Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

CR III > Pharm > Flashcards

Pharm Flashcards

1
Q

Aliskiren

A
  • Potent Renin Inhibitor
    • Long half-life (>24 hours)
    • Orally Active
    • Low Bioavailability
  • MOA
    • Supression of plasma renin activity → decreasing the levels of Ang I and II
    • Induces compensatory increase renin secretion
  • Indication
    • Primary hypertension (Not a first-line agent)
  • Contraindication
    • Pregnancy
    • Bilateral Renal Artery Stenosis
  • Adverse Effects
    • GI Disturbances
    • Headache
    • Dizziness
    • Angioedema
    • Cough
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Captopril

A
  • ACE Inhibitor
  • Shortest half-life
  • MOA
    • Inhibits conversion of Ang I to Ang II → Reducing levels of circulating and locally formed Ang II
  • Indication
    • Hypertension (First-Line)
    • Heart Failure
    • Acute MI
    • Chronic Renal Failure
    • Reduce Adverse Cardiovascular Events in High-Risk Patients
  • Contraindications
    • Pregnancy
    • Bilateral Renal Artery Stenosis
  • Adverse Effects
    • Hypotension
    • Hyperkalemia
    • Renal Function Impairment
    • Dry Cough
    • Skin Rash (Vessel Relaxation)
    • Dizziness
    • Headache
    • Impaired Taste
    • GI Disturbances
    • Angioedema (Serious, but Rare)
    • Proteinuria
    • Neutropenia
    • Glycosuria
    • Hepatotoxicity
  • Drug Interactions
    • NSAIDs - may impair hypotensive effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the consequences of taking an ACE Inhibitor?

A
  • Compensatory increase in plasma renin activity and Ang I levels due to removal of feedback inhibition of Ang II
  • Decrease in aldosterone levels
  • Generation of Ang II by alternative pathways
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the benificial effects of ACE Inhibitors?

A
  • Lower BP
  • Improve Arterial Compliance
  • Decrease Afterload
  • May prevent/reverse vascular and ventricular remodeling and hypertrophy
  • Improve Renal Perfusion
    • Lower Intraglomerular Pressure
  • May Improve Insulin Sensitivity and Glucose Metabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Enalapril

A
  • ACE Inhibitor
    • Prodrug converted to enalaprilat by an esterase in liver
    • Enalaprilat may be administered via I.V. in hypertensive emergencies
  • MOA
    • Inhibits conversion of Ang I to Ang II → Reducing levels of circulating and locally formed Ang II
  • Indication
    • Hypertension (First-Line)
    • Heart Failure
    • Acute MI
    • Chronic Renal Failure
    • Reduce Adverse Cardiovascular Events in High-Risk Patients
  • Contraindications
    • Pregnancy
    • Bilateral Renal Artery Stenosis
  • Adverse Effects
    • Hypotension
    • Hyperkalemia
    • Renal Function Impairment
    • Dry Cough
    • Skin Rash (Vessel Relaxation)
    • Dizziness
    • Headache
    • Impaired Taste
    • GI Disturbances
    • Angioedema (Serious, but Rare)
    • Proteinuria
    • Neutropenia
    • Glycosuria
    • Hepatotoxicity
  • Drug Interactions
    • NSAIDs - may impair hypotensive effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Lisinopril

A
  • ACE Inhibitor
    • Lysine derivative of enalaprilat
    • Enalaprilat may be administered via I.V. in hypertensive emergencies
  • MOA
    • Inhibits conversion of Ang I to Ang II → Reducing levels of circulating and locally formed Ang II
  • Indication
    • Hypertension (First-Line)
    • Heart Failure
    • Acute MI
    • Chronic Renal Failure
    • Reduce Adverse Cardiovascular Events in High-Risk Patients
  • Contraindications
    • Pregnancy
    • Bilateral Renal Artery Stenosis
  • Adverse Effects
    • Hypotension
    • Hyperkalemia
    • Renal Function Impairment
    • Dry Cough
    • Skin Rash (Vessel Relaxation)
    • Dizziness
    • Headache
    • Impaired Taste
    • GI Disturbances
    • Angioedema (Serious, but Rare)
    • Proteinuria
    • Neutropenia
    • Glycosuria
    • Hepatotoxicity
  • Drug Interactions
    • NSAIDs - may impair hypotensive effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Losartan

A
  • AT1 Receptor Blocker (Ang II Receptor Blocker)
    • Highly bound to plasma proteins
    • Poorly/Do NOT Cross the BBB
  • Orally Active
    • Undergoes extensive first-pass hepatic metabolism
    • Active metabolite longer half-life than parent compound
  • MOA
    • Selectively block AT1 Receptors
  • Indication
    • Hypertension
    • Heart Failure
    • Diabetic Nephropathy
    • Patients Intolerant to ACE Inhibitors
  • Contraindications
    • Pregnancy
    • Bilateral Renal Artery Stenosis
  • Adverse Effects
    • Hypotension (First-Dose)
    • Hyperkalemia
    • Renal Function Impairment
    • Skin Rash (Vessel Relaxation)
    • Dizziness
    • Headache
    • Impaired Taste
    • GI Disturbances
    • Less Chance of Angioedema compared to ACE Inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Candesartan

A
  • AT1 Receptor Blocker (Ang II Receptor Blocker)
    • Highly bound to plasma proteins
    • Poorly/Do NOT Cross the BBB
  • Prodrug
  • MOA
    • Selectively block AT1 Receptors
  • Indication
    • Hypertension
    • Heart Failure
    • Diabetic Nephropathy
    • Patients Intolerant to ACE Inhibitors
  • Contraindications
    • Pregnancy
    • Bilateral Renal Artery Stenosis
  • Adverse Effects
    • Hypotension (First-Dose)
    • Hyperkalemia
    • Renal Function Impairment
    • Skin Rash (Vessel Relaxation)
    • Dizziness
    • Headache
    • Impaired Taste
    • GI Disturbances
    • Less Chance of Angioedema compared to ACE Inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Olmesartan

A
  • AT1 Receptor Blocker (Ang II Receptor Blocker)
    • Highly bound to plasma proteins
    • Poorly/Do NOT Cross the BBB
  • Prodrug
  • MOA
    • Selectively block AT1 Receptors
  • Indication
    • Hypertension
    • Heart Failure
    • Diabetic Nephropathy
    • Patients Intolerant to ACE Inhibitors
  • Contraindications
    • Pregnancy
    • Bilateral Renal Artery Stenosis
  • Adverse Effects
    • Hypotension (First-Dose)
    • Hyperkalemia
    • Renal Function Impairment
    • Skin Rash (Vessel Relaxation)
    • Dizziness
    • Headache
    • Impaired Taste
    • GI Disturbances
    • Less Chance of Angioedema compared to ACE Inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Icatibant

A
  • Bradykinin B2 Antagonist
  • MOA
    • Blocks bradykinin B2 receptors, reducing vascular permeability
  • Indication
    • Acute Hereditary and ACE Inhibitor-Associated Angioedema
      • Reduced symptoms more rapidly than glucocoticoids and antihistamines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Bosentan

A
  • Endothelin Receptor Antagonist
    • Nonselective ETA/ETB antagonist
  • Orally Active
  • MOA
    • Block ET receptors, relaxing vascular smooth muscle
  • Indication
    • Pulmonary Arterial Hypertension
  • Contraindication
    • Pregnancy (Teratogenic)
  • Adverse Effects
    • Headache
    • Flushing
    • Hypotension
    • Peripheral Edema
    • Palpitations
    • Elevation of Liver Enzymes (Chronic Therapy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Macitentan

A
  • Endothelin Receptor Antagonist
    • Nonselective ETA/ETB antagonist
  • Orally Active
  • MOA
    • Block ET receptors, relaxing vascular smooth muscle
  • Indication
    • Pulmonary Arterial Hypertension
  • Contraindication
    • Pregnancy (Teratogenic)
  • Adverse Effects
    • Headache
    • Flushing
    • Hypotension
    • Peripheral Edema
    • Palpitations
    • Elevation of Liver Enzymes (Chronic Therapy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Ambrisentan

A
  • Endothelin Receptor Antagonist
    • Selective ETA antagonist
  • MOA
    • Block ET receptors, relaxing vascular smooth muscle
  • Indication
    • Pulmonary Arterial Hypertension
  • Contraindication
    • Pregnancy (Teratogenic)
  • Adverse Effects
    • Headache
    • Flushing
    • Hypotension
    • Peripheral Edema
    • Palpitations
    • Elevation of Liver Enzymes (Chronic Therapy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Nesiritide

A
  • Natriuretic Peptide Agonist
    • Recombinant Human BNP
  • Given via I.V.
  • Indications
    • Acute Decompensated Congestive Heart Failure
  • Pharmcological Effects
    • Relax arteries and veins
    • Promote diuresis and natriuresis
    • Decrease cardiovascular remodeling
    • Lower blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Sacubitril

A
  • Neprilysin Inhibitor
  • Prodrug
    • ​Activated to LBQ657 by de-ethylation via esterases
  • MOA
    • Inhibits neprilysin (responsible for ANP and BNP degradation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Entresto

A
  • Sacubitril and Valsartan
  • MOA
    • Enhance effects of ANP and BNP
    • Block Effects of Ang II
  • Indication
    • Chronic Heart Failure w/ Reduced Ejection Fraction
  • Contraindication
    • Hypersensitivity to sacubitril or valsartan
    • History of Angioedema
    • Concomitant use of ACE Inhibitors, AT1 Antagonist, or Aliskiren
17
Q

Acetazolamide

A
  • Carbonic Anhydrase Inhibitor
  • MOA
    • Inhibit Carbonic Anhydrase
    • Promotes HCO3- and Na+ Excretion → Increased Urine pH and Volume
  • Tolerance develops after 3-4 days due to metabolic acidosis caused by HCO3- excretion
  • Reduce formation of HCO3- in aqueous humor and cerebrospinal fluid
    • Decreases rate of formation of aqueous humor and cerbrospinal fluid
    • Lowers Intraocular Pressure and Cerbrospinal Pressure
  • Rapidly Absorbed/NOT Metabolized/Max Action @ 2 hours/Persists for 12 Hours
  • Indications
    • Glaucoma
    • Urinary Acidosis
    • Metabolic Alkalosis
    • Acute Mountain Sickness
  • Adverse Effects
    • Metabolic Acidosis
    • Renal Stones
    • Renal Potassium Wasting
18
Q

Furosemide

A
  • Loop Diuretic
    • Most Efficacious of All Diuretics
  • Sulfonamide
  • Pharmacokinetics
    • Rapidly absorbed
    • Half-Life = 2 hours
    • Onset of Effect
      • Lasts 6-8 hours
      • Peaks 1-2 hours
      • Within 1 hour
    • Can be given parenterally
    • Extensively bound to plasma proteins
    • Secreted by organic acid secretory system in Proximal Tubule
      • Competes w/ Uric Acid
      • May induce gout attack
    • 60-65% Eliminated via Renal Route
    • 35-40% Eliminated by Metabolism
  • MOA
    • Inhibits Na/K/2Cl cotransport in thick ascending limb → increased excretion of NaCl
      • Increases Na delivery to distal convoluted tuble and collecting tubule
    • Enhance Ca and Mg excretion
    • Increase K Secretion
    • Increased excretion of NaCl, H2O, Mg, and Ca in urine
  • Adverse Effects
    • Hypokalemic Metabolic Alkalosis
    • Hypomagnesemia
    • Hyperuricemia
    • Hyperglycemia
    • Hyperlipidemia
    • Ototoxicity
    • Hyponatremia
19
Q

Bumetanide

A
  • Loop Diuretic
    • Most Efficacious of All Diuretics
  • Sulfonamide
  • Pharmacokinetics
    • Rapidly absorbed
    • Half-Life = 1-1.5 hours
    • Onset of Effect
      • Within 30-60 Minutes
      • Peaks 1-2 hours
      • Lasts 4-6 hours
    • Extensively bound to plasma proteins
    • Secreted by organic acid secretory system in Proximal Tubule
      • Competes w/ Uric Acid
      • May induce gout attack
    • 60-65% Eliminated via Renal Route
    • 35-40% Eliminated by Metabolism
  • MOA
    • Inhibits Na/K/2Cl cotransport in thick ascending limb → increased excretion of NaCl
      • Increases Na delivery to distal convoluted tuble and collecting tubule
    • Enhance Ca and Mg excretion
    • Increase K Secretion
    • Increased excretion of NaCl, H2O, Mg, and Ca in urine
  • Adverse Effects
    • Hypokalemic Metabolic Alkalosis
    • Hypomagnesemia
    • Hyperuricemia
    • Hyperglycemia
    • Hyperlipidemia
    • Ototoxicity
    • Hyponatremia
20
Q

Ethacrynic Acid

A
  • Loop Diuretic
    • Most Efficacious of All Diuretics
  • Pharmacokinetics
    • Rapidly absorbed
    • Half-Life = 1 hour
    • Onset of Effect
      • Within 30 Minutes
      • Peaks 2 hours
      • Lasts 6-8 hours
    • Extensively bound to plasma proteins
    • Secreted by organic acid secretory system in Proximal Tubule
      • Competes w/ Uric Acid
      • May induce gout attack
    • 60-65% Eliminated via Renal Route
    • 35-40% Eliminated by Metabolism
  • MOA
    • Inhibits Na/K/2Cl cotransport in thick ascending limb → increased excretion of NaCl
      • Increases Na delivery to distal convoluted tuble and collecting tubule
    • Enhance Ca and Mg excretion
    • Increase K Secretion
    • Increased excretion of NaCl, H2O, Mg, and Ca in urine
  • Adverse Effects
    • Hypokalemic Metabolic Alkalosis
    • Hypomagnesemia
    • Hyperuricemia
    • Hyperglycemia
    • Hyperlipidemia
    • Ototoxicity
    • Hyponatremia
21
Q

Torsemide

A
  • Loop Diuretic
    • Most Efficacious of All Diuretics
  • Sulfonamide
  • Pharmacokinetics
    • Rapidly absorbed
    • Half-Life = 3-4 hours
    • Onset of Effect
      • Within 1 hour
      • Peaks 1-2 hours
      • Lasts 12-16 hours
    • Extensively bound to plasma proteins
    • Secreted by organic acid secretory system in Proximal Tubule
      • Competes w/ Uric Acid
      • May induce gout attack
    • 70% Eliminated via Hepatic Metabolism
    • 30% Eliminated by Renal Route
  • MOA
    • Inhibits Na/K/2Cl cotransport in thick ascending limb → increased excretion of NaCl
      • Increases Na delivery to distal convoluted tuble and collecting tubule
    • Enhance Ca and Mg excretion
    • Increase K Secretion
    • Increased excretion of NaCl, H2O, Mg, and Ca in urine
  • Adverse Effects
    • Hypokalemic Metabolic Alkalosis
    • Hypomagnesemia
    • Hyperuricemia
    • Hyperglycemia
    • Hyperlipidemia
    • Ototoxicity
    • Hyponatremia
22
Q

Hydrochlorothiazide

A
  • Thiazide Diuretics
  • Chemically Related to Sulfonamides
  • Pharmacokinetics
    • Bound to plasma proteins
    • Secreted by organic acid secretory system in PT (compete w/ uric acid)
    • Primarily excreted in urine
  • MOA
    • Inhibit Na/Cl cotransporter in distal convoluted tubule leading to decreased Na and Cl reabsorption
    • Enhance Ca reabsorption in PT and DCT
  • Adverse Effects
    • Hypokalemic metabolic alkalosis and hyperuricemia
    • Hypersensitivity reactions
    • Hypercalcemia
    • Hyperlipidemia
    • Hyperglycemia
    • Chronic Dilutional Hyponatremia
  • Indications
    • Edema
      • Chronic Heart Failure
      • Acute Pulmonary Edema
    • Nonedematous
      • Hypertension
      • Diabetic Insipidus
      • Nephrolithiasis and Osteoporosis
      • Hypercalcemia
23
Q

Indapamide

A
  • Thiazide-Like Diuretics
  • Pharmacokinetics
    • Don’t accumulate in patients w/ renal impairment
  • MOA
    • Block Na-Cl reabsorption in the distal convoluted tubule
    • Block Na reabsorption in proximal tubule
  • Adverse Effects
    • Hypokalemic metabolic alkalosis and hyperuricemia
    • Hypersensitivity reactions
    • Hypercalcemia
    • Chronic Dilutional Hyponatremia
  • Indications
    • Can be combined w/ loop diuretics to induce urine formation in patients with <20 ml/min GFR
24
Q

Metolazone

A
  • Thiazide-Like Diuretic
  • Pharmacokinetics
    • Don’t accumulate in patients w/ renal impairment
  • MOA
    • Block Na-Cl reabsorption in the distal convoluted tubule
    • Block Na reabsorption in proximal tubule
  • Adverse Effects
    • Hypokalemic metabolic alkalosis and hyperuricemia
    • Hypersensitivity reactions
    • Hypercalcemia
    • Chronic Dilutional Hyponatremia
  • Indications
    • Can be combined w/ loop diuretics to induce urine formation in patients with <20 ml/min GFR
25
Spironolactone
* Aldosterone Receptor Antagonist * Non-selective Antagonist * Potassium Sparing * Prodrug * Metabolized to canrenone (active metabolite) * MOA * Reduce Na reabsorption subsequently K excretion * Decrease H secretion * Pharmacokinetics * Rapid absorption * \>90% bound to plasma protein * Rapidly/Extensively metabolized * Onset = 24-48 Hours * Duration = 48-72 Hours * Half-Life = 1.6 hours Spironolactone 10-35 hours Canrenone * Primarily Excreted in Urine * Only diuretic that DOES NOT need to get into the lumen of the renal tubule * Indication * Hyperaldosteronism * Primary * Secondary * Hepatic Cirrhosis * Chronic Heart Failure * Edema * Hypertension * Adverse Effects * Hyperkalemia * Metabolic Acidosis * Gynecomastia * Contraindication * Renal Insufficiency * Serum K+ \>5.0 mEq/L * Treatment w/ other K-sparing diuretics * Oral potassium supplement
26
Eplerenone
* Aldosterone Receptor Antagonist * Selective Antagonist * Potassium Sparing * Prodrug * Metabolized to canrenone (active metabolite) * MOA * Reduce Na reabsorption subsequently K excretion * Decrease H secretion * Pharmacokinetics * Rapid absorption * \>90% bound to plasma protein * Rapidly/Extensively metabolized * Onset = 24-48 Hours * Duration = 48-72 Hours * Half-Life = 1.6 hours Spironolactone 10-35 hours Canrenone * Primarily Excreted in Urine * Only diuretic that DOES NOT need to get into the lumen of the renal tubule * Indication * Hyperaldosteronism * Primary * Secondary * Hepatic Cirrhosis * Chronic Heart Failure * Edema * Hypertension * Adverse Effects * Hyperkalemia * Metabolic Acidosis * Gynecomastia * Contraindication * Renal Insufficiency * Serum K+ \>5.0 mEq/L * Treatment w/ other K-sparing diuretics * Oral potassium supplement
27
Triamterene
* Potassium Sparing Diuretic * Na Channel Blocker * MOA * Block Na channels in luminal membrane of late distal tubules and collecting tubules * Thus inhibiting Na influx and K secretion * Pharmacokinetics * Rapid Absorption * Bound to proteins * Onset of Action = 2-4 Hours * Peak Effect = 6-8 Hours * Duration of Action = 12-16 Hours * Metabolized to sulfate conjugate and hydroxyltriamterene (active metabolite) * Half-Life = Approx. 3 Hours * Primarily Excreted by Glomerular Filtration and Organic Base Transport System Secretion * Indications * Edema * Hypertension * Contraindication * Renal Insufficiency * Serum Potassium \>5.0 mEq/L * Treatment w/ other potassium sparing diuretics * Oral admin of potassium * Adverse Effects * Hyperkalemia
28
Amiloride
* Potassium Sparing Diuretic * Na Channel Blocker * MOA * Block Na channels in luminal membrane of late distal tubules and collecting tubules * Thus inhibiting Na influx and K secretion * Pharmacokinetics * Rapid Absorption * Bound to proteins * Onset of Action = 2 Hours * Peak Effect = 6-10 Hours * Duration of Action = 24 Hours * Half-Life = 6-9 Hours * Excreted unchanged in urine and feces * Secreted into proximal tubule by organic base transport * Indications * Edema * Hypertension * Contraindication * Renal Insufficiency * Serum Potassium \>5.0 mEq/L * Treatment w/ other potassium sparing diuretics * Oral admin of potassium * Adverse Effects * Hyperkalemia
29
Patiromer
* Used to treat Hyperkalemia * MOA * Binds to excess K+ in the colon promoting K+ excretion * Indication * Non-life threatening hyperkalemia *

CR III (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions