphincter tone and impairs ulcer healing.
π Review NSAID use β a major cause of ulcers that no acid suppressant fully undoes.
π Pick-the-drug table
If the question mentionsβ¦
Think
Because
Burning at the IV site during an antiemetic push
Stop promethazine now
Extravasation risk of severe tissue injury
Lip smacking and tongue movements after weeks of a GI drug
Metoclopramide
Tardive dyskinesia
Muscle aches + dark urine on a lipid drug
Statin rhabdomyolysis
Myoglobin release
"Take it an hour before meals and don't take it with your other pills"
Sucralfate
Needs acid; binds other drugs
Powder that must be mixed with fluid
Cholestyramine
Never taken dry
Diabetic with early satiety, bloating and vomiting of old food
Metoclopramide for gastroparesis
Prokinetic effect
Confused older adult recently started on an acid drug
H2 blocker with renal impairment
Dose needs renal adjustment
Very high triglycerides
Fibric acid derivative
Largest triglyceride reduction
Patient on clopidogrel needing acid suppression
Pantoprazole over omeprazole
Less interference with clopidogrel activation
β οΈ Statin + fibrate β the combination to question
Adding a fibric acid derivative to a statin raises the risk of myopathy and rhabdomyolysis, and the risk is described as highest with gemfibrozil.
πͺ Reinforce muscle-symptom teaching whenever both are on the list.
π§ͺ Renal function and creatine kinase are followed more closely.
π Any new muscle pain in a patient on both is reported, not observed.
π§ Two lipid drugs = double the muscle homework.
𧬠Ezetimibe β the add-on
Zetia works in the intestine, not the liver, so it is often added to a statin when LDL is still above target, or used alone when a statin is not tolerated.
π½οΈ Can be taken with or without food.
π§² If a bile acid sequestrant is also prescribed, ezetimibe is spaced away from it.
πͺ Muscle symptoms are still reported, especially in combination therapy.
π Phenergan burnsStop at the first report of pain at the site
π§² Sticky drugs need spaceSucralfate & cholestyramine bind other medicines
πͺ Muscles & liverThe two statin monitoring words
π― Cover & check β 8 rapid-fire questions
Q1: What exactly does a proton pump inhibitor block, and why is that stronger than an H2 blocker?
It blocks the HβΊ/KβΊ-ATPase proton pump, the final step of acid production, so acid is shut off no matter which stimulus triggered it. An H2 blocker only blocks the histamine pathway.
Q2: When is sucralfate given and why?
On an empty stomach β commonly about an hour before meals and at bedtime β because it needs acid to form its protective paste, and food and other drugs interfere with it.
Q3: A patient receiving IV promethazine says the site burns. What is the priority action?
Stop the infusion or injection immediately and assess the site. Promethazine extravasation can cause tissue necrosis and gangrene.
Q4: Which antiemetic on this page blocks serotonin, and which blocks dopamine and histamine?
Ondansetron blocks 5-HT3 serotonin receptors. Promethazine blocks dopamine D2 and histamine H1 receptors, which is why it also sedates and has anticholinergic effects.
Q5: Why is metoclopramide usually limited to about 12 weeks?
Because of the boxed warning for tardive dyskinesia; the risk grows with duration and cumulative dose and the movements may be irreversible.
Q6: What two symptoms make you suspect rhabdomyolysis in a statin patient?
Unexplained muscle pain, tenderness or weakness, plus dark tea- or cola-colored urine.
Q7: How does cholestyramine lower LDL?
It binds bile acids in the intestine so they are eliminated in the faeces instead of being reabsorbed. The liver then uses more cholesterol to make replacement bile acids, lowering serum LDL.
Q8: Which lipid class is chosen mainly for very high triglycerides?
The fibric acid derivatives β fenofibrate and gemfibrozil. Combining them with a statin raises myopathy risk.