NAPLEX NABP North American Pharmacist Licensure Examination Free Practice Exam Questions (2025 Updated)

LN should be on docusate sodium/Senna for constipation and ondansetron for N/V. Dexamethasone has an off label use for N/V that is chemotherapy-associated. It is mostly used as an anti-inflammatory or immunosuppressant agent. Hydromorphone does not cause hyperglycemia. The most common side effects of opioids are nausea, vomiting and constipation.

Sulfonylureas work in beta cells in the pancreas that are still functioning to enhance insulin secretion. Alpha- Glucosidase Inhibitors stop α-glucosidase enzymes in the small intestine and delay digestion and absorption of starch and disaccharides which lowers the levels of glucose after meals. DPP4 blocks the degradation ofGLP-1, GIP, and a variety of other peptides, including brain natriuretic peptide. Glucagon-like peptide-1 receptor agonists work in various organs of the body. Glucagon-like peptide-1 receptor agonists enhance glucose homeostasis through: (i) stimulation of insulin secretion; (ii) inhibition of glucagon secretion; (iii) direct and indirect suppression of endogenous glucose production; (iv) suppression of appetite; (v) enhanced insulin sensitivity secondary to weight loss; (vi) delayed gastric emptying, resulting in decreased postprandial hyperglycaemia.Thiazolidinediones are the only true insulin-sensitising agents, exerting their effects in skeletaland cardiac muscle, liver,and adipose tissue. It ameliorates insulin resistance, decreases visceral fat.Biguanides work in liver, muscle, adipose tissue via activation of AMP-activated protein kinase (AMPK) reduce hepatic glucose production. SGLT2 inhibitors work in the kidneys to inhibit sodium-glucose transport

proteins to reabsorb glucose into the blood from muscle cells; overall this helps to improve insulin release from the beta cells of the pancreas.

This patient shows symptoms of acute sinusitis. The most common etiology of which is viruses. Indications that an infection is viral as opposed to bacterial included a shorter infection tie (less than 10 days) and no purulent discharge (hers is watery). She does not show any evidence of a complication developing and even notes that her symptoms are improving. If her symptoms were attributed to a bacterium, then the most common cause of acute sinusitis is Streptococcus pneumoniae followed by Haemophilus influenza, then Moraxella catarrhalis. Anaerobic species such as Bacteroides fragilis and Staphylococcus aureus are more commonly found in patients with chronic sinusitis (sinusitis lasting longer than 12 weeks). This is important to realize before indiscriminately providing antibiotics for these patients.

A type III hypersensitivity reaction is mediated by immune complex deposition. In lupus, auto-antibodies are formed and these complexes are deposited in other tissues, especially in the kidneys, skin, and joints. Graves disease and myasthenia gravis are examples of type II but in some classification systems they are called type V reactions. The auto-antibodies created in Graves attack TSH receptors in the thyroid, whereas in

Myasthenia the target is the acetylcholine receptor. Hashimoto’s thyroiditis is usually considered an example of a combination of type II and IV reactions, as T cells are directed at thyroid antigens and antibodies are also produced. Allergic rhinitis is a classic example of a type I, IgE mediated reaction.

Drugs mainly interact with the receptors by means of chemical forces or bonds. There are three major types of drug receptor bonds: - Covalent - Electrostatic - Hydrophobic Covalent bonds are very strong bonds and in most of the cases they are irreversible under biologic conditions. For example, the covalent bond between the acetyl group of aspirin and cyclo-oxygenase enzyme (target enzyme present on the platelets) does not breaks easily. The platelet aggregation effect of aspirin lasts long after free acetyl-salicylic acid has disappeared from the blood (about 15 minutes) and it is reversed only by the synthesis of new cyclo-oxygenase enzyme in new platelets which takes a long time. Hence the effect of aspirin is seen after the drug is stopped. Among the drug receptor interactions, electrostatic bond is much more commonly found than covalent bond. The electrostatic bonds vary from relatively strong linkages between permanently charged ionic molecules to weaker hydrogen bonds and very weak induced dipole interactions such as van der Waals force. The electrostatic bonds are weaker than covalent bonds. Hydrophobic bonds are usually very weak bonds and probably important in the interactions of highly lipid soluble drugs with the lipids of cell membranes and perhaps in the interactions of the drugs with the internal walls of receptor “pockets”.

ABW = 85 kg IBW = 50 kg + 2.3 kg (4) = 59.2 kg 85/59.2 = 1.44 AdjBW = 59.2 kg + 0.4(85 kg-59.2 kg) = 69.52

kg CrCl (IBW) = [(140-84) 59.2]/(72 × 1.4) = 32.8 CrCl (AdjBW) = [(140-84) 69.52]/(72 × 1.4) = 38.6

Correct: E. Shigella can cause bloody diarrhea, and frequently affects young children and institutionalized patients. The pathogen is highly contagious, and is spread via fecal-oral transmission. The pathogen can lead to severe dehydration, and even cause febrile seizures in young patients. For clinically stable patients who can be managed via outpatient therapy, the optimal treatment is via PO TMP-SMX to decrease the risk of person-

to-person transmission. Choice A – Erythromycin is the first line treatment for bloody diarrhea caused by the pathogen campylobacter. However, for the purposes of decreasing transmissibility of suspected Shigella, TMP-SMX remains the mainstay of therapy. Choices B + C – Oral metronidazole and oral vancomycin can both be used in the treatment of Clostridium deficile. Alternatively, intravenous metronidazole can be given if the patient is unable to tolerate oral medications. Choice D – Oral quinolones can be used in cases of bloody diarrhea in which salmonella is the suspected pathogen. Salmonella is caused by the ingestion of contaminated poultry and/or eggs, and can ultimately lead to bacteremia in 5-10% of cases.

Metformin should be stopped when eGFR falls below 30. This is the only cutoff that is recommended for absolute discontinuing. If the eGFR falls between 30-44 while ontherapy, benefits and risks of discontinuing should be evaluated. New initiation is only recommended when eGFR >45.

The only bile acid sequestrant, colesevelam (Welchol), has been shown to increase triglycerides through mechanism of: activation of phosphatidic acid phosphatase with promotes triglyceride synthesis. GLP-1 agonists work on GLP 1 receptors to increase insulin secretion, decrease glucagon secretion, and increase satiety. Thiazolidinediones activate nuclear transcription factor PPAR gamma to increase insulin sensitivity. SGLT2 inhibitors inhibit glucose reabsorption in the kidney. Alpha-glucosidase inhibitors slow down digestion and absorptions of carbs in the gut.

Correct: A. Migraine headaches typically affect females more often than males, and patients most frequently present in their early 20s. Classic symptoms of migraine include throbbing headaches lasting between 2–24 hours in duration, with triggers such as red wine, fasting, stress, and menses. Primary prevention is aimed at the identification and avoidance of triggers. Over the counter NSAIDS can be used if symptoms persist. Failing this, PRN abortive therapy is indicated, including the triptans (e.g. – sumatriptan) and metoclopramide. Choice B – Gabapentin is an anticonvulsant that is considered to be a second-line, prophylactic treatment for recurrent migraine headaches. Its utility is limited by its lengthy side effect profile. Choice C – Amitriptyline, a tricyclic antidepressant, can also be utilized for migraine prophylaxis. However, it will not abort a migraine currently in progress, and extensive side effects limit its use. Choices D + E – Propranolol and diltiazam are beta-blockers and calcium channel blockers, respectively. As with the anticonvulsants and tricyclic antidepressants, these

are considered migraine prophylaxis and will not interrupt a migraine once it has begun.

Clopidogrel and ticlopidine are ADP receptor pathway inhibitors. The irreversible inhibition of the ADP- dependent pathway of platelet activation is thought to be the result of covalent modification and inactivation of the platelet P2Y ADP receptor. This receptor is coupled to the inhibition of adenylyl cyclase. Both drugs are prodrugs and undergo conversion to active metabolites in the liver. However, clopidogrel must undergo oxidation by hepatic P450 enzymes to its active form. This is significant because many drugs are metabolized the hepatic P450 enzymes, including statins, and clopidogrel may interact with these medications. Clopidogrel is a second-generation thienopyridine and ticlopidine is a first-generation thienopyridine. Both drugs are indicated in combination with aspirin to prevent stent thrombosis. Eptifibatide is a GPIIb-IIIa receptor antagonist that is used to treat unstable angina and non-ST segment elevation myocardial infarction. Eptifibatide is also used to reduce ischemic events in patients who are undergoing percutaneous coronary intervention. The drug is a synthetic peptide that directly antagonizes the GPIIb-IIIa receptor on the platelet. Aspirin is an antiplatelet drug that works by inhibition of synthesis of prostaglandins. Prostaglandin G2 is the result of a synthesis pathway that is activated by platelets and endothelial cells, and results in localized

vasoconstriction and induction of platelet aggregation, as well as causing release of platelet granules. Warfarin is an anticoagulant that acts on vitamin K-dependent reactions in the coagulation pathway. Vitamin K is necessary for hepatic synthesis of coagulation factors II, VII, IX and X, protein C and protein S. Vitamin K- dependent carboxylation is necessary for induction of enzymatic activity of these coagulation factors. Take- home message: Clopidogrel, a second-generation thienopyridine ADP receptor pathway inhibitor, is indicated in combination with aspirin to prevent stent thrombosis in patients who undergo percutaneous coronary intervention after myocardial infarction. Clopidogrel is a prodrug that must undergo oxidation by hepatic P450 enzymes, and therefore may affect the activity of statins and other drugs dependent on the hepatic P450 enzymes.

Metformin is held in patients with reduced renal function due to an increased risk of lactic acidosis. Metformin has a Boxed Warning for lactic acidosis, which is a rare but serious metabolic complication. Lactic acidosis can occurs due to an accumulation of metformin (5 mcg/mL or more). It is fatal in about 50% of cases. Lactic acidosis has also been reported to occur in those with diabetes who have significant renal function impairment. Lactic acidosis occurs when there are elevated blood lactate levels of 5 mmol/L or more, decreased blood pH, electrolyte disturbances with an increased anion gap, and an increased lactate/pyruvate ratio. Normal lactic acid level <2.0 mmol/L.

Common GI side effects of Valproic Acid and Divalproex Sodium are Weight gain, Nausea, Vomiting, Diarrhea, abdominal pain, dyspepsia. Divalproex sodium or valproic acid affects reproductive endocrine function in women. Menstrual irregularities defined as amenorrhea, oligomenorrhea, and prolonged cycles were common. Gynecomastia is not a side effect of Divalproex Sodium. For list of drugs that causes gynecomastia refer the reference. Gingival hyperplasia is a well-known side effect of phenytoin.

80kg person = 15mg/kg/day = 1200mg/day 80mg /5ml = 1200mg/X X= 75mL/day / 4 doses = 18.75 mL per dose

B: A variety of drugs have been found to be of some value in the prevention and treatment of vomiting, especially cancer chemotherapy-induced vomiting. With the exception of thioridazine, most of the neuroleptic drugs have antiemetic effects that are mediated by blocking D2 dopaminergic receptors of the chemoreceptor trigger zone of the medulla. Phenothiazines, such as prochlorperazine, were the first drugs shown to be effective antiemetic agents and act by blocking dopamine receptors. They are effective against low to moderately emetogenic chemotherapeutic agents (for example, fluorouracil and doxorubicin). Although increasing the dose improves antiemetic activity, side effects, including hypotension and restlessness, are dose limiting. Other adverse reactions include extrapyramidal symptom and sedation. A: Serotonin 5-HT3 antagonist is incorrect. The specific antagonists of the 5-HT3 receptor, ondansetron and granisetron, selectively block 5-HT3 receptors in the periphery and in the brain (chemoreceptor trigger zone). C: Cannabinoids related is incorrect. Cannabinoids are marijuana derivatives including dronabinol and nabilone and are effective against moderately emetogenic chemotherapy. However, they are seldom first-line antiemetics because of serious side effects. D: Blockage of prostaglandins is incorrect. Dexamethasone and methylprednisolone used alone are effective against mildly to moderately emetogenic chemotherapy. Their antiemetic mechanism is not known, but it may involve blockade of prostaglandins. E: H2 receptor antagonist is incorrect. Antagonists of histamine H2 receptor block the action of histamine at all H2 receptors; their chief clinical use is as inhibitors of gastric acid secretion.

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Explanation

The direct Coombs test is used to test for autoimmune hemolyticanemia – a condition in which the body attacks red blood cells, leading to anemia. Some drugs can cause a positive direct Coombs test – methyldopa being one of the most well-known (via IgG-mediated type II hypersensitivity reaction). Other drugs that can cause this effect include quinidine (IgM-mediated activation) and penicillins (at very high doses).

Amoxicillin is a penicillin and so should be avoided in patients even with a non-immediate allergy. Acute treatment should be administered with one of the other listed options.

Since the bioavailability of levothyroxine is roughly 50% (given in the QUESTION NO:). To convert the home dose to intravenous, it would be 50% of the oral dose. So 50% of oral 75 mcg would be 37.5 mcg intravenously.

Because SGLT2 inhibitors work by preventing reabsorption of glucose in the kidneys, this increases frequency of urination. All of the options are monitoring requirements since the hydration status, blood pressure, blood glucose, and renal function may all be changed from increased urination (from the mechanism of the drug).