ATI RN
Pharmacology Across the Lifespan ATI Questions
Question 1 of 5
A patient with heart failure is prescribed furosemide. Furosemide works primarily by:
Correct Answer: A
Rationale: The correct answer is A: Inhibiting sodium reabsorption in the kidneys. Furosemide is a loop diuretic that acts on the ascending loop of Henle in the kidneys to inhibit the reabsorption of sodium and chloride ions. This leads to increased excretion of water and electrolytes, reducing fluid volume and relieving congestion in heart failure patients. Choice B is incorrect because furosemide does not directly inhibit aldosterone. Choice C is incorrect because furosemide does not affect myocardial contractions but rather fluid balance. Choice D is incorrect because furosemide's primary mechanism of action is not related to relaxing vascular smooth muscle.
Question 2 of 5
A 45-year-old man with a history of depression is started on sertraline. Sertraline is classified as:
Correct Answer: A
Rationale: The correct answer is A: A selective serotonin reuptake inhibitor (SSRI). Sertraline belongs to this class of antidepressants, which work by blocking the reuptake of serotonin, thereby increasing its levels in the brain. This helps alleviate symptoms of depression. Sertraline is not classified as a serotonin-norepinephrine reuptake inhibitor (SNRI) like venlafaxine (Effexor) or duloxetine (Cymbalta), nor a tricyclic antidepressant (TCA) such as amitriptyline. It is also not a monoamine oxidase inhibitor (MAOI) like phenelzine (Nardil) or selegiline (Emsam). SSRI is the most appropriate classification for sertraline based on its mechanism of action and therapeutic use in depression.
Question 3 of 5
Angina is caused by:
Correct Answer: D
Rationale: The correct answer is D because angina is caused by an inadequate supply of oxygen to the heart muscle, leading to chest pain. Extreme binding of noradrenaline due to upregulation can lead to increased constriction of blood vessels, reducing blood flow to the heart. This exacerbates the oxygen supply-demand imbalance, triggering angina. A: Blocking beta1 receptors with constant noradrenaline binding would decrease the effects of noradrenaline, potentially reducing heart rate and blood pressure, but it would not directly cause angina. B: Activating beta2 receptors would cause vasodilation, increasing blood flow to the heart, which is opposite to the mechanism of angina. C: Beta1 receptors not being active anymore would lead to a decrease in heart rate and contractility, but this state would not directly induce angina.
Question 4 of 5
A 30-year-old man presented to the clinic with a 2-month history of right-side head pain recurring on a weekly basis. His headaches were usually preceded by unformed flashes of light, bilaterally, and were associated with nausea, vomiting, and photophobia. The headaches were not relieved by aspirin or ibuprofen and usually lasted all day unless he was able to sleep. A drug acting on which of the following receptors would be most appropriate to stop the migraine attack in this patient?
Correct Answer: D
Rationale: The correct answer is D: 5-HT1B/1D serotonergic receptors. Migraine headaches are believed to be caused by neurovascular dysfunction involving serotonin pathways. Activating 5-HT1B/1D receptors can help constrict blood vessels and inhibit the release of pro-inflammatory neuropeptides, thus relieving migraine symptoms. Beta-2 adrenergic (choice A) receptors are not typically involved in migraine pathophysiology. GABAergic (choice B) drugs may be used for other types of headaches but are not specific for migraines. M1 cholinergic (choice C) drugs are not commonly used for migraine treatment as they do not target the serotonin pathways involved in migraines.
Question 5 of 5
A48-year-old woman suffering from allergic urticaria started a treatment with loratadine. The decreased synthesis of which of the following substances most likely mediated the therapeutic effect of the drug in the patient's disease?
Correct Answer: C
Rationale: The correct answer is C: Inositol triphosphate. Loratadine is an antihistamine used to treat allergic conditions like urticaria by blocking histamine receptors. Histamine binds to H1 receptors on cells, leading to the activation of phospholipase C, which cleaves phosphatidylinositol 4,5-bisphosphate into inositol triphosphate (IP3) and diacylglycerol. IP3 triggers the release of intracellular calcium stores, leading to various cellular responses including allergic reactions. By blocking histamine receptors, loratadine reduces the synthesis of IP3, hence mediating its therapeutic effect. Choice A (cAMP) is incorrect because loratadine does not directly affect the cAMP pathway. Choice B (cGMP) is incorrect as it is not involved in the mechanism of action of loratadine. Choice D (Cyclooxygenase-1) is incorrect as