Renal II - Diuretics Flashcards
Mechanism of diuretic action:
Definition of diuretics?
Role of clinically useful diuretics?
Mechanism of diuretic action:
Diuretics increase rate of urine flow
Clinically useful diuretics also increase renal excretion of Na+ (natriuresis) along with Cl-
Mechanism of diuretic action:
Most clinical applications of diuretics are directed toward reducing ___ ___ __ by decreasing total-body NaCl content. However they modify excretion of other ___ as well as ___ __.
Mechanism of diuretic action:
Most clinical applications of diuretics are directed toward reducing extracellular fluid volume by decreasing total-body NaCl content. However, they modify excretion of other ions as well as uric acid.
Mechanism of diuretic action:
A sustained positive or negative Na+ balance is ____ with ____. Diuretics cause a sustained net ___ in total body Na+ but the time course is ___.
What is this due to? This results from?
Mechanism of diuretic action:
A sustained positive or negative Na+ balance is incompatible with life. Diuretics cause a sustained net deficit in total body Na+ but the time course is finite.
This is due to DIURETIC BREAKING which results from renal compensatory mechanisms that bring Na_ excretion in balance with Na+ intake
Mechanism of diuretic action:
What are the breaking mechanisms (aka renal compensatory mechanisms) that bring Na+ excretion in balance with intake?
Mechanism of diuretic action:
Breaking mechanisms:
Activation of SNS and RAAS
Decrease arterial BP (which reduces pressure natriuresis)
Hypertrophy of renal epithelial cells
Increased expression of renal epithelial transporters
(Possible involvement of hormones such as ANP)
Clinical applications of diuretics:
Primarily used in the treatment of?
Diuretics are primarily used in the treatment of
a. Hypertension (both chronic and acute)
b. CHF
c. Renal failure (to maintain flow or decrease damage)
d. Nephrotic syndrome
e. Cirrhosis (primarily for edema accompanying cirrhosis)
Clinical diuretic agents:
What are the different drug categories?
Drug catergories
a. Carbonic anhydrase inhibitors
b. Loop diuretics
c. Potassium sparing diuretics
d. Amiloride diuretics
e. Thiazides (and thiazide like diuretics)
Clinical diuretic agents:
Where are carbonic acid anhydrase inhibitors? Not primarily used as?
Carbonic anhydrase inhibitors are in the proximal convoluted tubule and are not primarily used as a diuretic but diuresis is a side effect
Clinical diuretic agents:
Where are loop diuretics?
Potentcy? Duration of action?
What do they inhibit?
What is its main effect?
Loop diuretics are in the thick ascending limb
They are the most potent and they are short acting
They inhibit the Na/2Cl/K triporter
They diminish the osmotic gradient
Clinical diuretic agents:
Where are potassium sparing diuretics?
K+ sparing diuretics are in the collecting duct
Clinical diuretic agents:
Where are the amiloride diuretics?
What do amiloride diuretics block?
What does spironolactone block?
Amiloride diuretics are in the collecting duct
Amiloride diuretics block Na+ uptake (Na+ channel blockers)
Spironolactone blocks aldosterone and the mineralocorticoid receptor
Clinical diuretic agents:
Where do the thiazide diuretics act?
What do they inhibit?
Potentcy?
Thiazide diuretics are in the distal convoluted tubule
They inhibit the NaCl cotransporter
They are not extremely potent but they are very effective
Clinical diuretic agents:
Function and location of osmotic diuretics?
Osmotic diuretics promote water excretion in areas of high permeability:
Proximal tubule, thin descending limb, and collecting ducts
Excretory and Renal Hemodynamic Effects:
- What classes cause increased K+ excretion?
- What drug increases excretion of Ca++? Dont use for who?
- What drugs do NOT mess with renal hemodynamics (RBF/GFR/FF/TGF)?
- CAI, Inhibitors of the NA/K/2Cl- transport, and inhibitors of the NaCl symport cause an increased excretion in K+
- Inhibitors of the Na+/2Cl/K symport increase excretion of Ca++ and its not for use in osteoporosis patients
- Inhibitors of NaCl symport, inhibitors of renal epithelial Na+ channels, and mineralocorticoid receptor antagonists dont mess with renal hemodynamics
Carbonic Anhydrase Inhibitors (CAI):
Three drugs?
Carbonic Anhydrase Inhibitors (CAI):
a. Acetazolamide
b. Dichlorphenamide
c. Methazolamide
Carbonic Anhydrase Inhibitors (CAI):
Normal mechanism of action:
- Where?
- How is sodium reabsorbed?
Carbonic Anhydrase Inhibitors (CAI):
Normal mechanism of action:
- PCT
- Na_ is reabsorbed via the Na/H ANTIporter
Carbonic Anhydrase Inhibitors (CAI):
Normal mechanism of action:
- The antiporter results in significant ___ extrusion into the PCT. What is this coupled to make?
- What is the role of carbonic anhydrase? What happens to the products?
Carbonic Anhydrase Inhibitors (CAI):
Normal mechanism of action:
- The antiporter results in significant H+ extrusion into the PCT. It is couples to HCO3-.
- Carbonic anhydraze catalyzes the cleavage of HCO3- into OH- and CO2. OH- couples with H+ to form water. CO2 diffuses into the cytoplasm of the epithelial cell
Carbonic Anhydrase Inhibitors (CAI):
Normal mechanism of action:
- Once CO2 is in the cell, what occurs?
- Where is the HCO3- then transported? What is the net result?
Carbonic Anhydrase Inhibitors (CAI):
Normal mechanism of action:
- Once in the cell, carbonic anhydrase II combines CO2 and OH- to HCO3-
- HCO3- is then cotransported with Na+ across the basolateral membrane. The net result is the reabsorption of bicarbonate and sodium via NBC1.
Carbonic Anhydrase Inhibitors (CAI):
Mechanism of action:
What is the function of Acetazolamide? Result?
Acetazolamide is going to inhibit both forms of carbonic anhydrase (the one on the apical membrane of the PCT and the one within the cell) and it results in a decreased sodium and bicarbonate absorption.
Carbonic Anhydrase Inhibitors (CAI):
Mechanism of action:
- CAIs almost completely abolish NaHCO3 reabsorption in the proximal tubule but only if they inhibit a ___ percentage of the enzyme. Why?
- What is sodium bicarbonate reabsorption linked to?
- What else do CAIs reduce secretion of? Where?
Carbonic Anhydrase Inhibitors (CAI):
Mechanism of action:
- High; need a high percentage of enzyme inhibition because there is a large excess of carbonic anhydrase in the PCT
- Water and Cl- (thus results in diuresis and decreased reabsorption of NaCl)
- CAIs reduce secretion of titratable acid in the collecting duct
Carbonic Anhydrase Inhibitors (CAI):
Effects on urinary ion secretion:
- Bicarbonate excretion and inhibition of titratable acid increases urine ____ and produces ____ ____.
- Fractional excretion of Na+ is as high as ___.
- Fractional excretion of K+ can be as much as ____.
This is due to increased delivery of ___ to the distal nephron, flow-dependent enhancement of K+ ____ in the ___ __ and activation of ____.
Carbonic Anhydrase Inhibitors (CAI):
Effects on urinary ion secretion:
- Bicarbonate excretion and inhibition of titrateable acid increases urine pH and produced metabolic acidosis
- Fractional excretion of Na+ is as high as 5% (high)
- Fractional excretion of K+ can be as much as 70%. This is due to increased delivery of Na+ to the distal nephron, flow dependent enhancement of K+ secretion in the collecting duct and activation of RAAS.
Carbonic Anhydrase Inhibitors (CAI):
Effects on urinary ion secretion:
- Effect on phosphate excretion?
- Effects of CAIs on renal excretion is ___ ___ because metabolic acidosis leads to a reduction in fitered ____.
Carbonic Anhydrase Inhibitors (CAI):
Effects on urinary ion secretion:
- Increase in phosphate excretion
- Effect of CAIs on renal excretion is self limiting because metabolic acidosis leads to a reduction in filtered bicarbonate
Carbonic Anhydrase Inhibitors (CAI):
Effects on renal hemodynamics:
Increased delivery of solutes to the ___ ___ triggers tubuloglomerular feedback, which ___ afferent arteriolar resistance and ___ RBF and ___
Carbonic Anhydrase Inhibitors (CAI):
Effects on renal hemodynamics:
Increased delivery of solutes to the macula densa triggers tubuloglomerulal feedback, which increases afferent arteriolar resistance and reduces RBF and GFR
Carbonic Anhydrase Inhibitors (CAI):
Affects CA in extrarenal tissues causing?
Carbonic Anhydrase Inhibitors (CAI):
Affects CA in extrarenal tissues causing:
- Decrease aqueous humor and IOP
- Parasthesia and somnolence; antoconvulsant
- Increase CO2 in tissue and decrease in expiration
- Reduce gastric acid secretion at high doses (but this is NOT therapeutic)
- Creation of acidosis
Carbonic Anhydrase Inhibitors (CAI):
Current applications?
Carbonic Anhydrase Inhibitors (CAI):
Current applications?
a. Open-angle glaucoma
b. Edema
c. Prophylaxis for altitude sicness
d. Correcting metabolic alkalosis
Carbonic Anhydrase Inhibitors (CAI):
Current applications:
- What are the two major indications for CAI?
- Edema: effectiveness? where does it act? Why is it not very useful long-term?
Carbonic Anhydrase Inhibitors (CAI):
Current applications:
- Glaucoma and correction of metabolic alkalosis
- This is not very effective for edema; acts at distal nephron sites; not good long-term because of the metabolic acidosis
Carbonic Anhydrase Inhibitors (CAI):
Adverse effects:
- CNS effects?
- Because these are ___ derivatives they cause similar symptoms including?
Carbonic Anhydrase Inhibitors (CAI):
Adverse effects:
- CNS only seen with very high doses
- CAIs are sulfonamide derivatives and can cause bone marrow depression, skin toxicity, sulfonamide like renal lesions, and allergic reactions
Carbonic Anhydrase Inhibitors (CAI):
More serious adverse effects can occur due to urinary alkalinization/metabolic acidosis:
- Diversion of renal ___ from urine into the circulation - this can worsen ___ _____.
- Can cause ___ formation and ureteral colic from precipitation of ____ in alkaline urine
Carbonic Anhydrase Inhibitors (CAI):
More serious adverse effects can occur due to urinary alkalinization/metabolic acidosis:
- Diversion of renal ammonia from urine into the circulation - this can worsen hepatic encephalopathy
- Can cause calculus formation and ureteral colic from precipitation of Ca2PO4 in alakine urine
Carbonic Anhydrase Inhibitors (CAI):
More serious adverse effects can occur due to urinary alkalinization/metabolic acidosis:
- Can worsen metabolic or ____ acidosis.
- Reduction of the urinary excretion rate of weak organic ___.
Carbonic Anhydrase Inhibitors (CAI):
More serious adverse effects can occur due to urinary alkalinization/metabolic acidosis:
- Can worsen metabolic or pulmonary acidosis
- Reduction of the urinary excretion rate of weak organic bases
Carbonic Anhydrase Inhibitors (CAI):
What are the two contraindications? Why?
Carbonic Anhydrase Inhibitors (CAI):
a. Hepatic cirrhosis (due to diversion of ammonia to circulation)
b. Hyperchloremic acidosis (bc it can worsen metabolic acidosis)
c. Severe COPD (bc it can worsen respiratory acidosis)
Osmotic diuretics:
These agents are ___ filtered at the glomerulus, have ___ reabsorption by the renal tubule, and are relatively ___. They cause a significant increase in?
Osmotic diuretics:
There agents are freely filtered at the glomerulus, have little reabsorption by the renal tubule, and are relatively inert. They cause a significant increase in plasma and tubular fluid osmolality
Osmotic diuretics:
Drugs? (2)
Osmotic diuretics:
Mannitol and glycerin
Osmotic diuretics:
Mechanism and site of action:
Primary action?
Osmotic diuretics:
Primary action is to reduce the vertical osmotic gradient in the Loop of henle (descending limb)
Osmotic diuretics:
Effects on urinary excretion:
Excretes what ions?
Osmotic diuretics:
Excretes nearly all electrolytes including Na, K, Ca, Mg, Cl, HCO3, and phosphate. (Effects on NaCl are modest however)
Osmotic diuretics:
Mannitol’s effect on renal hemodynamics?
Osmotic diuretics:
Mannitol INCREASES RBF (by dilating the afferent arteriole) but total GFR is UNCHANGED
Osmotic diuretics:
Therapeutic uses:
- Attenuates decreased ___ in acute renal failure (PRIMARY USE)
- Reduce ___ edema and __ mass before and after ____. (also a common use)
Osmotic diuretics:
Therapeutic uses:
- Attenuates decreased GFR in acute renal failure
- Reduces cerebral edema and brain mass before and after neurosurgery.
Osmotic diuretics:
Therapeutic uses cont:
- Used for ___ disequilibrium syndrome. By increasing extracellular fluid osmolarity, osmotic diuretics remove excess ___ from tissues caused by too ___ a removal of ___ from the extracellular fluid caused by ____/ peritoneal ____.
- Control ____ during acute attacks of ___. Used pre and postoperatively.
Osmotic diuretics:
Therapeutic uses:
- Used for dialysis disequilibrium syndrome. By increasing exctracellular fluid osmolarity, osmotic diuretics remove excess water from tissue caused by too fast a removal of solutes from the extracellular fluid caused by hemodialysis/ peritoneal dialysis
- Controls IOP during acute attacks of glaucoma
Osmotic diuretics:
Adverse effects: (essentially extensions of effects to expand ECFV and reduce ICFV)
- What can occur in patients with CHF?
- What is associated with tissue swelling/damage?
- ____ and dehydration (too much low osmolarity diuresis: loss of water in excess of ___)
Osmotic diuretics:
Adverse effects: (essentially extensions of effects to expand ECFV and reduce ICFV)
- Patients with CHF can get pulmonary edema
- hyponatremia (HA, nausea, vomitting)
- HypERnatremia and dehydration (too much low osmolarity diuresis: loss of water in excess of Na+)
Osmotic diuretics:
- Contraindications for all osmotic diuretics?
- Contraindications for urea?
- Contraindications for mannitol?
- What can glycerin cause when metabolized?
Osmotic diuretics:
- All are contraindicated in anuric patients (renal dis.)
- Urea is contraindicated with impaired liver function and in patients with active cranial bleeding
- Mannitol - contraindicated in active cranial bleeding
- Glycerin can cause hypERglycemia
Loop Diuretics:
What do they inhibit? What else are they called?
Loop Diuretics:
They inhibit the Na/2Cl/K symporter; also known as high-ceiling diuretics
Loop Diuretics:
4 drugs?
Loop Diuretics:
a. Furosemide
b. Bumetanide
c. Ethacrynic acid
d. Torsemide
Loop Diuretics:
Mechanism of action:
- Why is Ca++ and Mg++ also excreted?
- What percent of filtered load of sodium is normally absorbed in the thick ascending limb?
- Loop diuretics reduce the action of the? Results in a reduction of?
Loop Diuretics:
- Ca/Mg is also excreted bc of the disruption of the positive transepithelial potential that normally pulls ions through
- 25% (very significant)
- They reduce the action of the counter current multiplier and thus reduce the vertical medullary osmotic gradient and the ability to concentrate urine
Loop Diuretics:
Effects on urinary excretion:
- Profound increased excretion of?
- Marked increased excretion of?
- Also increases the urinary excretion of ___ and ___ __ and this can be dangerous.
Loop Diuretics:
- Profound excretion of NaCl
- Marked excretion of Ca/Mg
- Also increases the urinary excretion of K+ and titratable acid and this can be dangerous
Loop Diuretics:
Effects on renal hemodynamics:
- Effect on RBF? How?
- Effect on GFR? How?
Loop Diuretics:
- Increases total RBF and redistributes RBF to the cortex (by prostaglandins)
- Does NOT decrease GFR (blocks TGF by inhibiting salt transport into the macula densa and the macula densa does NOT detect NaCl concentration in the tubule)
Loop Diuretics:
Other actions:
- In regards to renin?
- What is can furosemide specifically do?
Loop Diuretics:
- Powerful stimulators of renin (not for long term use because it causes heart and CV changes)
- Furosemide increases systemic venous capacitance and decreases LV filling pressure. Can reduce pulmonary edema even before diuresis begins
Loop Diuretics:
Therapeutic actions:
- Types of edema is this beneficial for?
- Good for treatment of life threatening _____ with the use of ____ saline
- What other two things are they good for?
Loop Diuretics:
Therapeutic actions
- This is good for acute pulmonary edema (strong diuresis w/ increased venous capacitance), edema/ascites of liver cirrhosis, and edema of nephrotic syndrome (often the ONLY drug capable of reducing massive edema from renal failure)
- hyponatremia; hypertonic
- Congestion in CHF and hypertension (not long term)
Loop Diuretics:
Why are they good for general drug overdoes?
Loop Diuretics:
They cause a washout - facilitate rapid elimination of the drug
Loop Diuretics:
Adverse effects:
What happens if too much of the drug is taken?
Loop Diuretics:
Overzealous effect can cause:
a. major depletion of body sodium and fluid
b. decreased GFR
c. CV collapse
d. Hypokalemia/hypomagnesemia/hypocalcemia
e. Alkalosis
Loop Diuretics:
Adverse effects:
- What happens to lipid profiles?
- Can cause ____, ____, hyperglycemia, skin rashes (_____), parasthesias, bone marrow _____, and GI disturbances.
Loop Diuretics:
Adverse effects
- Increase LDL/cholesterol/triglycerides, Decrease HDL
- ototoxicity; hyperuricemia; photosensitivity; depression
Loop Diuretics:
Who is this contraindicated in?
Loop Diuretics:
Contraindicatons
a. Postmenopausal osteopenic women
b. Patients with severe Na/water depletion
c. Patients with hypersensitivity to sulfonamides
d. Anuric patients that are unresponsive to a trial dose of loop diuretic
Thiazide diuretics: (sulfonamides)
What do they inhibit? Result?
Thiazide diuretics:
They inhibit NaCl symport and primarily increase NaCl rather than NaHCO3 excretion
Thiazide diuretics:
Drug examples? (3)
Thiazide diuretics:
a. Chlorothiazide
b. Hydrochlorothiazide
c. Chlorthalidone
Thiazide diuretics:
Thiazides inhibit NCC1 resulting in increased Na excretion but also increase epithelial cell absorption of ____
Thiazide diuretics:
calcium
Thiazide diuretics:
Effects on urinary excretion:
- What can the maximum excretion of NaCl be?
- There is an increased excretion of __ and ____ ___ that can be problematic.
- Increases the excretion of ___ ___ but is reduced following chronic administration
Thiazide diuretics:
Effects on urinary excretion:
- 5% (bc 90% is reabsorbed before reaching the DCT)
- Increased excretion of K+ and titrateable acid
- Increased excretion of uric acid
Thiazide diuretics:
Effects on urinary excretion:
- Decreases ___ excretion: this is a chronic effect, What are the benefits?
- Urine concentration?
Thiazide diuretics:
Effects on urinary excretion:
- Decreases Ca++ excretion (reabsorption in the DCT); dont want to lose calcium and also decreases kidney stones
- Thiazide diuretics do not alter the kidney’s ability to concentrate urine
Thiazide diuretics:
Effects on renal hemodynamics:
Effects on RBF? GFR? TGF?
Thiazide diuretics:
Essentially NO effect on RBF/GFR/TGF
Thiazide diuretics:
Therapeutic actions? (4)
Thiazide diuretics:
a. Treatment of edema
b. Hypertension
c. Calcium nepholithiasis and osteoporosis
d. Nephrogenic diabetes insipidus
Thiazide diuretics:
Treatment for edema in what situations? What is it not useful for?
Thiazide diuretics:
Edema with CHF, cirrhosis, and renal disease: not useful for renal failure
Thiazide diuretics:
First line agent to do what?
Thiazide diuretics:
First line agent for hypertension: to lower BP
Thiazide diuretics:
How do thiazides help nephrogenic diabetes insipidus?
Thiazide diuretics:
It reduces urine volume by 50%. but really - unknown
Thiazide diuretics:
Adverse side effects:
- Worried most about?
- There is a decrease in ___ tolerance and hyperglycemia (unmask latent ___ )
- Incidence of ___ ____ is greater with thiazides than other antihypertensives
- May also cause?
Thiazide diuretics:
- Worried most about hypokalemia, as well as metabolic alkalosis
- Decrease in glucose tolerance: diabetes
- Greater incidence of erectile dysfunction
- Hyperlipidemia
Thiazide diuretics:
Who is this contraindicated in?
Thiazide diuretics:
Patients with sulfonamide hypersensitivity
Thiazide diuretics:
Drug interactions:
It is potentially lethal when combined with _____. Why?
Thiazide diuretics:
Quinidine:
K+ depletion from thiazides plus prolonged QT interval qith quinidine leads to early after depolarizations. This could then lead to torsades de pointes and fatal ventricullar fibrillation
K+ sparing diuretics - inhibitors of renal epithelial Na channels:
Why are they usually used?
Drug?
K+ sparing diuretics - inhibitors of renal epithelial Na channels:
Used for their antikaliuretic actions to offset effects of other diuretics that increase K+ excretion
Amiloride
K+ sparing diuretics - inhibitors of renal epithelial Na channels:
Mechanism of action:
Cells in the late distal tubule/CT have apical epithelial ___ channels that create a lumen ___ transepithelial potential difference. This voltage drives the secretion of ___ and ___ into the lumen. ____ and amiloride block the ___ channel in the luminal membrane. This indirectly inhibits excretion of?
K+ sparing diuretics - inhibitors of renal epithelial Na channels:
Mechanism of action:
Cells in the late distal tubule/CT have apical epithelial Na+ channels that creat a lumen negative transepithelial potential difference. This voltage drives the secretion of K+ and H+ into the lumen. Triamterene and amiloride block the Na+ channel in the luminal membrane. This indirectly inhibits the excretion of K+, H+, Ca++, and Mg++
K+ sparing diuretics - inhibitors of renal epithelial Na channels:
Effects on renal hemodynamics?
K+ sparing diuretics - inhibitors of renal epithelial Na channels:
No effects on hemodynamics and do not alter TGF
K+ sparing diuretics - inhibitors of renal epithelial Na channels:
- Uses?
- What is the main adverse effect?
- Contraindicated in? Why?
K+ sparing diuretics - inhibitors of renal epithelial Na channels:
- Used only in Combination with other diuretics for treatment of edema or hypertension
- Hyperkalemia
- Hyperkalemic patients or those at risk of developing hyperkalemia; can cause arrhythmias easily
K+ sparing diuretics - mineralocorticoid receptor antagonist:
What are the 2 drugs?
Also referred to as?
K+ sparing diuretics - mineralocorticoid receptor antagonist:
a. Spironolactone
b. Eplerenon
Also known as aldosterone antagonists
K+ sparing diuretics - mineralocorticoid receptor antagonist:
Mechanism of action:
In normal situations, aldosterone binds to ___ and regulates the expression of multiple gene products called ____ ____ ____ (AIPs). The AIPs ____ Na+ conductance of the ____ membrane and sodium pump of the ___ membrane and enhance transepithelial ___ transport. This increases the lumen ___ transepithelial potential which is the driving force for secretion of ___ and ___.
K+ sparing diuretics - mineralocorticoid receptor antagonist:
Mechanism of action
In normal situations, aldosterone binds to MR and regulates the expression of multiple gene products called aldosterone induced proteins. The AIPs increase Na+ conductance of the luminal membrane and the sodium pump of the basolateral membrane and enhance transepithelial NaCl transport. This increases the lumen negative transepithelial potential which is the driving force for secretion of K+ and H+
K+ sparing diuretics - mineralocorticoid receptor antagonist:
- MR antatonists are the only diuretics that do not require access to the ___ ___ to induce diuresis.
- When are MR antagonists more effective?
K+ sparing diuretics - mineralocorticoid receptor antagonist:
- tubular lumen
- More effective when levels of aldosterone in the body is higher
K+ sparing diuretics - mineralocorticoid receptor antagonist:
Therapeutic uses:
- Drug of choice for?
- Diuretic of choice in patients with?
- Coadministration with thiazide or loop diuretics in the treatment of ___ and ____
- Reduces what in CHF?
K+ sparing diuretics - mineralocorticoid receptor antagonist:
Therapeutic uses:
- Drug of choice for primary hyperaldosteronism
- Diuretic of choice for hepatic cirrhosis
- Coadminister for treatment of edema and hypertension
- Reduces morbidity, mortality, and ventricular arrhythmias in CHF
K+ sparing diuretics - mineralocorticoid receptor antagonist:
Adverse effects:
- May cause life threatening _____ (this is the principle risk)
- What are CNS adverse effects?
- Contraindicated in patients with ___ ___.
K+ sparing diuretics - mineralocorticoid receptor antagonist:
Adverse effects:
- May cause life threatening hyperkalemia
- drowsiness, lethargy, ataxia, confusion, and headache
- Contraindicated in patients with peptic ulcers
K+ sparing diuretics - mineralocorticoid receptor antagonist:
Spironolactone:
- What type of receptors does it have affinity for? What side effects can it induce?
- Chronic administration can lead to increased risk for what type of malignancy?
K+ sparing diuretics - mineralocorticoid receptor antagonist:
Spironolactone
- Affinity toward progesterone and androgen receptors and thus induces side effects such as gynecomastia, impotence, and menstrual irregulaties
- Increased risk for breast cancer
B-Type Natriuretic Peptide:
Stimulates ____ and ___ similar to ANP
Drug?
Only approved for?
B-Type Natriuretic Peptide:
Stimulates natriuresis and diuresis similar to ANP
Drug = Nesiritide
Only approve for short term management of decompensated heart failur
B-Type Natriuretic Peptide:
3 Actions?
DECREASES pulmonary capillary wedge pressure/TPR
INCREASES stroke volume
B-Type Natriuretic Peptide:
Associated with a lower incidence of ____ than dobutamine which was the previous drug of choice for ___ ___ ___.
2 adverse effects?
B-Type Natriuretic Peptide:
Associated with a lower incidence of arrhythmias than dobutamine which was the previous drug of choice for decompensated heart failure
Adverse effects: Hypotension and Increased risk of renal dysfunction
