WBR0735

Author	[[PageAuthor::Rim Halaby, M.D. [1]]]
Exam Type	ExamType::USMLE Step 1
Main Category	MainCategory::Pharmacology, MainCategory::Physiology
Sub Category
Prompt	[[Prompt::A 52 year old male patient presents to the physician's office complaining of headache and blurry vision. His past medical history is only significant for dyslipidemia. He states that his blood pressure has been elevated on several previous occasions, but he has not been receiving any anti-hypertensive medication. Currently, he only takes rosuvastatin. He has no reported allergies. His vital signs show a temperature of 36.8 degrees C (98.24 degrees F), a heart rate of 72 bpm, and a blood pressure measuring 158/92 mmHg. The physician decides to start the patient on a medication that also inhibits the breakdown of bradykinin. Based on the image below, at which level of the renin-angiotensin pathway does the prescribed medication act? ]]
Answer A	AnswerA::A
Answer A Explanation	AnswerAExp::Renin is the enzyme that converts angiotensinogen to angiotensin I. Renin inhibitors act at this level.
Answer B	AnswerB::B
Answer B Explanation	AnswerBExp::ACE is the enzyme that converts angiotensin I to angiotensin II. ACE-inhibitors act at this level.
Answer C	AnswerC::C
Answer C Explanation	AnswerCExp::ACE-I does not act at the level of the AT I receptor.
Answer D	AnswerD::D
Answer D Explanation	AnswerDExp::Angiotensin II receptor blockers (ARB) act at this level of the pathway.
Answer E	AnswerE::E
Answer E Explanation	AnswerEExp::ACE-I does not act at this level of the pathway.
Right Answer	RightAnswer::B
Explanation	[[Explanation::The prescribed medication to treat the patient's hypertension is most likely an angiotensin-converting enzyme (ACE) inhibitor. It is indicated for the management of hypertension and has compelling indications in specific cases such as the diabetic nephropathy due to its role in reducing proteinuria, which might by itself be injurious to the kidneys, and in left ventricular hypertrophy due to its role in preventing ventricular remodeling. Classical side effects of ACE-I are angioedema, cough, and hyperkalemia. Cough is caused by the action of ACE-I in inhibiting bradykinin breakdown, leading to its local accumulation with activation of inflammatory peptides and release of histamine. Educational Objective: A classical side effect of ACE-I is dry cough. ACE-inhibitors act by preventing the production of Reference: Karlberg BE. Cough and inhibition of the renin-angiotensin system. J Hypertens Suppl. 1993; 11(3):S49-S52. Educational Objective: References: ]]
Approved	Approved::No
Keyword	WBRKeyword::angiotensin, WBRKeyword::angiotensinogen, WBRKeyword::receptor, WBRKeyword::blocker, WBRKeyword::converting, WBRKeyword::enzyme, WBRKeyword::ACE, WBRKeyword::inhibitor, WBRKeyword::ACE inhibitor, WBRKeyword::cough, WBRKeyword::bradykinin, WBRKeyword::side, WBRKeyword::effect
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Order in Linked Questions	LinkedOrder::