Angiotensin-Converting Enzymes Quiz
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Questions and Answers

What happens if RAAS is blocked in a patient with severe renal impairment (S.creatinine > 3 mg/dl)?

  • It will improve renal function.
  • It will aggravate renal failure. (correct)
  • It will stabilize blood pressure.
  • It will have no effect on renal function.

    • Which of the following ACE inhibitors contains a sulfhydryl (SH) group?

  • Fosinopril
  • Lisinopril
  • Captopril (correct)
  • Benazepril

    • Which ACE inhibitor is a prodrug and requires metabolic activation?

  • Lisinopril
  • Captopril
  • Enalapril (correct)
  • Benazepril

    • What is the mechanism of action of ACE inhibitors regarding bradykinin?

    <p>They prevent the degradation of bradykinin.</p> Signup and view all the answers

    How frequently should Captopril be administered to achieve therapeutic efficacy?

    <p>Every 8 hours</p> Signup and view all the answers

    Which of the following is an effect of inhibition of the RAAS?

    <p>Decreased formation of Ang-II.</p> Signup and view all the answers

    What distinguishes Aliskiren from other RAAS inhibitors?

    <p>It inhibits renin release.</p> Signup and view all the answers

    Which ACE inhibitor does not undergo significant metabolism by the liver?

    <p>Lisinopril</p> Signup and view all the answers

    What physiological condition triggers the release of renin from the juxtaglomerular cells?

    <p>Decreased glomerular filtration rate</p> Signup and view all the answers

    Which receptor does Angiotensin II primarily act on to maintain GFR despite decreased RBF?

    <p>AT1 receptors in the efferent arterioles</p> Signup and view all the answers

    What is a consequence of Angiotensin II acting on AT1 receptors outside the kidneys?

    <p>Cell hypertrophy and apoptosis</p> Signup and view all the answers

    In the context of renal ischemia, which of the following is a potential outcome if RAAS is activated?

    <p>Acute tubular necrosis</p> Signup and view all the answers

    How does the RAAS system contribute to maintaining renal function in states of low renal blood flow?

    <p>By stimulating systemic vasoconstriction</p> Signup and view all the answers

    What changes in kidney function can lead to acute oliguria?

    <p>Decreased renal blood flow and GFR</p> Signup and view all the answers

    What role does Angiotensin II play in the kidneys during low renal perfusion states?

    <p>Stimulates secretion of aldosterone</p> Signup and view all the answers

    What effect does persistent activation of the RAAS have on renal tissues?

    <p>Induces cell hypertrophy and apoptosis</p> Signup and view all the answers

    Renin is released from the juxtaglomerular cells in response to increased renal blood flow.

    <p>False</p> Signup and view all the answers

    Angiotensin II has no effect on the efferent arterioles of the kidney.

    <p>False</p> Signup and view all the answers

    The activation of the RAAS can lead to systemic vasodilation in various tissues.

    <p>False</p> Signup and view all the answers

    Acute tubular necrosis may develop as a result of renal ischemia.

    <p>True</p> Signup and view all the answers

    Angiotensin II contributes to cellular hypertrophy and apoptosis in some tissues.

    <p>True</p> Signup and view all the answers

    The RAAS system helps to increase renal blood flow when there is a decrease in blood volume.

    <p>True</p> Signup and view all the answers

    A decrease in renal blood flow and glomerular filtration rate directly triggers the release of aldosterone.

    <p>False</p> Signup and view all the answers

    Vasoconstriction of the efferent arterioles helps maintain adequate GFR even with low renal blood flow.

    <p>True</p> Signup and view all the answers

    Inhibitors of the RAAS can potentially improve renal function in cases of severe renal impairment.

    <p>False</p> Signup and view all the answers

    Captopril is a prodrug that requires liver metabolism to become active.

    <p>False</p> Signup and view all the answers

    Bradykinin is degraded by Angiotensin-converting enzyme (ACE).

    <p>True</p> Signup and view all the answers

    All ACE inhibitors listed are classified as prodrugs.

    <p>False</p> Signup and view all the answers

    Blocking Angiotensin II formation will lead to decreased vascular constriction and reduced salt and water retention.

    <p>True</p> Signup and view all the answers

    ACE inhibitors that contain a sulfhydryl (SH) group have a higher likelihood of causing immune side effects.

    <p>True</p> Signup and view all the answers

    Angiotensin-converting enzyme inhibitors must be administered every 8 hours to achieve therapeutic efficacy.

    <p>False</p> Signup and view all the answers

    Lisinopril requires renal metabolism and is not effective in patients with kidney impairment.

    <p>False</p> Signup and view all the answers

    What initiates the release of renin from juxtaglomerular cells?

    <p>A decrease in renal blood flow (RBF) leads to renal ischemia, which triggers renin release.</p> Signup and view all the answers

    How does Angiotensin II help maintain GFR despite decreased RBF?

    <p>Angiotensin II causes vasoconstriction of the efferent arterioles, thereby maintaining adequate GFR.</p> Signup and view all the answers

    Describe the systemic effects of Angiotensin II upon activation of AT1 receptors.

    <p>Angiotensin II causes systemic vasoconstriction, cellular hypertrophy, and apoptosis in various tissues.</p> Signup and view all the answers

    What condition can result from acute oliguria induced by renal ischemia?

    <p>Acute tubular necrosis may develop as a consequence of prolonged renal ischemia and acute oliguria.</p> Signup and view all the answers

    Explain the consequence of sustained RAAS activation on renal tissues.

    <p>Persistent RAAS activation leads to cellular hypertrophy and apoptosis, contributing to renal damage.</p> Signup and view all the answers

    What is the relationship between renal blood flow and glomerular filtration rate?

    <p>A decrease in renal blood flow directly leads to a decrease in glomerular filtration rate.</p> Signup and view all the answers

    What triggers the compensatory mechanisms of the RAAS in response to decreased kidney perfusion?

    <p>Renal ischemia caused by decreased renal blood flow activates the RAAS as a compensatory response.</p> Signup and view all the answers

    Identify the negative effects of Angiotensin II on tissues outside the kidneys.

    <p>Angiotensin II can induce vascular constriction, hypertrophy, and apoptosis in non-renal tissues.</p> Signup and view all the answers

    What is the primary risk of blocking RAAS in patients with severe renal impairment (S.creatinine > 3 mg/dl)?

    <p>It can aggravate renal failure.</p> Signup and view all the answers

    How do ACE inhibitors affect bradykinin levels in the body?

    <p>ACE inhibitors prevent the degradation of bradykinin.</p> Signup and view all the answers

    Which class of drug includes β-blockers, α-methyldopa, and clonidine in relation to RAAS inhibition?

    <p>These drugs are inhibitors of renin release.</p> Signup and view all the answers

    Identify a key pharmacological property that differentiates captopril from other ACE inhibitors.

    <p>Captopril contains a sulfhydryl (SH) group.</p> Signup and view all the answers

    Which ACE inhibitors listed are classified as prodrugs?

    <p>Fosinopril and Enalapril are classified as prodrugs.</p> Signup and view all the answers

    What is the role of angiotensin II in relation to glomerular filtration rate (GFR)?

    <p>Angiotensin II helps maintain GFR despite low renal blood flow.</p> Signup and view all the answers

    Describe the impact of ACE inhibitors on aldosterone release.

    <p>ACE inhibitors inhibit aldosterone release.</p> Signup and view all the answers

    What is the significance of using an ACE inhibitor like lisinopril in patients with mild renal impairment (S.creatinine up to 3 mg/dl)?

    <p>Lisinopril can be safely used to block RAAS in mild renal impairment.</p> Signup and view all the answers

    The renin-angiotensin-aldosterone (RAAS) system is activated in response to ↓ RBF and ↓ GFR due to renal ______.

    <p>ischemia</p> Signup and view all the answers

    Renin is released from the juxtaglomerular cells as a rescue message to initiate stimulation of the ______ system.

    <p>RAAS</p> Signup and view all the answers

    Angiotensin II acts on AT1 receptors causing ______ of the efferent arterioles to maintain GFR.

    <p>vasoconstriction</p> Signup and view all the answers

    Activation of AT1 receptors outside the kidneys causes systemic ______, hypertrophy, and apoptosis.

    <p>vasoconstriction</p> Signup and view all the answers

    Chronic activation of the RAAS can lead to ______ renal tissues and may induce degenerative changes.

    <p>damaging</p> Signup and view all the answers

    Acute oliguria may develop due to renal ______ resulting from activation of the RAAS.

    <p>ischemia</p> Signup and view all the answers

    Angiotensin II plays a role in maintaining adequate GFR despite decreases in renal ______ flow.

    <p>blood</p> Signup and view all the answers

    The release of ______ is a compensatory mechanism in response to decreased renal perfusion.

    <p>renin</p> Signup and view all the answers

    Inhibition of the RAAS will correct the hypertension but also will ↓ GFR and aggravate _____ if renal ischemia was grave.

    <p>RF</p> Signup and view all the answers

    Inhibitors of plasma renin activity include _____ such as aliskiren.

    <p>drugs</p> Signup and view all the answers

    Normal S.creatinine is _____ mg/dl.

    <p>0.3-1.2</p> Signup and view all the answers

    Captopril, zofenopril, and alacepril are examples of SH-containing _____ inhibitors.

    <p>ACE</p> Signup and view all the answers

    ACE inhibitors inhibit Ang-converting enzyme (ACE) leading to the inhibition of both Ang-II formation and _____ release.

    <p>aldosterone</p> Signup and view all the answers

    If S.creatinine is up to 3 mg/dl, you can block the RAAS, but blocking the RAAS is dangerous if S.creatinine is greater than _____ mg/dl.

    <p>3</p> Signup and view all the answers

    ACE inhibitor frequency of administration varies, with Captopril being administered every _____ hours.

    <p>8</p> Signup and view all the answers

    Bradykinin is prevented from degradation primarily through the action of _____ inhibitors.

    <p>ACE</p> Signup and view all the answers

    Match the following ACE inhibitors with their pharmacological properties:

    <p>Captopril = Contains SH group and causes immune side effects Fosinopril = Prodrug with liver and kidney metabolism Lisinopril = No significant liver metabolism Enalapril = Prodrug and does not cause immune side effects</p> Signup and view all the answers

    Match the following substances with their role in the RAAS system:

    <p>Renin = Initiates RAAS activation in response to decreased RBF Angiotensin II = Promotes vasoconstriction and increases blood pressure Aldosterone = Stimulates sodium and water retention Bradykinin = Potent vasodilator degraded by ACE</p> Signup and view all the answers

    Match the following statements about RAAS inhibition with their outcomes:

    <p>Inhibition of RAAS = Corrects hypertension but may reduce GFR β-blockers = Inhibitors of renin release ACE inhibitors = Inhibit formation of Angiotensin II Aliskiren = Direct inhibitor of plasma renin activity</p> Signup and view all the answers

    Match the following drugs with their administration frequency:

    <p>Captopril = Every 8 hours Fosinopril = Every 12 hours Lisinopril = Once every 24 hours Enalapril = Every 12 hours</p> Signup and view all the answers

    Match the following ACE inhibitors with their types regarding SH group presence:

    <p>Captopril = SH-containing drug Fosinopril = Non SH-containing drug Benazepril = Non SH-containing drug Alacepril = SH-containing drug</p> Signup and view all the answers

    Match the following conditions with their implications for RAAS blocking:

    <p>S.creatinine up to 3 mg/dl = Blocking RAAS is permissible Severe renal impairment = Blocking RAAS can worsen renal failure Mild renal impairment = RAAS can be effectively blocked Renal ischemia = Inhibition may cause adverse outcomes</p> Signup and view all the answers

    Match the following mechanisms of action to their effects:

    <p>ACE Inhibition = Decreases Ang II formation and aldosterone release Bradykinin Preventing Degradation = Leads to increased vasodilation Inhibition of salt and water retention = Reduces blood pressure Vasodilation = Facilitated by increased bradykinin levels</p> Signup and view all the answers

    Match the following RAAS inhibitors with their specific types:

    <p>Captopril = SH-containing ACE inhibitor Ramipril = Non SH-containing ACE inhibitor Clonidine = α2-adrenergic agonist and RAAS inhibitor Aliskiren = Direct renin inhibitor</p> Signup and view all the answers

    Match the following components of the RAAS system with their functions:

    <p>Renin = Initiates the RAA system response Angiotensin II = Maintains GFR despite reduced RBF Aldosterone = Increases sodium reabsorption in kidneys AT1 receptors = Mediates vasoconstriction in systemic circulation</p> Signup and view all the answers

    Match the following outcomes with the corresponding triggers of the RAAS system:

    <p>Renal ischemia = Stimulates renin release from juxtaglomerular cells Decreased renal blood flow = Activates the compensatory mechanism of RAAS Acute oliguria = May lead to acute tubular necrosis Systemic vasoconstriction = Results from Angiotensin II acting on AT1 receptors</p> Signup and view all the answers

    Match the following effects of Angiotensin II with their specific vascular impacts:

    <p>Efferent arterioles constriction = Helps maintain GFR despite low RBF Cell hypertrophy = Contributes to degenerative changes in tissues Apoptosis = Results from prolonged stimulation of AT1 receptors Systemic vascular resistance = Increased by systemic effects of Angiotensin II</p> Signup and view all the answers

    Match the ACE inhibitors with their notable characteristics:

    <p>Captopril = Contains a sulfhydryl group Lisinopril = Does not require liver metabolism Enalapril = Is a prodrug activated by the liver Ramipril = Used for cardiovascular protection</p> Signup and view all the answers

    Match the following pathophysiological states with their relation to RAAS activation:

    <p>Acute tubular necrosis = Potential outcome of ischemia due to RAAS activation Increased renal perfusion = Aimed to mitigate effects of reduced blood flow Cellular hypertrophy = A long-term effect of sustained Angiotensin II exposure Systemic vasodilation = Can result from RAAS modulation in certain contexts</p> Signup and view all the answers

    Match the following statements about renal function with their implications on RAAS:

    <p>↓ RBF and ↓ GFR = Trigger for renin release Angiotensin II action = Supports renal function despite low perfusion Inhibition of RAAS = May improve renal outcomes in specific scenarios Chronic activation of RAAS = Harms renal tissue integrity over time</p> Signup and view all the answers

    Match the following concepts related to the RAAS system with their descriptions:

    <p>Juxtaglomerular cells = Location of renin secretion Angiotensin II effects = Leads to varying degrees of vasoconstriction RAAS system response = Compensatory mechanism for hemodynamic stability Renal blood flow dynamics = Essential for maintaining glomerular filtration rate</p> Signup and view all the answers

    Match the following ACE inhibitor characteristics with their implications in therapy:

    <p>Captopril = Associated with immune-mediated side effects Enalapril = Requires activation for therapeutic effect Lisinopril = Eliminated primarily by the kidneys Ramipril = Demonstrated renal and cardiovascular protective effects</p> Signup and view all the answers

    Study Notes

    Overview of RAAS and ACE Inhibitors

    • RAAS (renin-angiotensin-aldosterone system) regulates blood pressure and fluid balance.
    • Renal ischemia leads to decreased renal blood flow (RBF) and glomerular filtration rate (GFR), risking acute tubular necrosis.
    • Juxtaglomerular cells release renin to initiate RAAS as a compensatory response.
    • Angiotensin II (Ang-II) activates AT1 receptors in kidney efferent arterioles, causing vasoconstriction (VC) to support GFR despite reduced RBF.
    • Ang-II also causes systemic VC and promotes cell hypertrophy and apoptosis in other tissues, leading to degenerative changes.

    Impact of Inhibiting RAAS

    • Inhibiting RAAS corrects hypertension but may worsen renal function in severe renal ischemia.
    • Normal serum creatinine (S.creatinine) levels range from 0.3-1.2 mg/dl; levels above 3 mg/dl indicate severe renal impairment.
    • In mild renal impairment (S.creatinine up to 3 mg/dl), RAAS blockade is generally safe.
    • In severe renal impairment, RAAS inhibition is dangerous and can exacerbate renal failure (RF).

    Types of Angiotensin-Converting Enzyme Inhibitors (ACEIs)

    • SH-containing drugs: Captopril, zofenopril, alacepril.
    • Non-SH-containing drugs: Enalapril, fosinopril, lisinopril, benazepril, ramipril.

    Pharmacological Properties of Selected ACEIs

    • Captopril

      • SH group: Yes
      • Immune side effects: Yes
      • Prodrug: No
      • Metabolism: Liver, kidney
      • Onset: 1-4 hours
      • Frequency: Every 8 hours
      • Sub-lingual dose: 25 mg

    • Fosinopril

      • SH group: No
      • Immune side effects: No
      • Prodrug: Yes
      • Metabolism: Liver, kidney
      • Frequency: Every 12 hours

    • Enalapril

      • SH group: No
      • Immune side effects: No
      • Prodrug: Yes
      • Metabolism: Liver
      • Frequency: Every 12 hours

    • Lisinopril

      • SH group: No
      • Immune side effects: No
      • Prodrug: No
      • Metabolism: No hepatic metabolism, kidney excretion
      • Frequency: Once daily

    • Benazepril

      • SH group: No
      • Immune side effects: No
      • Prodrug: Yes
      • Metabolism: Liver
      • Frequency: Once daily

    Mechanism of Action of ACEIs

    • ACEIs block angiotensin-converting enzyme (ACE) in vascular endothelium.
    • Result in:
      • Reduced formation of Ang-II and aldosterone, decreasing vasoconstriction and salt & water retention.
      • Inhibition of bradykinin degradation, enhancing vasodilation effects.

    Overview of RAAS and ACE Inhibitors

    • RAAS (renin-angiotensin-aldosterone system) regulates blood pressure and fluid balance.
    • Renal ischemia leads to decreased renal blood flow (RBF) and glomerular filtration rate (GFR), risking acute tubular necrosis.
    • Juxtaglomerular cells release renin to initiate RAAS as a compensatory response.
    • Angiotensin II (Ang-II) activates AT1 receptors in kidney efferent arterioles, causing vasoconstriction (VC) to support GFR despite reduced RBF.
    • Ang-II also causes systemic VC and promotes cell hypertrophy and apoptosis in other tissues, leading to degenerative changes.

    Impact of Inhibiting RAAS

    • Inhibiting RAAS corrects hypertension but may worsen renal function in severe renal ischemia.
    • Normal serum creatinine (S.creatinine) levels range from 0.3-1.2 mg/dl; levels above 3 mg/dl indicate severe renal impairment.
    • In mild renal impairment (S.creatinine up to 3 mg/dl), RAAS blockade is generally safe.
    • In severe renal impairment, RAAS inhibition is dangerous and can exacerbate renal failure (RF).

    Types of Angiotensin-Converting Enzyme Inhibitors (ACEIs)

    • SH-containing drugs: Captopril, zofenopril, alacepril.
    • Non-SH-containing drugs: Enalapril, fosinopril, lisinopril, benazepril, ramipril.

    Pharmacological Properties of Selected ACEIs

    • Captopril

      • SH group: Yes
      • Immune side effects: Yes
      • Prodrug: No
      • Metabolism: Liver, kidney
      • Onset: 1-4 hours
      • Frequency: Every 8 hours
      • Sub-lingual dose: 25 mg

    • Fosinopril

      • SH group: No
      • Immune side effects: No
      • Prodrug: Yes
      • Metabolism: Liver, kidney
      • Frequency: Every 12 hours

    • Enalapril

      • SH group: No
      • Immune side effects: No
      • Prodrug: Yes
      • Metabolism: Liver
      • Frequency: Every 12 hours

    • Lisinopril

      • SH group: No
      • Immune side effects: No
      • Prodrug: No
      • Metabolism: No hepatic metabolism, kidney excretion
      • Frequency: Once daily

    • Benazepril

      • SH group: No
      • Immune side effects: No
      • Prodrug: Yes
      • Metabolism: Liver
      • Frequency: Once daily

    Mechanism of Action of ACEIs

    • ACEIs block angiotensin-converting enzyme (ACE) in vascular endothelium.
    • Result in:
      • Reduced formation of Ang-II and aldosterone, decreasing vasoconstriction and salt & water retention.
      • Inhibition of bradykinin degradation, enhancing vasodilation effects.

    Overview of RAAS and ACE Inhibitors

    • RAAS (renin-angiotensin-aldosterone system) regulates blood pressure and fluid balance.
    • Renal ischemia leads to decreased renal blood flow (RBF) and glomerular filtration rate (GFR), risking acute tubular necrosis.
    • Juxtaglomerular cells release renin to initiate RAAS as a compensatory response.
    • Angiotensin II (Ang-II) activates AT1 receptors in kidney efferent arterioles, causing vasoconstriction (VC) to support GFR despite reduced RBF.
    • Ang-II also causes systemic VC and promotes cell hypertrophy and apoptosis in other tissues, leading to degenerative changes.

    Impact of Inhibiting RAAS

    • Inhibiting RAAS corrects hypertension but may worsen renal function in severe renal ischemia.
    • Normal serum creatinine (S.creatinine) levels range from 0.3-1.2 mg/dl; levels above 3 mg/dl indicate severe renal impairment.
    • In mild renal impairment (S.creatinine up to 3 mg/dl), RAAS blockade is generally safe.
    • In severe renal impairment, RAAS inhibition is dangerous and can exacerbate renal failure (RF).

    Types of Angiotensin-Converting Enzyme Inhibitors (ACEIs)

    • SH-containing drugs: Captopril, zofenopril, alacepril.
    • Non-SH-containing drugs: Enalapril, fosinopril, lisinopril, benazepril, ramipril.

    Pharmacological Properties of Selected ACEIs

    • Captopril

      • SH group: Yes
      • Immune side effects: Yes
      • Prodrug: No
      • Metabolism: Liver, kidney
      • Onset: 1-4 hours
      • Frequency: Every 8 hours
      • Sub-lingual dose: 25 mg

    • Fosinopril

      • SH group: No
      • Immune side effects: No
      • Prodrug: Yes
      • Metabolism: Liver, kidney
      • Frequency: Every 12 hours

    • Enalapril

      • SH group: No
      • Immune side effects: No
      • Prodrug: Yes
      • Metabolism: Liver
      • Frequency: Every 12 hours

    • Lisinopril

      • SH group: No
      • Immune side effects: No
      • Prodrug: No
      • Metabolism: No hepatic metabolism, kidney excretion
      • Frequency: Once daily

    • Benazepril

      • SH group: No
      • Immune side effects: No
      • Prodrug: Yes
      • Metabolism: Liver
      • Frequency: Once daily

    Mechanism of Action of ACEIs

    • ACEIs block angiotensin-converting enzyme (ACE) in vascular endothelium.
    • Result in:
      • Reduced formation of Ang-II and aldosterone, decreasing vasoconstriction and salt & water retention.
      • Inhibition of bradykinin degradation, enhancing vasodilation effects.

    Overview of RAAS and ACE Inhibitors

    • RAAS (renin-angiotensin-aldosterone system) regulates blood pressure and fluid balance.
    • Renal ischemia leads to decreased renal blood flow (RBF) and glomerular filtration rate (GFR), risking acute tubular necrosis.
    • Juxtaglomerular cells release renin to initiate RAAS as a compensatory response.
    • Angiotensin II (Ang-II) activates AT1 receptors in kidney efferent arterioles, causing vasoconstriction (VC) to support GFR despite reduced RBF.
    • Ang-II also causes systemic VC and promotes cell hypertrophy and apoptosis in other tissues, leading to degenerative changes.

    Impact of Inhibiting RAAS

    • Inhibiting RAAS corrects hypertension but may worsen renal function in severe renal ischemia.
    • Normal serum creatinine (S.creatinine) levels range from 0.3-1.2 mg/dl; levels above 3 mg/dl indicate severe renal impairment.
    • In mild renal impairment (S.creatinine up to 3 mg/dl), RAAS blockade is generally safe.
    • In severe renal impairment, RAAS inhibition is dangerous and can exacerbate renal failure (RF).

    Types of Angiotensin-Converting Enzyme Inhibitors (ACEIs)

    • SH-containing drugs: Captopril, zofenopril, alacepril.
    • Non-SH-containing drugs: Enalapril, fosinopril, lisinopril, benazepril, ramipril.

    Pharmacological Properties of Selected ACEIs

    • Captopril

      • SH group: Yes
      • Immune side effects: Yes
      • Prodrug: No
      • Metabolism: Liver, kidney
      • Onset: 1-4 hours
      • Frequency: Every 8 hours
      • Sub-lingual dose: 25 mg

    • Fosinopril

      • SH group: No
      • Immune side effects: No
      • Prodrug: Yes
      • Metabolism: Liver, kidney
      • Frequency: Every 12 hours

    • Enalapril

      • SH group: No
      • Immune side effects: No
      • Prodrug: Yes
      • Metabolism: Liver
      • Frequency: Every 12 hours

    • Lisinopril

      • SH group: No
      • Immune side effects: No
      • Prodrug: No
      • Metabolism: No hepatic metabolism, kidney excretion
      • Frequency: Once daily

    • Benazepril

      • SH group: No
      • Immune side effects: No
      • Prodrug: Yes
      • Metabolism: Liver
      • Frequency: Once daily

    Mechanism of Action of ACEIs

    • ACEIs block angiotensin-converting enzyme (ACE) in vascular endothelium.
    • Result in:
      • Reduced formation of Ang-II and aldosterone, decreasing vasoconstriction and salt & water retention.
      • Inhibition of bradykinin degradation, enhancing vasodilation effects.

    Overview of RAAS and ACE Inhibitors

    • RAAS (renin-angiotensin-aldosterone system) regulates blood pressure and fluid balance.
    • Renal ischemia leads to decreased renal blood flow (RBF) and glomerular filtration rate (GFR), risking acute tubular necrosis.
    • Juxtaglomerular cells release renin to initiate RAAS as a compensatory response.
    • Angiotensin II (Ang-II) activates AT1 receptors in kidney efferent arterioles, causing vasoconstriction (VC) to support GFR despite reduced RBF.
    • Ang-II also causes systemic VC and promotes cell hypertrophy and apoptosis in other tissues, leading to degenerative changes.

    Impact of Inhibiting RAAS

    • Inhibiting RAAS corrects hypertension but may worsen renal function in severe renal ischemia.
    • Normal serum creatinine (S.creatinine) levels range from 0.3-1.2 mg/dl; levels above 3 mg/dl indicate severe renal impairment.
    • In mild renal impairment (S.creatinine up to 3 mg/dl), RAAS blockade is generally safe.
    • In severe renal impairment, RAAS inhibition is dangerous and can exacerbate renal failure (RF).

    Types of Angiotensin-Converting Enzyme Inhibitors (ACEIs)

    • SH-containing drugs: Captopril, zofenopril, alacepril.
    • Non-SH-containing drugs: Enalapril, fosinopril, lisinopril, benazepril, ramipril.

    Pharmacological Properties of Selected ACEIs

    • Captopril

      • SH group: Yes
      • Immune side effects: Yes
      • Prodrug: No
      • Metabolism: Liver, kidney
      • Onset: 1-4 hours
      • Frequency: Every 8 hours
      • Sub-lingual dose: 25 mg

    • Fosinopril

      • SH group: No
      • Immune side effects: No
      • Prodrug: Yes
      • Metabolism: Liver, kidney
      • Frequency: Every 12 hours

    • Enalapril

      • SH group: No
      • Immune side effects: No
      • Prodrug: Yes
      • Metabolism: Liver
      • Frequency: Every 12 hours

    • Lisinopril

      • SH group: No
      • Immune side effects: No
      • Prodrug: No
      • Metabolism: No hepatic metabolism, kidney excretion
      • Frequency: Once daily

    • Benazepril

      • SH group: No
      • Immune side effects: No
      • Prodrug: Yes
      • Metabolism: Liver
      • Frequency: Once daily

    Mechanism of Action of ACEIs

    • ACEIs block angiotensin-converting enzyme (ACE) in vascular endothelium.
    • Result in:
      • Reduced formation of Ang-II and aldosterone, decreasing vasoconstriction and salt & water retention.
      • Inhibition of bradykinin degradation, enhancing vasodilation effects.

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    Description

    Test your knowledge on Angiotensin-Converting Enzyme Inhibitors (ACEIs) and their role in the renin-angiotensin-aldosterone system (RAAS). This quiz covers key concepts related to renal function and the effects of ACE inhibitors on renal ischemia. Perfect for students in pharmacology and medicine.

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