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CRRAB Week 6 > ADH and Diuretics > Flashcards

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
Q

What additional benefit do the aldosterone receptor inhibitors have in heart failure?

A

they prevent the fibrotic changes in the kidneys and heart caused by aldosterone (which is high in CHF)

26
Q

What are the side effeccts of the K sparing diuretics?

A 
hyperkalemia (duh)
hyperchloremic metabolic acidosis
Gynecomastia (spironolactone)
acute renal failure (specific to triamterene and indomethacin)
kidney stones
27
Q

Vasopressin is the naturally occuring antidiuretic hormone, so what is the synthetic congener?

A

desmopressin

28
Q

What are vasopressin and desmopressin used for?

A

diabetes insipidus

bed-wetting

29
Q

How does ADH work?

A

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
Q

What is the major osmotic diuretic?

A

mannitol

31
Q

How does mannitol work?

A

it’s a big old sugar that doesn’t get reabsorbed (filtration rate = excretion rate), so it promotes H2O excretion by osmotic forces

32
Q

What are the uses of mannitol/

A

reduce body water
reduce intracranial pressure
reduce intraocular pressure

33
Q

What are some toxicities of mannitol?

A 
extracellular volume expansion
dehydration
hperkalemia
hypernatremia
hyponatremia when renal function is low?
34
Q

What is the major carbonic anhydrase inhibitor?

A

acetazolamide

35
Q

Why is acetazolamide not really helpful as a diuretic?

A

because carbonic ahydrase is too important of an enzyme and works in a lot of places in the body

36
Q

What do we use acetazolamide for?

A

glaucoma
produce urinary alkalinization
produce metabolic acidosis
to treat acute mountain sickness

37
Q

What are the side effects of acetazolamide?

A

hyperchloremic metabolic acidosis
renal stones
renal potassium wasting

38
Q

What is the major pathology related to the organic anion transporters?

A

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
Q

What drugs can we use to treat gout that act in the kidney? How do they work?

A

probenicid and sulfinpyrazone

they inhibit a renal OAT to facilitate the excretion - the uric acid doesn’t get reabsorbed

40
Q

How does allopurinol work?

A

it blocks santhine oxidase so you don’t get xanthine ocnverted to uric acid

41
Q

How does colchicine work for gout?

A

it’s a microtubule inhibitor with anti-inflamamtory properties

CRRAB Week 6 (8 decks)

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