RAAS (RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM) STUDY GUIDE QUESTIONS WITH ANSWERS 2023-2024
1. The nurse who administers spironolactone to a patient with
... [Show More] heart failure should recognize that it promotes improvement by what mechanism?
it blocks the action of aldosterone
2. The renin-angiotensin-aldosterone system plays an important role in maintaining blood pressure. Which compound in this system is most powerful at raising blood pressure?
Angiotensin II
3. The nurse is reviewing medication records of several different patients. Which patients should the nurse closely monitor for hyperkalemia? Select all that apply.
A patient taking triamterene and a direct renin inhibitor, A patient taking spironolactone and angiotensin receptor blocker, A patient taking amiloride and an angiotensin-converting enzyme (ACE) inhibitor
4. The nurse is administering captopril to a patient with heart failure. Which best describes the effects of this drug?
Blocks production of angiotensin II
5. Which side effects should the nurse monitor for in a patient who takes enalapril? Select all that apply.
Hyperkalemia, Intractable cough
6. A patient has reduced cardiac output. Which compensatory response would the nurse expect to occur in this patient?
Activation of the renin-angiotensin-aldosterone system (RAAS)
7. A patient is prescribed lisinopril 40 mg by mouth once a day for hypertension. For which therapeutic effect should the nurse monitor?
decrease in blood pressure
8. The nurse is teaching a patient prescribed captopril for the treatment of hypertension. Which instructions should the nurse include? Select all that apply.
Expect a persistent dry cough, Avoid potassium salt substitutes, Report difficulty in breathing immediately
9. The nurse is caring for a patient with bipolar disorder treated with lithium. The patient has a new prescription for captopril for hypertension. The combination of these two drugs makes which assessment particularly important?
lithium level
10. The nurse is caring for a patient with renal artery stenosis who has been prescribed benazepril. Which laboratory result indicates an adverse effect of this drug?
Serum creatinine level of 2.3 mg/dL
11. Which medication works by preventing angiotensin II from binding with its receptor sites?
candesartan
12. The nurse is caring for a patient who takes an angiotensin-converting enzyme (ACE) inhibitor. If the patient develops a persistent nonproductive cough, what should the nurse do?
Notify the provider of the new development
13. The nurse administers candesartan to a patient. Which assessment finding should the nurse use as a clinical indicator of the therapeutic effectiveness of the medication?
blood pressure reduction
14. The nurse is administering 8:00 a.m. medications for hypertension. Which drugs should the nurse identify as aldosterone antagonists? Select all that apply.
Eplerenone, Spironolactone
15. The nurse determines that the patient is experiencing an adverse effect of enalapril if which effect is noted?
Patient has a dry, hacking cough
16. What is the goal of the renin-angiotensin-aldosterone system (RAAS)?
Increase the blood pressure
17. When the RAAS is activated due to a change in body hemodynamics, the __________________ stimulates the ___________________ cells in the kidneys to release _______________.
sympathetic nervous system; juxtaglomerular; renin
18. What component of the RAAS (renin-angiotensin-aldosterone system) is created and found in the liver that is activated by renin?
Angiotensinogen
19. What is the role of ACE in the renin-angiotensin-aldosterone system?
It converts angiotensin I into angiotensin II
20. Select all the roles of angiotensin II when it is activated in the renin-angiotensin-aldosterone system
Triggers the release of aldosterone
Increases the blood volume
Increases systemic vascular resistance
Causes the release of ADH (antidiuretic hormone)
21. During RAAS activation, what gland releases aldosterone?
Adrenal cortex
22. What is the role of aldosterone?
It causes the kidneys to keep sodium and water.
23. During the renin-angiotensin-aldosterone system activation, what gland releases antidiuretic hormone (ADH)?
Pituitary
24. What is the role of the antidiuretic hormone during RAAS?
Causes the kidneys to keep water
24. Select below the CORRECT sequence in how the renin-angiotensin-aldosterone system works:
Renin-> Angiotensinogen -> Angiotensin I -> ACE -> Angiotensin II
25. What is angiotensinogen?
Renin substrate/α2-globulin
26. Where is angiotensinogen primarily synthesized?
Liver
27. Angiotensinogen is primarily synthesized in the liver but can also be made on a localized level in?
Vasculature, heart, brain, adrenal gland, kidney
28. Where is Renin made?
Kidney
29. Which rate limiting step is catalyzed by Renin?
Conversion of Angiotensinogen to Angiotensin I
30. What can cause an increase in Renin release?
Decreased BP, decreased Na or Cl delivery to macula dense, and an increase in SNS tone
31. What can cause a decrease in Renin release?
Ang II short loop negative feedback, stimulation of AT1R, and Na loading (4-5g)
32. Which cells in the kidney release Renin?
JG cells (stimulation of β1 receptors)
33. What is the body's 2nd most potent vasoconstrictor that drives aldosterone secretion?
Angiotensin II
34. Renin release and CV homeostasis diagram
Angiotensin I does not have much physiological activity so it is catalyzed to Angiotensin II by which enzyme?
ACE (Kininase II)
33. Where is the highest expression of ACE?
Endothelial cells of pulmonary vasculature
34. ACE is a nonspecific enzyme with which other substrates?
Bradykinin, neurotensin, substance P
35. What is the physiological effect of bradykinin?
Vasodilator by stimulating formation of nitric oxide and PGI2
36. Ang II Type 1 receptor (AT1R) diagram
What type of GPCR is AT2R?
Gi
32. What is the effect of AT2R stimulation?
Vasodilation via activation of phosphatases and opening of K channels, K flows out, hyperpolarization occurs and muscles relax
33. AT1R v. AT2R
What is the body's most potent vasoconstrictor?
Endothelin
34.What are physiological actions of Ang II?
Increased vascular tone (vasoconstriction) which increases TPR, positive inotropism (increased force of contraction due to increased calcium), and positive chronotropism (increased HR)
35. Why is positive chronotropism caused by Ang II not usually observable?
Reflex bradycardia due to baroreceptors
36. What effect does Ang II have on NE? [Show Less]