WBR0735
| Author | [[PageAuthor::Yazan Daaboul, M.D. (Reviewed by Yazan Daaboul, M.D.)]] |
|---|---|
| Exam Type | ExamType::USMLE Step 1 |
| Main Category | MainCategory::Pharmacology, MainCategory::Physiology |
| Sub Category | SubCategory::Vascular |
| Prompt | [[Prompt::A 52-year-old man presents to the physician's office complaining of headache and blurry vision. His past medical history is only significant for dyslipidemia. He states that he often uses an electronic sphygmomanometer while resting at home. His blood pressure was elevated on several previous occasions in the past, but he has not been receiving any anti-hypertensive medication. In the clinic, his blood pressure is 158/92 mmHg, heart rate is 72/min, and temperature is 36.8 °C (98.24 °F). The physician decides to start the patient on a medication that also inhibits the breakdown of bradykinin. Based on the diagram 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 as first line agent for the management of hypertension, and has compelling indications in specific cases such as diabetic nephropathy and left ventricular hypertrophy. Classical adverse effects of ACE-I are angioedema, cough, and hyperkalemia. Cough is caused by the action of ACE-I that inhibits bradykinin breakdown, resulting in the accumulation of bradykinin with activation of inflammatory peptides and release of histamine. Educational Objective: A classical adverse effect of ACE-I is dry cough. ACE-inhibitors act by inhibiting the breakdown of bradykinin, resulting in the accumulation of bradykinin with activation of inflammatory peptides and release of histamine. |
| Approved | Approved::Yes |
| Keyword | WBRKeyword::Angiotensin, WBRKeyword::Angiotensinogen, WBRKeyword::Receptor, WBRKeyword::Blocker, WBRKeyword::Converting, WBRKeyword::Adverse effect, WBRKeyword::Adverse, WBRKeyword::Enzyme, WBRKeyword::ACE, WBRKeyword::Inhibitor, WBRKeyword::ACE inhibitor, WBRKeyword::Cough, WBRKeyword::Bradykinin, WBRKeyword::Side, WBRKeyword::effect |
| Linked Question | Linked:: |
| Order in Linked Questions | LinkedOrder:: |
