ADH and Diuretics Flashcards

1
Q

How much plasma is filtered by the kidneys in a day?

A

180 L

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2
Q

Where in the kidney do the loop diuretics work?

A

the ascending limb of the LOOP of henle (LOOP)

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3
Q

Where in the nephron do thiazide diuretics work?

A

in the distal convoluted tubule

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4
Q

Where in the nephron do Potassium sparing diuretics work?

A

the cortical collecting tubule

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5
Q

Where is ADH active?

A

in the medullary collecting duct

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6
Q

Where in the nephrone do the osmotic diuretics work?

A

in the proximal tubule and/or the descending limb of the LOH

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7
Q

What are two examples of Loop diuretics?

A

furosemide (Lasix) and bumetanide

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8
Q

What do loop diuretics do?

A

they inhibit the Na/K/2 Cl pump in the thick ascending limb of the lOH

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9
Q

What percentage of Na is reabsorbed in this area - the thick ascending limb of the LOH?

A

about 25%

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10
Q

WHat happens in general to the osmolarity in the tubule of the thick ascending limb of the LOH?

A

It goes hypo-osmolar because Na, K and Cl are pumped out but water remains inside since there are no aquaporins here

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11
Q

What is the effect of the loop diuretics on osmolarity within the tubulet hen?

A

They prevent this decrease in osmolarity because they inhibit the Na, K and Cl from moving out of the tubule.

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12
Q

What effect do the loop diuretics have on Na, Cl and K excretion?

A

Increased NaCl excretion and increased K excretion because some of the increased nehron Na is exchanged for K in the cortical collecting tubule

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13
Q

What are the major uses of loop diuretics?

A
  1. pulmonary edema
  2. other edematous conditions (CHF)
  3. hyperkalemia
  4. acute renal failure
  5. anion overdose
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14
Q

Why aren’t the loop diuretics used for HTN?

A

Because htey have a much greater impact on systemic electrolyte levels than the thiazide diuretics and thus have more severe side effects

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15
Q

What are three thiazide diuretics?

A

chlorthalidone
hydrochlorothiazide
metalazone

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16
Q

What do the thiazides do?

A

they block the NaCl transporter in the distal convoluted tubule

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17
Q

What percentage of NaCl reabsorbtion occurs in the distal convoluted tubule?

A

not much - only 8%.

18
Q

What do the htiazides to to Na, Cl and K excretion

A

increased NaCl excretion

increase K excretion because some of the increased Na is exchanged for K in the cortical collecting tubule

19
Q

What are the major uses of the thiazides?

A

hypertension!
heart failure
nephrolithiasis caused by hypercalcemia
nephrogenic diabetes insipidus

20
Q

What are the major side effects of the htiazides?

A
hyperglycemia
hyperuricemia
hypokalemia
hyperlipidemia
hyponatremia
allergic reactions
21
Q

Why do the thiazides cause hyperglycemia? Do you still use them in diabetics?

A

Thiazides are sulfonylureas and will bind to an SUR receptor on a potassium channel controlling insulin release
when it binds, the K channel opens and you get an efflux of K and you hyperpolarize the beta cell
This inhibits the beta cell’s release of insulin release
thus, increasing blood glucose

22
Q

What are the potassium sparing diuretics?

A

spironolactone
eplerenone
amiloride
triamterene

23
Q

What are the two mechanisms of the K sparing diuretics?

A

spironolactone and eplerenon are aldosterone receptor inhibitors
amiloride and triamterene inhibit Na exchange for K and H in the cortical collecting duct

24
Q

What are the major uses of the K sparing diuretics?

A

hyperaldosteornism

prevent potassium wasting caused by other diuretics

25
What additional benefit do the aldosterone receptor inhibitors have in heart failure?
they prevent the fibrotic changes in the kidneys and heart caused by aldosterone (which is high in CHF)
26
What are the side effeccts of the K sparing diuretics?
``` hyperkalemia (duh) hyperchloremic metabolic acidosis Gynecomastia (spironolactone) acute renal failure (specific to triamterene and indomethacin) kidney stones ```
27
Vasopressin is the naturally occuring antidiuretic hormone, so what is the synthetic congener?
desmopressin
28
What are vasopressin and desmopressin used for?
diabetes insipidus | bed-wetting
29
How does ADH work?
It ultimately activates G protein coupled receptors in the collecting duct to recruit aquaporin channels this makes water more likely to reabsorb , making urine more concentrated
30
What is the major osmotic diuretic?
mannitol
31
How does mannitol work?
it's a big old sugar that doesn't get reabsorbed (filtration rate = excretion rate), so it promotes H2O excretion by osmotic forces
32
What are the uses of mannitol/
reduce body water reduce intracranial pressure reduce intraocular pressure
33
What are some toxicities of mannitol?
``` extracellular volume expansion dehydration hperkalemia hypernatremia hyponatremia when renal function is low? ```
34
What is the major carbonic anhydrase inhibitor?
acetazolamide
35
Why is acetazolamide not really helpful as a diuretic?
because carbonic ahydrase is too important of an enzyme and works in a lot of places in the body
36
What do we use acetazolamide for?
glaucoma produce urinary alkalinization produce metabolic acidosis to treat acute mountain sickness
37
What are the side effects of acetazolamide?
hyperchloremic metabolic acidosis renal stones renal potassium wasting
38
What is the major pathology related to the organic anion transporters?
gout - they transport small hydrophilic molecules into or out of the nephron, including urate (driven by symport or antiport exchane of molecules for dicarboxylates)
39
What drugs can we use to treat gout that act in the kidney? How do they work?
probenicid and sulfinpyrazone they inhibit a renal OAT to facilitate the excretion - the uric acid doesn't get reabsorbed
40
How does allopurinol work?
it blocks santhine oxidase so you don't get xanthine ocnverted to uric acid
41
How does colchicine work for gout?
it's a microtubule inhibitor with anti-inflamamtory properties