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Pharm exam 2 > CV-Duretics > Flashcards

CV-Duretics Flashcards

1
Q

Carbonic anhydrase inhibitors MOA

A

Carbonic anhydrase is needed for HCO3- reabsorbtion and HCO3 formation

dec in PCT reabsorption leads to inc aff arteriol resistnce, and dec in RBF AND GFR

inc in bicarb sectrion leads to diuresis and K+ resorb

Bicarbonate reabsorption by the PCT is thus dependent on CA, and inhibition of CA thus causes a major loss of HCO3- into the urine.

inhibition of CA results in a major loss of HCO3–, causing metabolic acidosis.

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2
Q

Osmotic diuretics MOA

A

 Osmotic Diuretics: freely filtered but poorly reabsorbed

inc tubular fluid osmotic pressure ↓ tubular fluid reabsorption
*acts mainly in thin lopp hemle, but also in distal tubule

Dec blood viscosity, ECV expansion, inhibition of renin release, all of which lead to INC RENAL BLOOD FLOW, remove NACL from renal medulla, dec medullary tonicity, and dec H20 extraction from the distal tubule.

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3
Q

Na+-K+-2Cl- cotransport (NKCC) inhibitors (loop diuretics) MOA

A

selectively inhibit NaCl reabsorption in the thick ascending limb of the loop of Henle. Due to the large NaCl absorptive capacity of this segment and the fact that the diuretic action of these drugs is not limited by development of acidosis, NKCC inhibitors are among the most efficacious diuretic agents available.

Inhibit Na+-K+-2Cl-
cotransporter (NKCC) 
inhibit reabsorption of solute
from TAL segments

Venodilation:↓ right atrial
pressure & pulmonary
capillary wedge pressure
within minutes (IV)

inc fractional Ca2+ excretion by 30% by decreasing the lumen-positive transepithelial potential that promotes paracellular Ca2+ reabsorption

inc fractional Mg2+ excretion > 60% by decreasing voltage-dependent paracellular transport

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4
Q

Thiazides and sulfonamide compounds MOA

A

inhibit DCT Na+-Cl-
cotransporter (NCC)
block coupled Na+ and Cl-
reabsorption

Inhibit NaCl transport predominantly in the distal
collecting ducts
 Some thiazides have significant carbonic anhydrase
inhibitory activity.
 Increase Ca2+ reabsorption, thereby decreasing Ca2+
excretion.
 Vasodilation: this effect is weaker than that of the NKCC
inhibitors.

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5
Q

Renal epithelial Na+ channel blockers MOA

A

amiloride blocks epithelial Na+ channels in the luminal membrane of principal cells in the late distal tubule and collecting duct by competing with Na+ for negatively charged areas within the Na+ channel pore and prevention of K+ loss

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6
Q

Aldosterone antagonists MOA

A

Antagonize aldosterone receptors in the renal collecting tubules

Decrease Na+ reabsorption natriuresis

Decrease loss of K+ in exchange for Na+

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7
Q

Carbonic anhydrase inhibitors Clinical use

A

1.Glaucoma
Glaucoma is the most common indication for CA inhibitors. CA is present in the ciliary body. CA inhibitors decrease aqueous humor production and intraocular pressure.

2.Acute mountain sickness
CA is present in the choroid plexus. By decreasing cerebrospinal fluid formation and by decreasing the pH of the cerebrospinal fluid and brain, CA inhibitors can increase ventilation and diminish symptoms of mountain sickness.

  1. to induce Urinary alkalization
    Uric acid, cystine, and other weak acids are most easily reabsorbed from acidic urine. Therefore, renal excretion of cystine (in cystinuria) and other weak acids can be enhanced by increasing urinary pH with CA inhibitors.

4.Edema: combined with NKCC or NCC inhibitors

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8
Q

Osmotic diuretics clinical use

A

Prophylaxis of acute renal failure (mannitol)

 expand the ECV
 maintain GFR
 inc tubular fluid flow
 prevent tubule obstruction from shed cell        
  constituents or crystals
 reduce renal edema

Cerebral edema
Osmotic diuretics alter Starling forces so that water leaves cells and reduces intracellular volume. This effect is used to reduce intracranial pressure in neurologic conditions.

Dialysis disequilibrium syndrome

Acute attacks of glaucoma

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9
Q

Na+-K+-2Cl- cotransport (NKCC) inhibitors (loop diuretics) clinical use

A

Pulmonary edema
Congestive heart failure
Acute renal failure
Hypercalcemia: Saline + loop diuretics

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10
Q

Thiazides and sulfonamide compounds clinical use

A

1 Hypertension - Less effective in patients with reduced
renal function

  1. Control of edema: congestive heart failure …
  2. Hypercalciuria
  3. Nephrolithiasis
    Thiazide diuretics reduce urinary excretion of Ca2+

5.Nephrogenic Diabetes Insipidus: thiazides 
increased renal Na+ reabsorption
recovery of Aquaporin-2 abundance
recovery of NCC, ENaC
thiazides can reduce urine volume by up to 50% in these patients. The mechanism of this paradoxical effect remains unknown.

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11
Q

Renal epithelial Na+ channel blockers Clinical use

A

used as K+-sparing agents in
hypokalemic alkalosis.

Used in combination with loop
diuretics / thiazides to prevent
hypokalemia caused by these agents

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12
Q

Aldosterone antagonists therapeutic effects..moa..

A

1.Prevention of LV remodeling and cardiac fibrosis
Inhibition of matrix metalloproteinases
Inhibition of protein kinase C

2.Prevention of sudden cardiac death
improve heart rate variability
reduce QT dispersion
reduce early morning rise in heart rate in HF patients
prevent severe hypokalemia

3.Hemodynamic effects
blood pressure reduction
modest diuresis and natriuresis

4.Vascular Effects
decrease vascular NAD(P)H oxidase activity
reduce the generation of reactive oxygen species
reverse endothelial dysfunction
increase nitric oxide bioactivity
retard the thrombotic response to injury

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13
Q

Carbonic anhydrase inhibitor adverse effects

A

1.Hyperchloremic metabolic acidosis (and urinary alk)
results from chronic reduction of body HCO3– stores by CA inhibitors and limits the diuretic efficacy of these drugs to 2 or 3 days. Unlike the diuretic effect, acidosis persists as long as the drug is continued.

  1. Renal stones
    phosphaturia and hypercalciuria occur during the bicarbonaturic response to inhibitors of carbonic anhydrase. calcium salts

3.Renal loss of K+ (aka Renal potassium wasting:)-prevent with simultaneous administration of potassium chloride.

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14
Q

Osmotic diuretics adverse effects

A

ECV expansion 

Risk of pulmonary edema in pts with heart failure
Hyponatremia: nausea, headache, vomiting
Hypernatremia: loss of water in excess of electrolytes, dehydration

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15
Q

Na+-K+-2Cl- cotransport (NKCC) inhibitors (loop diuretics) adverse effects

A
  1. Hyponatremia
    hypotension, reduced GFR, circulatory collapse, thromboembolic episodes, and in patients with liver disease, hepatic encephalopathy.

2.Hypokalemia
cardiac arrhythmias, particularly in patients taking cardiac glycosides, if dietary K is low.

  1. Hypocalcemia/hypomagnesia
    Increased Mg2+ and Ca2+ excretion may result in hypomagnesemia (a risk factor for cardiac arrhythmias) and hypocalcemia (rarely leading to tetany).
  2. Ototoxicity
    tinnitus, hearing impairment, deafness, vertigo, and a sense of fullness in the ear, more frequent with IV least with oral
  3. Hyperuricemia
    occasionally leading to gout).
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16
Q

Thiazides and sulfonamide compounds adverse effects

A

Hypokalemic metabolic alkalosis and hyperuricemia: similar to those observed with loop diuretics.

  1. Impaired glucose tolerance
  2. hyperlipidemia
  3. hyponaturemia
  4. allergic rxns
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17
Q

Renal epithelial Na+ channel blockers adverse effects

A
  1. Glucose tolerance and photosensitization
  2.  Interstitial nephritis and renal stones.
  3. Hyperkalemia
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18
Q

Aldosterone antagonists adverse effects

A

1.Hyperkalemia
2. Metabolic acidosis in cirrhotic patients
3.Effects due to binding to other steroid receptors:
gynecomastia
impotence, decreased libido
hirsutism
deepening of the voice
menstrual irregularities

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19
Q

Carbonic anhydrase inhibitors contraindications

A

cirrhosis ( plasma NH4+), Carbonic anhydrase inhibitor-induced alkalinization of the urine will decrease urinary excretion of NH4+ and may contribute to the development of hyperammonemia and hepatic encephalopathy in patients with cirrhosis.

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20
Q

Osmotic diuretics contraindications

A

Anuria due to renal disease

Impaired liver function (urea)

Active cranial bleeding (mannitol & urea

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21
Q

Na+-K+-2Cl- cotransport (NKCC) inhibitors (loop diuretics contraindications

A

Severe Na+ and volume depletion
 Hypersensitivity to sulfonamides (for sulfonamide-based loop diuretics)
 Anuria unresponsive to a trial dose of loop diuretic

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22
Q

Thiazides and sulfonamide compounds contraindications

A

hypersensitivity to sulfonamides

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23
Q

Renal epithelial Na+ channel blockers contraindications

A

hyperkalemia
renal failure (results in hypeer K), patients receiving other K+-sparing
diuretics, patients taking angiotensin-converting enzyme
inhibitors, or patients taking K+ supplements). Even NSAIDs can increase the likelihood of hyperkalemia in patients receiving Na+-channel inhibitors.

24
Q

g

A

g

25
Q

g

A

g

26
Q

g

A

g

27
Q

Glomerulus Diuretic with Major Action

A

0

28
Q

Proximal convoluted tubule (PCT) Diuretic with Major Action

A

CARBONIC ANHYDRASE INHIBITORS: (Acetazolamide)

29
Q

Primary Transporters and Drug Targets at Apical Membrane of the Proximal convoluted tubule (PCT)

A

Na+/H+ exchanger (NHE3), carbonic anhydrase

30
Q

osmotic diuretics

A

**Mannitol,Glycerin, Isosorbide, Urea

31
Q

Clinical use of osmotic diuretics, prophylaxis of acute renal failure

A

 Mannitol is effective in attenuating the reduction in GFR associated with ATN when administered before the ischemic insult or offending nephrotoxin.
 Mechanisms: the renal protection afforded by mannitol may be due to
o removal of obstructing tubular casts
o dilution of nephrotoxic substances in the tubular fluid, and/or
o reduction of swelling of tubular elements via osmotic extraction of water.

32
Q

Dialysis disequilibrium syndrome -clin ue osmotic diuertetic, mannitol

A

Too rapid a removal of solutes from the extracellular fluid by hemodialysis or peritoneal dialysis results in a reduction in the osmolality of the extracellular fluid. Consequently, water moves from the extracellular compartment into the intracellular compartment, causing hypotension and CNS symptoms (i.e., headache, nausea, muscle cramps, restlessness, CNS depression, and convulsions). Osmotic diuretics increase the osmolality of the extracellular fluid compartment and thereby shift water back into the extracellular compartment.

33
Q

clinical use osmotic diuretic (mannitol) acute glaucoma

A

By increasing the osmotic pressure of the plasma, osmotic diuretics extract water from the eye and are used to reduce intraocular pressure (IOP) during acute glaucoma attacks and for short-term reductions in IOP both pre- and post-operatively.

34
Q

NKCC inhibitors (loop diuretics)

A

**Furosemide (Lasix), Bumetanide, Ethacrynic acid

35
Q

NCC Inhibitors (Thiazides & Sulfonamides

A

***Chlorthalidone, Hydrochlorothiazide, Metolazone, Indapamide

36
Q

INHIBITORS OF RENAL EPITHELIAL SODIUM CHANNELS

A

***Amiloride, Triamterene

37
Q

CARBONIC ANHYDRASE INHIBITORS

A

(Acetazolamide)

38
Q

ALDOSTERONE RECEPTOR ANTAGONISTS

A

***Spironolactone, Eplerenone)

39
Q

Aldosterone antags clinical use

A
  1. edema and hypertension (coadministered with thiazide or loop diuretics)
  2. added to standard therapy of heart failure
  3. primary hyperaldosteronism
4. refractory edema associated with secondary aldosteronism 
 cardiac failure
 hepatic cirrhosis
 nephrotic syndrome
 severe ascites
40
Q

Cortical collecting tubule (CCT) normal functions

A

Na+ reabsorption (due to aldosterone(2–5%) coupled to K+ and H+ secretion

41
Q

Cortical collecting tubule (CCT) transporters and drug targets

A

Na channels (ENaC), K channels, H transporter, aquaporins

42
Q

Cortical collecting tubule (CCT) diuretic with major influence

A

K+-sparing diuretics, such as aldosterone atagonists **(Spironalactone), inhibitors of renal epithelium NA+ channcels (Amiloride?!?!???)

43
Q

Medulary collecting duct functions

A

Water reabsorption under vasopressin control

44
Q

Medulary collecting duct transporters

A

Aquaporins

45
Q

Medulary collecting duct main duretics of influcence

A

Vasopressin antagonist such as osmotic agents **(Mannitol) and ADH antagonists (????) maybe Amiloride??!?!

46
Q

Distal convoluted tubule (DCT) functions

A

Active reabsorption of 4–8% of filtered Na+ and Cl–; Ca2+ reabsorption under parathyroid hormone control

47
Q

Distal convoluted tubule (DCT) transporters

A

Na/Cl (NCC)

48
Q

Distal convoluted tubule (DCT) main duretics of influcence

A

Thiazides (Chlorthiazides)

49
Q

Thick ascending limb of Henle’s loop (TAL) functions

A

Active reabsorption of 15–25% of filtered Na+, K+, Cl–; secondary reabsorption of Ca2+ and Mg+

50
Q

Thick ascending limb of Henle’s loop (TAL) transporters

A

Na/K/2Cl (NKCC2)

51
Q

Thick ascending limb of Henle’s loop (TAL) duretics of influence

A

NKCC inhibitors (loop diuretics) (furosemide)

52
Q

parts of tubule systrem with no duretics that target the,

A

Glomerulus
Proximal tubule, straight segments
Thin descending limb of Henle’s loop

53
Q

Proximal convoluted tubule (PCT) functions

A

Reabsorption of 65% of filtered Na+, K+, Ca2+, and Mg2+; 85% of NaHCO3, and nearly 100% of glucose and amino acids. Isosmotic reabsorption of water.

54
Q

Proximal convoluted tubule (PCT) transporters

A

Na+/H+ exchanger (NHE3), carbonic anhydrase

55
Q

Proximal convoluted tubule (PCT) duretics of influence

A

Carbonic anhydrase inhibitors (acetazolamide)

Pharm exam 2 (8 decks)

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