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296 Cards in this Set
- Front
- Back
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What is Hypertension?
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-Systolic blood pressure of 140mm Hg or
-higher or a diastolic blood pressure of 90mm Hg or higher |
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What is Hypertension?
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-Systolic blood pressure of 140mm Hg or
-higher or a diastolic blood pressure of 90mm Hg or higher |
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What is Hypertension?
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-Systolic blood pressure of 140mm Hg or
-higher or a diastolic blood pressure of 90mm Hg or higher |
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What is Hypertension?
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-Systolic blood pressure of 140mm Hg or
-higher or a diastolic blood pressure of 90mm Hg or higher |
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Describe Primary Hypertension
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Characterizes 90% of hypertensive patients
-For these patients the cause is unknown |
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Describe Primary Hypertension
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Characterizes 90% of hypertensive patients
-For these patients the cause is unknown |
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Describe Primary Hypertension
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Characterizes 90% of hypertensive patients
-For these patients the cause is unknown |
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Describe Primary Hypertension
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Characterizes 90% of hypertensive patients
-For these patients the cause is unknown |
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What type of killer is hypertension described as?
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The Silent Killer
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What type of killer is hypertension described as?
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The Silent Killer
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What type of killer is hypertension described as?
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The Silent Killer
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What type of killer is hypertension described as?
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The Silent Killer
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What is Secondary Hypertension?
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10% of HTN patients
-For these pts the cause is KNOWN. |
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What enzyme converts angiotensinogen to angiotensin I?
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RENIN
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What is Secondary Hypertension?
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10% of HTN patients
-For these pts the cause is KNOWN. |
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What is the purpose of ACE?
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To convert Angiotensin I to Angiotensin II
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What is the purpose of ACE?
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To convert Angiotensin I to Angiotensin II
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What is the purpose of ACE?
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To convert Angiotensin I to Angiotensin II
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What is the purpose of ACE?
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To convert Angiotensin I to Angiotensin II
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What is Secondary Hypertension?
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10% of HTN patients
-For these pts the cause is KNOWN. |
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Name the causes of increased Cardiac Output?
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-Increased fluid volume (excess sodium and water)
-Excess stimulation of RAAS -Sympathetic nervous system overactivity |
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Name the causes of increased Cardiac Output?
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-Increased fluid volume (excess sodium and water)
-Excess stimulation of RAAS -Sympathetic nervous system overactivity |
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Name the causes of increased Cardiac Output?
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-Increased fluid volume (excess sodium and water)
-Excess stimulation of RAAS -Sympathetic nervous system overactivity |
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Name the causes of increased Cardiac Output?
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-Increased fluid volume (excess sodium and water)
-Excess stimulation of RAAS -Sympathetic nervous system overactivity |
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What is Secondary Hypertension?
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10% of HTN patients
-For these pts the cause is KNOWN. |
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How is the PVR increased?
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-Excess stimulation of RAAS
-Sympathetic Nervous System |
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How is the PVR increased?
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-Excess stimulation of RAAS
-Sympathetic Nervous System |
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How is the PVR increased?
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-Excess stimulation of RAAS
-Sympathetic Nervous System |
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How is the PVR increased?
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-Excess stimulation of RAAS
-Sympathetic Nervous System |
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What is the equation for BP?
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BP= cardiac output (CO) x peripheral vascular resistance (PVR)
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What does water follow?
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Sodium
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What does water follow?
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Sodium
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What does water follow?
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Sodium
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What does water follow?
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Sodium
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What is the equation for BP?
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BP= cardiac output (CO) x peripheral vascular resistance (PVR)
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How does the body react to diuretics?
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-Increases Urine Volume
-Decrease blood pressure |
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How does the body react to diuretics?
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-Increases Urine Volume
-Decrease blood pressure |
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How does the body react to diuretics?
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-Increases Urine Volume
-Decrease blood pressure |
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How does the body react to diuretics?
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-Increases Urine Volume
-Decrease blood pressure |
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What is the equation for BP?
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BP= cardiac output (CO) x peripheral vascular resistance (PVR)
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What does it mean to increase urine volume?
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Remove sodium and water from the body
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What does it mean to increase urine volume?
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Remove sodium and water from the body
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What does it mean to increase urine volume?
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Remove sodium and water from the body
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What does it mean to increase urine volume?
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Remove sodium and water from the body
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What is the equation for BP?
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BP= cardiac output (CO) x peripheral vascular resistance (PVR)
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What is a long term effect of diuretics?
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Decreases PVR --> decrease in sodium content of smooth muscle cells
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What is a long term effect of diuretics?
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Decreases PVR --> decrease in sodium content of smooth muscle cells
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What is a long term effect of diuretics?
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Decreases PVR --> decrease in sodium content of smooth muscle cells
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What is a long term effect of diuretics?
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Decreases PVR --> decrease in sodium content of smooth muscle cells
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What is Cardiac Output?
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Stroke Volume x Heart Rate
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Name the 2 examples of B-Blockers
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-Labetalol (Trandate)
-Metoprolol (Lopressor, Toprol XL) |
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Name the 2 examples of B-Blockers
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-Labetalol (Trandate)
-Metoprolol (Lopressor, Toprol XL) |
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Name the 2 examples of B-Blockers
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-Labetalol (Trandate)
-Metoprolol (Lopressor, Toprol XL) |
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Name the 2 examples of B-Blockers
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-Labetalol (Trandate)
-Metoprolol (Lopressor, Toprol XL) |
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What is Cardiac Output?
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Stroke Volume x Heart Rate
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What is the mechanism of action for B-Blockers?
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-Block B1 receptors in cardiac muscle
-Inhibits the release of Renin from the kidneys |
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What is the mechanism of action for B-Blockers?
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-Block B1 receptors in cardiac muscle
-Inhibits the release of Renin from the kidneys |
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What is the mechanism of action for B-Blockers?
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-Block B1 receptors in cardiac muscle
-Inhibits the release of Renin from the kidneys |
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What is the mechanism of action for B-Blockers?
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-Block B1 receptors in cardiac muscle
-Inhibits the release of Renin from the kidneys |
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What is Cardiac Output?
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Stroke Volume x Heart Rate
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When B1 receptors are blocked, what effects do we see on CO and HR?
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-Decrease in Heart Rate (negative chronotropic effects)
-Decrease in Cardiac Output (negative inotropic effects |
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When B1 receptors are blocked, what effects do we see on CO and HR?
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-Decrease in Heart Rate (negative chronotropic effects)
-Decrease in Cardiac Output (negative inotropic effects |
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When B1 receptors are blocked, what effects do we see on CO and HR?
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-Decrease in Heart Rate (negative chronotropic effects)
-Decrease in Cardiac Output (negative inotropic effects |
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When B1 receptors are blocked, what effects do we see on CO and HR?
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-Decrease in Heart Rate (negative chronotropic effects)
-Decrease in Cardiac Output (negative inotropic effects |
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What is Cardiac Output?
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Stroke Volume x Heart Rate
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What actions do only some B-Blockers have on BP?
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-Some agents inhibit activity of the sympathetic nervous system
-Some agents DIRECTLY decrease peripheral vascular resistance |
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What actions do only some B-Blockers have on BP?
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-Some agents inhibit activity of the sympathetic nervous system
-Some agents DIRECTLY decrease peripheral vascular resistance |
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What actions do only some B-Blockers have on BP?
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-Some agents inhibit activity of the sympathetic nervous system
-Some agents DIRECTLY decrease peripheral vascular resistance |
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What actions do only some B-Blockers have on BP?
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-Some agents inhibit activity of the sympathetic nervous system
-Some agents DIRECTLY decrease peripheral vascular resistance |
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What 2 systems control blood pressure?
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-Sympathetic NS
-Renin-angiotensin-aldosterone system (RAAS) |
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What effects to B-Blockers have on blood volume?
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None!
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What effects to B-Blockers have on blood volume?
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None!
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What effects to B-Blockers have on blood volume?
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None!
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What effects to B-Blockers have on blood volume?
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None!
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What 2 systems control blood pressure?
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-Sympathetic NS
-Renin-angiotensin-aldosterone system (RAAS) |
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Which type of B-Blockers are contraindicated for asthma patients? Why?
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Non-selective B-Blockers because they can attache to B2 receptors in the lungs and cause bronchio constriction
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Which type of B-Blockers are contraindicated for asthma patients? Why?
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Non-selective B-Blockers because they can attache to B2 receptors in the lungs and cause bronchio constriction
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Which type of B-Blockers are contraindicated for asthma patients? Why?
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Non-selective B-Blockers because they can attache to B2 receptors in the lungs and cause bronchio constriction
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Which type of B-Blockers are contraindicated for asthma patients? Why?
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Non-selective B-Blockers because they can attache to B2 receptors in the lungs and cause bronchio constriction
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What 2 systems control blood pressure?
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-Sympathetic NS
-Renin-angiotensin-aldosterone system (RAAS) |
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What is important to keep in mind with selective B-Blockers?
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Their selectivity is not absolute.
-Once you increase the dose, selectivity becomes non-selective |
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What is important to keep in mind with selective B-Blockers?
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Their selectivity is not absolute.
-Once you increase the dose, selectivity becomes non-selective |
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What is important to keep in mind with selective B-Blockers?
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Their selectivity is not absolute.
-Once you increase the dose, selectivity becomes non-selective |
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What is important to keep in mind with selective B-Blockers?
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Their selectivity is not absolute.
-Once you increase the dose, selectivity becomes non-selective |
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What 2 systems control blood pressure?
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-Sympathetic NS
-Renin-angiotensin-aldosterone system (RAAS) |
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Describe the Intrinsic Sympathomimetic activity (ISA) of B-Blockers.
Is this good or bad? |
-Causes activation of adrenergic receptors producing effects similar to stimulation of the SNS
-Bad effect |
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Describe the Intrinsic Sympathomimetic activity (ISA) of B-Blockers.
Is this good or bad? |
-Causes activation of adrenergic receptors producing effects similar to stimulation of the SNS
-Bad effect |
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Describe the Intrinsic Sympathomimetic activity (ISA) of B-Blockers.
Is this good or bad? |
-Causes activation of adrenergic receptors producing effects similar to stimulation of the SNS
-Bad effect |
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Describe the Intrinsic Sympathomimetic activity (ISA) of B-Blockers.
Is this good or bad? |
-Causes activation of adrenergic receptors producing effects similar to stimulation of the SNS
-Bad effect |
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What effect does the sympathetic NS have on BP?
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It works in the short term
-Ex: Regulation of BP laying down to standing up |
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What aspect of B-Blockers allow them to be widely distributed throughout the body?
What occurs during the hepatic metabolism of these B-Blockers? |
-Their lipid solubility
-The Lipid soluble agents undergo more extensive first pass hepatic metabolism |
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What aspect of B-Blockers allow them to be widely distributed throughout the body?
What occurs during the hepatic metabolism of these B-Blockers? |
-Their lipid solubility
-The Lipid soluble agents undergo more extensive first pass hepatic metabolism |
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What aspect of B-Blockers allow them to be widely distributed throughout the body?
What occurs during the hepatic metabolism of these B-Blockers? |
-Their lipid solubility
-The Lipid soluble agents undergo more extensive first pass hepatic metabolism |
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What aspect of B-Blockers allow them to be widely distributed throughout the body?
What occurs during the hepatic metabolism of these B-Blockers? |
-Their lipid solubility
-The Lipid soluble agents undergo more extensive first pass hepatic metabolism |
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What effect does the sympathetic NS have on BP?
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It works in the short term
-Ex: Regulation of BP laying down to standing up |
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Does Lebatolol have Beta Selectivity?
Alpha blockade? ISA Activity? What degree is it's lipid solubility? |
-NO selectivity
-Yes alpha blockade -No ISA activity -Moderate Lipid solubility |
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Does Lebatolol have Beta Selectivity?
Alpha blockade? ISA Activity? What degree is it's lipid solubility? |
-NO selectivity
-Yes alpha blockade -No ISA activity -Moderate Lipid solubility |
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Does Lebatolol have Beta Selectivity?
Alpha blockade? ISA Activity? What degree is it's lipid solubility? |
-NO selectivity
-Yes alpha blockade -No ISA activity -Moderate Lipid solubility |
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Does Lebatolol have Beta Selectivity?
Alpha blockade? ISA Activity? What degree is it's lipid solubility? |
-NO selectivity
-Yes alpha blockade -No ISA activity -Moderate Lipid solubility |
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What effect does the sympathetic NS have on BP?
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It works in the short term
-Ex: Regulation of BP laying down to standing up |
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What type of B-Blocker is Metoprolol?
Does it have alpha Blockade? Does it have ISA activity? What is its lipid solubiltiy? |
-B1 selective B-Blocker
-No alpha blockade -No ISA activity -Moderate lipid solubility |
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What type of B-Blocker is Metoprolol?
Does it have alpha Blockade? Does it have ISA activity? What is its lipid solubiltiy? |
-B1 selective B-Blocker
-No alpha blockade -No ISA activity -Moderate lipid solubility |
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What type of B-Blocker is Metoprolol?
Does it have alpha Blockade? Does it have ISA activity? What is its lipid solubiltiy? |
-B1 selective B-Blocker
-No alpha blockade -No ISA activity -Moderate lipid solubility |
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What type of B-Blocker is Metoprolol?
Does it have alpha Blockade? Does it have ISA activity? What is its lipid solubiltiy? |
-B1 selective B-Blocker
-No alpha blockade -No ISA activity -Moderate lipid solubility |
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What effect does the sympathetic NS have on BP?
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It works in the short term
-Ex: Regulation of BP laying down to standing up |
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What cautions should be taken when taking pts off B-Blockers?
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-Must taper off over several weeks to avoid rebound hypertension
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What cautions should be taken when taking pts off B-Blockers?
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-Must taper off over several weeks to avoid rebound hypertension
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What cautions should be taken when taking pts off B-Blockers?
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-Must taper off over several weeks to avoid rebound hypertension
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What cautions should be taken when taking pts off B-Blockers?
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-Must taper off over several weeks to avoid rebound hypertension
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How does RAAS effect BP?
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-Long Term effect
-Helps control of Na+/H2O levels. |
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Why should you keep watch of diabetics on B-blockers?
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-Keep watch of poorly controlled diabetic patients because they can MASK the signs and symptoms of HYPOGLYCEMIA!
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Why should you keep watch of diabetics on B-blockers?
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-Keep watch of poorly controlled diabetic patients because they can MASK the signs and symptoms of HYPOGLYCEMIA!
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Why should you keep watch of diabetics on B-blockers?
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-Keep watch of poorly controlled diabetic patients because they can MASK the signs and symptoms of HYPOGLYCEMIA!
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Why should you keep watch of diabetics on B-blockers?
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-Keep watch of poorly controlled diabetic patients because they can MASK the signs and symptoms of HYPOGLYCEMIA!
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How does RAAS effect BP?
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-Long Term effect
-Helps control of Na+/H2O levels. |
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What are the adverse effects of B-Blockers?
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-Blocking B2 leads to bronchoconstriction
-Bradycardia -Weight Gain -CNS: sleep disturbances, depression, confusion, agitation, psychosis -Hypotension |
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What are the adverse effects of B-Blockers?
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-Blocking B2 leads to bronchoconstriction
-Bradycardia -Weight Gain -CNS: sleep disturbances, depression, confusion, agitation, psychosis -Hypotension |
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What are the adverse effects of B-Blockers?
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-Blocking B2 leads to bronchoconstriction
-Bradycardia -Weight Gain -CNS: sleep disturbances, depression, confusion, agitation, psychosis -Hypotension |
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What are the adverse effects of B-Blockers?
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-Blocking B2 leads to bronchoconstriction
-Bradycardia -Weight Gain -CNS: sleep disturbances, depression, confusion, agitation, psychosis -Hypotension |
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How does RAAS effect BP?
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-Long Term effect
-Helps control of Na+/H2O levels. |
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How should a pt on B-Blockers get out of bed?
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They should sit for a period of time before getting up.
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How should a pt on B-Blockers get out of bed?
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They should sit for a period of time before getting up.
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How should a pt on B-Blockers get out of bed?
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They should sit for a period of time before getting up.
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How should a pt on B-Blockers get out of bed?
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They should sit for a period of time before getting up.
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How does RAAS effect BP?
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-Long Term effect
-Helps control of Na+/H2O levels. |
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List the most common Angiotensin-Converting Enzyme Inhibitors (ACEI)
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-Captopril (Capoten)
-Enalapril (Vasotec) -Lisinopril (Prinivil, Zestril) |
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List the most common Angiotensin-Converting Enzyme Inhibitors (ACEI)
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-Captopril (Capoten)
-Enalapril (Vasotec) -Lisinopril (Prinivil, Zestril) |
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List the most common Angiotensin-Converting Enzyme Inhibitors (ACEI)
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-Captopril (Capoten)
-Enalapril (Vasotec) -Lisinopril (Prinivil, Zestril) |
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List the most common Angiotensin-Converting Enzyme Inhibitors (ACEI)
|
-Captopril (Capoten)
-Enalapril (Vasotec) -Lisinopril (Prinivil, Zestril) |
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What do HTN patients lack that non-HTN patients have?
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An Na+/H2O concetration set point and regulatory system
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What is the MOA of ACEIs?
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-Inhibit RAAS by preventing conversion of I --> II. Inhibit ACE
-Inhibiting II --> decreased PVR -->decreased blood pressure |
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What is the MOA of ACEIs?
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-Inhibit RAAS by preventing conversion of I --> II. Inhibit ACE
-Inhibiting II --> decreased PVR -->decreased blood pressure |
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What is the MOA of ACEIs?
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-Inhibit RAAS by preventing conversion of I --> II. Inhibit ACE
-Inhibiting II --> decreased PVR -->decreased blood pressure |
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What is the MOA of ACEIs?
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-Inhibit RAAS by preventing conversion of I --> II. Inhibit ACE
-Inhibiting II --> decreased PVR -->decreased blood pressure |
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What do HTN patients lack that non-HTN patients have?
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An Na+/H2O concetration set point and regulatory system
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What effect to do ACEIs have on bradykinin and prostaglandins? What does this do?
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-Limits the degradation of bradykinin (increases vasodilation)
-Increases synthesis of vasodilating prostaglandins |
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What effect to do ACEIs have on bradykinin and prostaglandins? What does this do?
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-Limits the degradation of bradykinin (increases vasodilation)
-Increases synthesis of vasodilating prostaglandins |
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What effect to do ACEIs have on bradykinin and prostaglandins? What does this do?
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-Limits the degradation of bradykinin (increases vasodilation)
-Increases synthesis of vasodilating prostaglandins |
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What effect to do ACEIs have on bradykinin and prostaglandins? What does this do?
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-Limits the degradation of bradykinin (increases vasodilation)
-Increases synthesis of vasodilating prostaglandins |
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What do HTN patients lack that non-HTN patients have?
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An Na+/H2O concetration set point and regulatory system
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What is the PRIMARY effect of ACEIs?
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Decreases Peripheral Vascular Resistance
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What is the PRIMARY effect of ACEIs?
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Decreases Peripheral Vascular Resistance
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What is the PRIMARY effect of ACEIs?
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Decreases Peripheral Vascular Resistance
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What is the PRIMARY effect of ACEIs?
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Decreases Peripheral Vascular Resistance
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What do HTN patients lack that non-HTN patients have?
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An Na+/H2O concetration set point and regulatory system
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What type of administration is used for ACEIs?
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All are oral except for enalaprilat which is IV.
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What type of administration is used for ACEIs?
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All are oral except for enalaprilat which is IV.
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What type of administration is used for ACEIs?
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All are oral except for enalaprilat which is IV.
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What type of administration is used for ACEIs?
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All are oral except for enalaprilat which is IV.
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Which receptor(s) does the Sympathetic NS act on to effect BP?
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-Activate B1: which increase HR and thus increase BP
-Activate A1 receptors which cause vasoconstriction and thus increase BP |
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What is the best way to start a patient on an ACEI?
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Start them on a short acting agent (Captopril) and then switch to a longer acting once they are adjusted.
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What is the best way to start a patient on an ACEI?
|
Start them on a short acting agent (Captopril) and then switch to a longer acting once they are adjusted.
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What is the best way to start a patient on an ACEI?
|
Start them on a short acting agent (Captopril) and then switch to a longer acting once they are adjusted.
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What is the best way to start a patient on an ACEI?
|
Start them on a short acting agent (Captopril) and then switch to a longer acting once they are adjusted.
|
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Which receptor(s) does the Sympathetic NS act on to effect BP?
|
-Activate B1: which increase HR and thus increase BP
-Activate A1 receptors which cause vasoconstriction and thus increase BP |
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WHat are the adverse effects of ACEIs?
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-Hyperkalemia--> arrhythmias
-Acute renal failure -angioedema -Cough |
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WHat are the adverse effects of ACEIs?
|
-Hyperkalemia--> arrhythmias
-Acute renal failure -angioedema -Cough |
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WHat are the adverse effects of ACEIs?
|
-Hyperkalemia--> arrhythmias
-Acute renal failure -angioedema -Cough |
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WHat are the adverse effects of ACEIs?
|
-Hyperkalemia--> arrhythmias
-Acute renal failure -angioedema -Cough |
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Which receptor(s) does the Sympathetic NS act on to effect BP?
|
-Activate B1: which increase HR and thus increase BP
-Activate A1 receptors which cause vasoconstriction and thus increase BP |
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Which adverse effect of ACEIs is considered a true allergy?
When can it occur? What should you do? |
-Angioedema
It can occur at any point while patient is taking medication. --If it occurs you must seek immediate medical attention and stop all medications that can can cause angioedemas |
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Which adverse effect of ACEIs is considered a true allergy?
When can it occur? What should you do? |
-Angioedema
It can occur at any point while patient is taking medication. --If it occurs you must seek immediate medical attention and stop all medications that can can cause angioedemas |
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Which adverse effect of ACEIs is considered a true allergy?
When can it occur? What should you do? |
-Angioedema
It can occur at any point while patient is taking medication. --If it occurs you must seek immediate medical attention and stop all medications that can can cause angioedemas |
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Which adverse effect of ACEIs is considered a true allergy?
When can it occur? What should you do? |
-Angioedema
It can occur at any point while patient is taking medication. --If it occurs you must seek immediate medical attention and stop all medications that can can cause angioedemas |
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Which receptor(s) does the Sympathetic NS act on to effect BP?
|
-Activate B1: which increase HR and thus increase BP
-Activate A1 receptors which cause vasoconstriction and thus increase BP |
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Which adverse effect of ACEIs is not a true allergy?
What is it caused by? |
Cough
-Caused by an increase in bradykinin=irritant to the lungs = dry coughing |
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Which adverse effect of ACEIs is not a true allergy?
What is it caused by? |
Cough
-Caused by an increase in bradykinin=irritant to the lungs = dry coughing |
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Which adverse effect of ACEIs is not a true allergy?
What is it caused by? |
Cough
-Caused by an increase in bradykinin=irritant to the lungs = dry coughing |
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Which adverse effect of ACEIs is not a true allergy?
What is it caused by? |
Cough
-Caused by an increase in bradykinin=irritant to the lungs = dry coughing |
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What does Angiotensin II act as and which tissues does if effect?
|
-It is a potent vasoconstrictor
-Acts on the blood vessels to cause vasoconstriction -Acts on the adrenal Cortex to enable Aldosterone to Increase Na+ and Water retention. |
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What drug interactions occur with ACEIs?
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Potassium supplements or potassium sparing drugs.
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|
What drug interactions occur with ACEIs?
|
Potassium supplements or potassium sparing drugs.
|
|
|
What drug interactions occur with ACEIs?
|
Potassium supplements or potassium sparing drugs.
|
|
|
What drug interactions occur with ACEIs?
|
Potassium supplements or potassium sparing drugs.
|
|
|
What does Angiotensin II act as and which tissues does if effect?
|
-It is a potent vasoconstrictor
-Acts on the blood vessels to cause vasoconstriction -Acts on the adrenal Cortex to enable Aldosterone to Increase Na+ and Water retention. |
|
|
As a nurse, what should you monitor for with pts on ACEIs?
|
-any situations that might lead to a drop in fluid volume (V/D, dehydration, diaphoresis)
-Administer on an empty stomach 1 hour before or 2 hours after meals |
|
|
As a nurse, what should you monitor for with pts on ACEIs?
|
-any situations that might lead to a drop in fluid volume (V/D, dehydration, diaphoresis)
-Administer on an empty stomach 1 hour before or 2 hours after meals |
|
|
As a nurse, what should you monitor for with pts on ACEIs?
|
-any situations that might lead to a drop in fluid volume (V/D, dehydration, diaphoresis)
-Administer on an empty stomach 1 hour before or 2 hours after meals |
|
|
As a nurse, what should you monitor for with pts on ACEIs?
|
-any situations that might lead to a drop in fluid volume (V/D, dehydration, diaphoresis)
-Administer on an empty stomach 1 hour before or 2 hours after meals |
|
|
What does Angiotensin II act as and which tissues does if effect?
|
-It is a potent vasoconstrictor
-Acts on the blood vessels to cause vasoconstriction -Acts on the adrenal Cortex to enable Aldosterone to Increase Na+ and Water retention. |
|
|
What is the most popular drug under Angiotensin Receptor blocking agents (ARBs)
|
Losartan (Cozaar)
|
|
|
What is the most popular drug under Angiotensin Receptor blocking agents (ARBs)
|
Losartan (Cozaar)
|
|
|
What is the most popular drug under Angiotensin Receptor blocking agents (ARBs)
|
Losartan (Cozaar)
|
|
|
What is the most popular drug under Angiotensin Receptor blocking agents (ARBs)
|
Losartan (Cozaar)
|
|
|
What does Angiotensin II act as and which tissues does if effect?
|
-It is a potent vasoconstrictor
-Acts on the blood vessels to cause vasoconstriction -Acts on the adrenal Cortex to enable Aldosterone to Increase Na+ and Water retention. |
|
|
Which patients are prescribed ARBs?
|
Ones that are intolerant to ACEIs
|
|
|
Which patients are prescribed ARBs?
|
Ones that are intolerant to ACEIs
|
|
|
Which patients are prescribed ARBs?
|
Ones that are intolerant to ACEIs
|
|
|
Which patients are prescribed ARBs?
|
Ones that are intolerant to ACEIs
|
|
|
What enzyme converts angiotensinogen to angiotensin I?
|
RENIN
|
|
|
What the MOA of ARBs?
|
Selectively blocks the vasoconstrictive effects of angtiotensin II by blocking binding of II to its receptor
|
|
|
What the MOA of ARBs?
|
Selectively blocks the vasoconstrictive effects of angtiotensin II by blocking binding of II to its receptor
|
|
|
What the MOA of ARBs?
|
Selectively blocks the vasoconstrictive effects of angtiotensin II by blocking binding of II to its receptor
|
|
|
What the MOA of ARBs?
|
Selectively blocks the vasoconstrictive effects of angtiotensin II by blocking binding of II to its receptor
|
|
|
What enzyme converts angiotensinogen to angiotensin I?
|
RENIN
|
|
|
What are the adverse effects of ARBs?
|
-hyperkalemia
-Acute Renal Failure -Angioedema |
|
|
What are the adverse effects of ARBs?
|
-hyperkalemia
-Acute Renal Failure -Angioedema |
|
|
What are the adverse effects of ARBs?
|
-hyperkalemia
-Acute Renal Failure -Angioedema |
|
|
What are the adverse effects of ARBs?
|
-hyperkalemia
-Acute Renal Failure -Angioedema |
|
|
What enzyme converts angiotensinogen to angiotensin I?
|
RENIN
|
|
|
What side affect do ACEIs have that ARBs do not?
|
cough
-ARBs do no have an effect on Bradykinin |
|
|
What side affect do ACEIs have that ARBs do not?
|
cough
-ARBs do no have an effect on Bradykinin |
|
|
What side affect do ACEIs have that ARBs do not?
|
cough
-ARBs do no have an effect on Bradykinin |
|
|
What side affect do ACEIs have that ARBs do not?
|
cough
-ARBs do no have an effect on Bradykinin |
|
|
What are some common drug interactions for ARBs?
|
-Potassium supplements
-Potassium sparing diuretics |
|
|
What are some common drug interactions for ARBs?
|
-Potassium supplements
-Potassium sparing diuretics |
|
|
What are some common drug interactions for ARBs?
|
-Potassium supplements
-Potassium sparing diuretics |
|
|
What are some common drug interactions for ARBs?
|
-Potassium supplements
-Potassium sparing diuretics |
|
|
Does a pt on ARBs have to consider mealtimes when administering the drug?
|
No, unlike pts on ACEIs
|
|
|
Does a pt on ARBs have to consider mealtimes when administering the drug?
|
No, unlike pts on ACEIs
|
|
|
Does a pt on ARBs have to consider mealtimes when administering the drug?
|
No, unlike pts on ACEIs
|
|
|
Does a pt on ARBs have to consider mealtimes when administering the drug?
|
No, unlike pts on ACEIs
|
|
|
Give an example of a Direct Renin Inhibitor
|
Aliskiren (Tekturna)
|
|
|
Give an example of a Direct Renin Inhibitor
|
Aliskiren (Tekturna)
|
|
|
Give an example of a Direct Renin Inhibitor
|
Aliskiren (Tekturna)
|
|
|
Give an example of a Direct Renin Inhibitor
|
Aliskiren (Tekturna)
|
|
|
Describe the MOA of Direct Renin Inhibitors
|
-Bind to the active site of renin, preventing the cleavage of angiotensinogen and the formation of angiotensin I
|
|
|
Describe the MOA of Direct Renin Inhibitors
|
-Bind to the active site of renin, preventing the cleavage of angiotensinogen and the formation of angiotensin I
|
|
|
Describe the MOA of Direct Renin Inhibitors
|
-Bind to the active site of renin, preventing the cleavage of angiotensinogen and the formation of angiotensin I
|
|
|
Describe the MOA of Direct Renin Inhibitors
|
-Bind to the active site of renin, preventing the cleavage of angiotensinogen and the formation of angiotensin I
|
|
|
What ultimate effect do DRIs have on the body?
|
They ultimately drop angiotensin II
|
|
|
What ultimate effect do DRIs have on the body?
|
They ultimately drop angiotensin II
|
|
|
What ultimate effect do DRIs have on the body?
|
They ultimately drop angiotensin II
|
|
|
What ultimate effect do DRIs have on the body?
|
They ultimately drop angiotensin II
|
|
|
What are the adverse effects of DRIs?
|
ANGIOEDEMA
-No cough! |
|
|
What are the adverse effects of DRIs?
|
ANGIOEDEMA
-No cough! |
|
|
What are the adverse effects of DRIs?
|
ANGIOEDEMA
-No cough! |
|
|
What are the adverse effects of DRIs?
|
ANGIOEDEMA
-No cough! |
|
|
Which drug cause angioedema?
|
-ACEIs
-ARBs -DRIs |
|
|
Which drug cause angioedema?
|
-ACEIs
-ARBs -DRIs |
|
|
Which drug cause angioedema?
|
-ACEIs
-ARBs -DRIs |
|
|
Which drug cause angioedema?
|
-ACEIs
-ARBs -DRIs |
|
|
What is the only effect that ACEIs/ARBs/DRIs have on blood pressure?
|
They only reduce PVR!
Have no effect on CO or Blood Volume! |
|
|
What is the only effect that ACEIs/ARBs/DRIs have on blood pressure?
|
They only reduce PVR!
Have no effect on CO or Blood Volume! |
|
|
What is the only effect that ACEIs/ARBs/DRIs have on blood pressure?
|
They only reduce PVR!
Have no effect on CO or Blood Volume! |
|
|
What is the only effect that ACEIs/ARBs/DRIs have on blood pressure?
|
They only reduce PVR!
Have no effect on CO or Blood Volume! |
|
|
What two classes of drugs fall under Calcium Channel Blockers?
|
-Dihydropyridines (DHP)
Non-Dihydropyridines (non-DHP) |
|
|
What two classes of drugs fall under Calcium Channel Blockers?
|
-Dihydropyridines (DHP)
Non-Dihydropyridines (non-DHP) |
|
|
What two classes of drugs fall under Calcium Channel Blockers?
|
-Dihydropyridines (DHP)
Non-Dihydropyridines (non-DHP) |
|
|
What two classes of drugs fall under Calcium Channel Blockers?
|
-Dihydropyridines (DHP)
Non-Dihydropyridines (non-DHP) |
|
|
What is the most common DHP?
What is the most common non-DHP? |
DHP = Amlodipine (Norvasc)
non-DHP = Diltiazem (Cardizem) |
|
|
What is the most common DHP?
What is the most common non-DHP? |
DHP = Amlodipine (Norvasc)
non-DHP = Diltiazem (Cardizem) |
|
|
What is the most common DHP?
What is the most common non-DHP? |
DHP = Amlodipine (Norvasc)
non-DHP = Diltiazem (Cardizem) |
|
|
What is the most common DHP?
What is the most common non-DHP? |
DHP = Amlodipine (Norvasc)
non-DHP = Diltiazem (Cardizem) |
|
|
What function do non-DHPs have that DHPs do not?
|
They lower HR --> lowers CO --> lowers BP
|
|
|
What function do non-DHPs have that DHPs do not?
|
They lower HR --> lowers CO --> lowers BP
|
|
|
What function do non-DHPs have that DHPs do not?
|
They lower HR --> lowers CO --> lowers BP
|
|
|
What function do non-DHPs have that DHPs do not?
|
They lower HR --> lowers CO --> lowers BP
|
|
|
What is the MOA of CCBs?
|
Calcium Channel Blockers
-Decreases PVR by blocking CALCIUM entry into smooth muscle --> vasodilation |
|
|
What is the MOA of CCBs?
|
Calcium Channel Blockers
-Decreases PVR by blocking CALCIUM entry into smooth muscle --> vasodilation |
|
|
What is the MOA of CCBs?
|
Calcium Channel Blockers
-Decreases PVR by blocking CALCIUM entry into smooth muscle --> vasodilation |
|
|
What is the MOA of CCBs?
|
Calcium Channel Blockers
-Decreases PVR by blocking CALCIUM entry into smooth muscle --> vasodilation |
|
|
Which CCB has a greater overall effect on BP?
|
DHP lower BP much more than non-DHPs
|
|
|
Which CCB has a greater overall effect on BP?
|
DHP lower BP much more than non-DHPs
|
|
|
Which CCB has a greater overall effect on BP?
|
DHP lower BP much more than non-DHPs
|
|
|
Which CCB has a greater overall effect on BP?
|
DHP lower BP much more than non-DHPs
|
|
|
Which CCB has a greater effect on HR?
|
non-DHP can lower HR, DHPs do not
|
|
|
Which CCB has a greater effect on HR?
|
non-DHP can lower HR, DHPs do not
|
|
|
Which CCB has a greater effect on HR?
|
non-DHP can lower HR, DHPs do not
|
|
|
Which CCB has a greater effect on HR?
|
non-DHP can lower HR, DHPs do not
|
|
|
What effect do DHPs have on HR?
|
They can actually increase HR causing REFLEX TACHYCARDIA
|
|
|
What effect do DHPs have on HR?
|
They can actually increase HR causing REFLEX TACHYCARDIA
|
|
|
What effect do DHPs have on HR?
|
They can actually increase HR causing REFLEX TACHYCARDIA
|
|
|
What effect do DHPs have on HR?
|
They can actually increase HR causing REFLEX TACHYCARDIA
|
|
|
-What are the adverse effects of Alodipine
|
-DHP
-Reflex tachycardia -Headache and flushing -Peripheral edema |
|
|
-What are the adverse effects of Alodipine
|
-DHP
-Reflex tachycardia -Headache and flushing -Peripheral edema |
|
|
-What are the adverse effects of Alodipine
|
-DHP
-Reflex tachycardia -Headache and flushing -Peripheral edema |
|
|
-What are the adverse effects of Alodipine
|
-DHP
-Reflex tachycardia -Headache and flushing -Peripheral edema |
|
|
Bradycardia and Cardiac arrest are adverse effects of what drug?
|
Diltiazem (Caedizem)
which is a non-DHP CCB |
|
|
Bradycardia and Cardiac arrest are adverse effects of what drug?
|
Diltiazem (Caedizem)
which is a non-DHP CCB |
|
|
Bradycardia and Cardiac arrest are adverse effects of what drug?
|
Diltiazem (Caedizem)
which is a non-DHP CCB |
|
|
Bradycardia and Cardiac arrest are adverse effects of what drug?
|
Diltiazem (Caedizem)
which is a non-DHP CCB |
|
|
What are the Direct Vasodilator agents?
|
-Hydralazine (Apresoline)
-Minoxidil (Loniten) Rogaine! |
|
|
What are the Direct Vasodilator agents?
|
-Hydralazine (Apresoline)
-Minoxidil (Loniten) Rogaine! |
|
|
What are the Direct Vasodilator agents?
|
-Hydralazine (Apresoline)
-Minoxidil (Loniten) Rogaine! |
|
|
What are the Direct Vasodilator agents?
|
-Hydralazine (Apresoline)
-Minoxidil (Loniten) Rogaine! |
|
|
What MOA is used by Direct Vasodilators?
|
-Causes artery relaxation (vasodilation) resulting in decreased blood pressure
|
|
|
What MOA is used by Direct Vasodilators?
|
-Causes artery relaxation (vasodilation) resulting in decreased blood pressure
|
|
|
What MOA is used by Direct Vasodilators?
|
-Causes artery relaxation (vasodilation) resulting in decreased blood pressure
|
|
|
What MOA is used by Direct Vasodilators?
|
-Causes artery relaxation (vasodilation) resulting in decreased blood pressure
|
|
|
What can occur is Direct Vasodilators are administered alone?
|
They can cause reflex tachycardia
∴They are usually combined with another drug |
|
|
What can occur is Direct Vasodilators are administered alone?
|
They can cause reflex tachycardia
∴They are usually combined with another drug |
|
|
What can occur is Direct Vasodilators are administered alone?
|
They can cause reflex tachycardia
∴They are usually combined with another drug |
|
|
What can occur is Direct Vasodilators are administered alone?
|
They can cause reflex tachycardia
∴They are usually combined with another drug |
|
|
What are the adverse effects of Direct Vasodilators? When do these affects usually take place?
|
-Tachycardia
-Fluid Retention -Usually occur early in administration |
|
|
What are the adverse effects of Direct Vasodilators? When do these affects usually take place?
|
-Tachycardia
-Fluid Retention -Usually occur early in administration |
|
|
What are the adverse effects of Direct Vasodilators? When do these affects usually take place?
|
-Tachycardia
-Fluid Retention -Usually occur early in administration |
|
|
What are the adverse effects of Direct Vasodilators? When do these affects usually take place?
|
-Tachycardia
-Fluid Retention -Usually occur early in administration |
|
|
What effects do Direct Vasodilators have on PVR?
On CO? On Blood Volume? |
PVR= ↓
CO = ↑ Blood Volume = ↑ |
|
|
What effects do Direct Vasodilators have on PVR?
On CO? On Blood Volume? |
PVR= ↓
CO = ↑ Blood Volume = ↑ |
|
|
What effects do Direct Vasodilators have on PVR?
On CO? On Blood Volume? |
PVR= ↓
CO = ↑ Blood Volume = ↑ |
|
|
What effects do Direct Vasodilators have on PVR?
On CO? On Blood Volume? |
PVR= ↓
CO = ↑ Blood Volume = ↑ |
|
|
What is Angina?
|
Pain caused by body's response to lack of O2 in the heart
|
|
|
What is Angina?
|
Pain caused by body's response to lack of O2 in the heart
|
|
|
What is Angina?
|
Pain caused by body's response to lack of O2 in the heart
|
|
|
What is Angina?
|
Pain caused by body's response to lack of O2 in the heart
|
