test 6 part 2 Flashcards

(36 cards)

1
Q

Diuretics

A

 Increase the volume of urine excreted

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2
Q

Proximal convoluted tubule reabsorption

A

 Almost 100%: glucose, amino acids, metabolites

 65%: H2O, Na, Cl, K, bicarbonate

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3
Q

Proximal convoluted tubule secretion

A

 H+
 Organic acids and bases
 Catecholamines
 Drugs/toxins

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4
Q

Descending loop of henle

A
  • H2O reabsorbed
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5
Q

Ascending loop of henle reabsorbed

A

 Impermeable to water!
 25%: Na, Cl, K
 Ca, bicarbonate, magnesium

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6
Q

Ascending loop of henle secreted

A

 H+

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7
Q

Early Distal convoluted tubule

A

 Impermeable to water!

 5%: Na, Cl, K reabsorbed

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8
Q

Late distal tubule and cortical collecting tubule reabsorbed

A
 H2O in the presence of Antidiuretic hormone (ADH)
 Principal cells
        - Na+
 Intercalated cells
        - Bicarb, K+, and H+
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9
Q

Late distal tubule and cortical collecting tubule excreted

A

 Principal cells
- K+
 Intercalated cells
- Bicarb, K+, and H+

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10
Q

Medullary collecting duct reabsorbed

A

 10%: Na, H2O (when ADH present)

 Urea

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11
Q

Medullary collecting duct secreted

A

 H+

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12
Q

Common uses of diuretics

A
Hypertension
Edema associated with
         Congestive heart failure
         Liver cirrhosis
         Corticosteroid therapy
         Renal dysfunction
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13
Q

Types of diuretics

A
Thiazide
Loop
Potassium-Sparing
Carbonic Anhydrase Inhibitors
Osmotic
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14
Q

Thiazide diuretics

A

Most widely used
Affect distal convoluted tubule
All have same Emax, different potencies
Effective orally
1-3 weeks for stable blood pressure reduction
- “low ceiling diuretics” = giving more than therapeutically required won’t do anything

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15
Q

Thiazide diuretics affect which transporter

A
  • Na/Cl cotransporter on luminal membrane

- in distal convoluted tubule

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16
Q

Thiazide diuretics enter lumen where and how

A
  • Secreted into the lumen in the proximal tubule via the organic acid secretory system
17
Q

Thiazide diuretic actions

A

 Increased excretion of Na and Cl
 Very hyperosmolar urine
 Unique to thiazides
 Loss of K+ (Na/K countertransport mech on luminal side)
 Sodium concentration in filtrate is high when it reaches distal tubule
 More K+ is exchanged for Na+
 Loss of Mg2+ (supplementation of Mg2+ required with chronic use)
 Decreased excretion of calcium
 Increased reabsorption in distal convoluted tubule
 Reduced PVR
 Over time volume status returns but PVR remains low

18
Q

Thiazide diuretics therapeutic uses

A

 Hypertension
 Heart failure
 Hypercalciuria
 Diabetes insipidus

19
Q

Thiazide diuretics adverse effects

A
 Potassium depletion
 Hyponatremia
 Hyperuricemia
 Volume depletion
 Hypercalcemia
 Hyperglycemia
20
Q

Loop diuretics

A

 Major action on ascending Loop of Henle
 Act on luminal side
 Highest efficacy in removing Na+ and Clfrom
the body
 Produce copious amounts of urine
 Oral or IV
 Rapid onset, short duration (2-4 hours)
- greatest diuretic effect

21
Q

Loop diuretics act on what transporter

A
  • Na/2Cl/K cotransporter luminal membrane

- ascending loop of henle

22
Q

Loop diuretics and renal blood flow

A

 Quick response
 May increase renal blood flow due to prostaglandin synthesis
 NSAIDS inhibit renal prostaglandin synthesis and can reduce the diuretic action

23
Q

Loop diuretics therapeutic uses

A

 Peripheral and pulmonary edema (HF)
 Emergency situations (Acute pulmonary edema)
 Hypercalcemia
 Hyperkalemia
- Diuretic of choice even in patients with compromised renal function

24
Q

Loop diuretics perfusion uses

A

 Remove extra fluid on CPB
 Treat hyperkalemia
 Help maintain urine production and renal function

25
Adult pump dose of loop diuretics
20-40 mg bolus
26
Loop diuretics adverse effects
```  Ototoxicity  Hyperuricemia  Acute hypovolemia  Potassium depletion  Hypomagnesemia ```
27
Potassium-sparing diuretics: aldosterone antagonists
 Block aldosterone action  Mediator proteins that normally stimulate the Na+/K+ pump are not produced  Retention of K+  Excretion of Na+
28
Potassium-sparing diuretics: aldosterone antagonists therapeutic uses
 Diuresis  Low efficacy in removing Na+ from body  Useful for retention of K+  Given in conjunction with thiazide or loop diuretics  Secondary hyperaldosteronism  Hepatic cirrhosis  Nephrotic syndrome  Heart failure  Resistant hypertension  Ascites  Polycystic ovary syndrome (high androgen levels)
29
Potassium-sparing diuretics: aldosterone antagonists adverse effects
 Gynecomastia in male patients  Menstrual irregularities in female patients  Hyperkalemia  Mental confusion
30
Potassium-sparing diuretics: Sodium channel blockers
- the Na/K counterstransport blocked  Not very efficacious  Used in combination with other diuretics for potassium sparing effects  Prevent the loss of potassium that occurs with thiazide and loop diuretics
31
Potassium-sparing diuretics: Sodium channel blockers adverse effects
 Increased uric acid  Renal stones  K+ retention
32
Carbonic Anhydrase inhibitors
 Much less efficacious than thiazide or loop diuretics  Often used for other pharmacologic actions  Inhibits carbonic anhydrase of proximal tubule
33
Carbonic Anhydrase inhibitors therapeutic uses
 Glaucoma  Correction of metabolic alkalosis  Mountain sickness
34
Osmotic diuretics - Mannitol (osmitrol)
 Alcohol and a sugar (similar to xylitol or sorbitol)  Not absorbed orally  IV
35
Osmotic diuretics - Mannitol (osmitrol) mechanism of action
 Elevates blood plasma osmolality  Enhanced flow of water from tissues into the plasma  Elevates tubular filtrate osmolality  Filtered, but not reabsorbed  Facilitates water excretion  Reduces water reabsorption  Inhibits reabsorption of sodium, chloride, and other solutes
36
Osmotic diuretics therapeutic uses
```  Reduce intracranial pressure  Acute renal failure  Shock  Drug toxicity  Trauma  Maintaining urine flow preserves long term kidney function! ```