Advanced Pharmacology Exam 3 (2026/2027) |
Latest Questions | 100% Verified Answers | A+
• Hypertension -✓✓Classification is determined based on the average of
two or more properly measured seated blood pressure measurements
from two or more more clinical encounters. If systolic and diastolic BP
yield different classifications, the highest category is used for the
purpose of determining a classification.
JNC VIII --> just know that these recommendations are much looser
than the JNC VII, and that pt with heart disease are no longer included in
guidelines!
• Blood Pressure -✓✓Based on the mathematical equation:
BP = CO (cardiac output) x SVR (systemic vascular resistance)
Increased BP can result either from increase in CO or increase in SVR
-These are controlled by the sympathetic nervous system and the RAAS
system!
• Regulation of Blood Pressure -✓✓Causes of increased CO:
-Increased fluid volume (excess sodium and water)
-Excess stimulation of the RAAS
-Sympathetic nervous system overactivity
Causes of increased SVR:
,-Excess stimulation of RAAS
-Sympathetic nervous system overactivity
• Diuretics -✓✓in the normal adult approx 180 L of fluid is filtered by
the kidneys each day (with 25,000 mEq of Na)
Balance is maintained by the reabsorption of sodium along the entire
length of the nephron --> as you move through the nephrons you have
less reabsorption (H2O follows Na!)
There are two decreases in BP:
-Initial BP decrease --> decrease blood volume resulting in decreased
CO; compensatory increase in SVR (activation of RAAS and SNS)
-Sustained BP decrease --> decreases SVR resulting in decreased Na-
content of smooth muscle cells
Decreased CO, Decreased SVR, Decreased Blood Vol.
Classified based on MOA in the nephron:
-carbonic anhydrase inhibitors
-loop diuretics
-thiazide diuretics
-K-sparing diuretics
,• Carbonic Anhydrase Inhibitors -✓✓Acetazolamide (Diamox)
Therapeutic uses: glaucoma, urinary alkalinization, metabolic alkalosis
(creates metabolic acidosis), acute mountain sickness
*NOT an effective class to use for diuresis and therefore not routinely
used to tx HTN (because not potent)
• Carbonic Anhydrase Inhibitor Mechanism of Action -✓✓Block
NaHCO3 reabsorption and cause diuresis predominantly in the proximal
tubule
Not as potent because not affecting the more potent channels
• Carbonic Anhydrase Inhibitor Adverse Effects -✓✓Hyperchloremic
metabolic acidosis --> losing Na and Bicarb!
Renal stones
Drowsiness
Paresthesias
Hypersensitivity reactions
*Note: these are not usually used as oral agents, these are the systemic
effects of oral use
, • Loop Diuretics -✓✓Furosemide (Lasix) --> 10-100% bioavailability
(oral = ~50%)
Bumetanide (Bumex) --> 80-100% bioavailability
Torsemide (Demadex) --> 80-100% bioavailability
Ethacrynic acid (Edecrin)
Oral and IV preparations
Short half-life (2-6 h) --> need to be administered multiple times each
day for continuous fluid removal
Excreted by the kidneys (prolonged renal half-life)
Therapeutic uses:
-states of volume overload *very effective for fluid elimination*
-less extensively used in the maintenance tx of HTN
-hyperkalemia --> works on other electrolytes
• Loop Diuretic Mechanism of Action -✓✓-Inhibits Na reabsorption in
the ascending limb of the Loop of Henle
-Promotes up to 25% Na and water excretion
-Increases urinary excretion of other electrolytes
*Most potent diuretics - inhibit up to 25% of Na and H2O reabsorption*
Latest Questions | 100% Verified Answers | A+
• Hypertension -✓✓Classification is determined based on the average of
two or more properly measured seated blood pressure measurements
from two or more more clinical encounters. If systolic and diastolic BP
yield different classifications, the highest category is used for the
purpose of determining a classification.
JNC VIII --> just know that these recommendations are much looser
than the JNC VII, and that pt with heart disease are no longer included in
guidelines!
• Blood Pressure -✓✓Based on the mathematical equation:
BP = CO (cardiac output) x SVR (systemic vascular resistance)
Increased BP can result either from increase in CO or increase in SVR
-These are controlled by the sympathetic nervous system and the RAAS
system!
• Regulation of Blood Pressure -✓✓Causes of increased CO:
-Increased fluid volume (excess sodium and water)
-Excess stimulation of the RAAS
-Sympathetic nervous system overactivity
Causes of increased SVR:
,-Excess stimulation of RAAS
-Sympathetic nervous system overactivity
• Diuretics -✓✓in the normal adult approx 180 L of fluid is filtered by
the kidneys each day (with 25,000 mEq of Na)
Balance is maintained by the reabsorption of sodium along the entire
length of the nephron --> as you move through the nephrons you have
less reabsorption (H2O follows Na!)
There are two decreases in BP:
-Initial BP decrease --> decrease blood volume resulting in decreased
CO; compensatory increase in SVR (activation of RAAS and SNS)
-Sustained BP decrease --> decreases SVR resulting in decreased Na-
content of smooth muscle cells
Decreased CO, Decreased SVR, Decreased Blood Vol.
Classified based on MOA in the nephron:
-carbonic anhydrase inhibitors
-loop diuretics
-thiazide diuretics
-K-sparing diuretics
,• Carbonic Anhydrase Inhibitors -✓✓Acetazolamide (Diamox)
Therapeutic uses: glaucoma, urinary alkalinization, metabolic alkalosis
(creates metabolic acidosis), acute mountain sickness
*NOT an effective class to use for diuresis and therefore not routinely
used to tx HTN (because not potent)
• Carbonic Anhydrase Inhibitor Mechanism of Action -✓✓Block
NaHCO3 reabsorption and cause diuresis predominantly in the proximal
tubule
Not as potent because not affecting the more potent channels
• Carbonic Anhydrase Inhibitor Adverse Effects -✓✓Hyperchloremic
metabolic acidosis --> losing Na and Bicarb!
Renal stones
Drowsiness
Paresthesias
Hypersensitivity reactions
*Note: these are not usually used as oral agents, these are the systemic
effects of oral use
, • Loop Diuretics -✓✓Furosemide (Lasix) --> 10-100% bioavailability
(oral = ~50%)
Bumetanide (Bumex) --> 80-100% bioavailability
Torsemide (Demadex) --> 80-100% bioavailability
Ethacrynic acid (Edecrin)
Oral and IV preparations
Short half-life (2-6 h) --> need to be administered multiple times each
day for continuous fluid removal
Excreted by the kidneys (prolonged renal half-life)
Therapeutic uses:
-states of volume overload *very effective for fluid elimination*
-less extensively used in the maintenance tx of HTN
-hyperkalemia --> works on other electrolytes
• Loop Diuretic Mechanism of Action -✓✓-Inhibits Na reabsorption in
the ascending limb of the Loop of Henle
-Promotes up to 25% Na and water excretion
-Increases urinary excretion of other electrolytes
*Most potent diuretics - inhibit up to 25% of Na and H2O reabsorption*
