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S2B5 Pharmacology > Diuretics I & II > Flashcards

Diuretics I & II Flashcards

1
Q

what are the ions reabsorbed/secreted in the

proximal tubule?

thick ascending loop of henle?

distal convluted tubule?

collected tubule?

A
  • reabsorbed: (note Na, Cl- reabsorbed at each segment)
    • proximal tubule: Na+, Cl- HCO3
    • thick ascending loop of henle: Na, Cl-, Ca+, Mg
    • distal convoluted tubule: Na-, CL- Ca
    • collecting tubule: Na, Cl-
  • secreted:
    • proximal tubule: H+
    • collecting tubule: H+, K+
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2
Q

carbonic anhydrase inhibitor diuretics act on what renal tubular segment?

A

proximal tubule

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3
Q

loop diuretics act on what tubular segment?

A

thick ascending loop of henle

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4
Q

thiazide diuretics act on what tubular segment?

A

distal convoluted tubule

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5
Q

K+ sparing diuretics act on what part of the tubular segment?

A

the collecting tubule

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6
Q
A
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7
Q
A
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8
Q

carbonic anhydrase inhibitors

  • renal MOA
A
  • MOA: multiple
    • renal: diuresis by acting on the proximal convoluted tubule
      • inhibits reabsorption of Na+, HCO3 and HCl-
        • recall from phys:
          • Na+/H antiporter takes up Na+ in exchange for H+
            • Na+ reabsorbed into blood by Na/K transporter
          • the secreted H+ combinates with bicarb to make H2CO3
          • H2CO3 dissociates back into back into H2O + CO2 via carbonic anhydrase
          • these products are reabsorbed into the cell and ultimately break down to release HCO3 (which is reabsorbed into the blood) and H+, which drives Na+/H antiport
            • (antiport necessary to drive Na+ reabsorption)
      • thus, inhibition of carbonic anhydrase impedes both Na+ and HCO3 reabsorption
        • since HCO3- starts the accumulate in the filtrate, the filtrate becomes basic.
        • the Cl-/base exchanger, which pumps base into the blood in exchange for sodium reabsorption, is now slowed
          • this slows Cl- reabsorption
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9
Q

net effects of carbonic anhydrase inhibitors

A
  • decreased reaborption Na, HCO3 and Cl
    • net effect:
      • reduced NaHCO3 and NaCl reabosprtion
      • increased tubular concentration of NaHCO3 and NaCl, which results in.
          1. DIURESIS (due to NaCl)
            * water follows NaCl into tubule
            * increased urine volume –> pee it out
          1. INCREASED URINE pH (due to NaHCO3)
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10
Q

why is tolerance to carbonic anhydrase inhibitor diuretics so common?

A
  • in response to basic urine pH resulting from CAIs, the body compensates with metabolic acidosis
    • the body provides H+ for the plasma
    • the plasma H+ diffuses into the cell, then drives the Na+/H+ antiporter, promoting Na+ reabsoprtion and H+ secretion (which then combines with HCO3-) to ultimately pull it back into the cell
      • though carbonic anhydrase can still inhibit CAIs, the Na+/H+ antiporter now works, Na+ enters the blood, followed by water –> high blood pressure
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11
Q

non-renal indications and MOAs of carbonic anhydrase inhibitors

A
  • CAIs used to treat high pressure in the eye and cerospinal system
    • glaucoma
      • in eye - carbonic anhydrase generates HCO3- that draws Na+ and fluid into the aqueous humor
        • _​_this increases the introocular pressure/
        • CAIs inhibit this process to lower introular pressure
    • cerebrospinal pressure
      • in brain - carbonic anhydrase generates HCO3- that draws inNa+ and fluid into the cerbrospinal fluid
        • increases cerobrospinal fluid pressure
        • CAIs inhibit this process

_(_dont fully understand the mechanisms here)

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12
Q

clinical uses of CAI

A
  • glaucoma
  • high cerobrospinal pressure
    • can also treat acute mountain sickness resulting from high cerocrospinal pressure:
      • sickness caused when high cranial pressure impedes oxygen extraction
        • CAIs lower pressure and allow for improved O2 intake/CO2 removed
  • urinary acidosis - CAIs increase urinary HCO3
  • compensatory metabolic alkalosis (resulting from excessive use of diuretics or respiratory acidosis)
    • CAIs increase urinary HCO3, neutralizing acidic urine so the body doesn’t have to
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13
Q

AEs of CAIs

A
  • metabolic acidosis (CAIs correct urinary acidosis, but resulting urinary alkalosis could induce compensatory metabolic alkalosis)
  • renal K+ wasting
  • renal stones (rarely)
    • due to K+, Ca+ excretion, these ions forms stones in tubules
  • parathesia
  • drowsiness
  • hypersensitivity reactions
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14
Q

name of CAI

A

acetazolamine (a sulfonamide)

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15
Q

loop diuretics MOA

A

loop diuretics act on the thick ascending loop of henle

  • here, they inhibit reabsoprtion of Na+, Cl-, Mg+, Ca+
    • recall from phys:
      • the NKCC2 transporter pumps Na+, K+ and 2Cl- into cell from filtrate
      • on basolateral side, the reabsorbed Na+ moves into the blood in exchange for K+ thru Na/K ATPase
      • the combined K+ increase in the cell drives K+ out of the cell into the filtrate
        • this increases the (+) charge in the filtrate
        • this drives cations Mg2+ and Ca2+ out of filtrate into cell –> into blood
          • combined reabsorption Na, CL-, Mg and Ca creates medullary hypertonicity
          • K+ secreted after initial reabsorption so does not contribute to this
    • loop diuretics work by:
      • inhibiting the NKCC2 transporter - inhibits all absorption resulting from that transporter (Na, Cl, Mg, Ca)
        • reduces medullary tonicity
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16
Q

overall effects of loop diuretics

A
  • decrease tonicity of medulla
    • this diminshes the the osmotic gradient that goes from the cortex to the medulla: typically, the solute reabsorbsion that occurs at the thick ascending limb establishes a interstitial concentration that increases from the cortex down into the medulla and promotes water reabsoprtion in the thin descending limb and collecting tubules
      • ​since loop diruetics inhibit reabsorption at TAL, they disrupt this gradient and impede water reabsorption at the thick descending limb at collecting tuubles
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17
Q

what are the loop diuretics?

A
  • furosemide
  • bumetanide
  • torsemide
  • ethacrynic acid
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18
Q

MOA of thiazide diuretics

A

thiazide diuretics act at the DCT (distal convoluted tubule)

  • at the DCT: Na, Cl, Ca++ reabsorbed
    • recall from phys:
      • a Na/K ATPase establishes a Na+ gradient that drives NCC, a NaCl cotransporter
        • NCC moves Na+ and Cl- from filtrate into cell for reaborption
  • thiazide diuretics block the NCC channel:
    • _​_this decreases Na+ and Cl- reabsorption
      • the decrease in intracellular [Na+] drives a Ca++/Na+ exchanger to move Na+ from the blood into the cell in exchange fro Ca++
        • –> increasing Ca++ reabsoprtion
    • they also may increase Ca++ reabsorption at the PCT as a result of volume depletion
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19
Q

net effects of thiazide diuretics

A
  • increased excretion of NaCl, water, and K+ (?)
  • increased reabsorption of of Ca++
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20
Q

contrast the effects of loop diuretics and thiazide diuretics on Ca++ movement and what this means in terms of their clinical uses

A

have opposite effects:

  • loop diuretics: decrease Ca++ reabsorption, increase tubular Ca++
    • thus can be used to treat with patients with hypercalcemia [high blood Ca++]
  • thiazide diuretics: increase Ca++ reabsorption, lower tubular Ca++
    • thus can be used to treat patients hyperuricemia
      • this can reduce the risk of gallstones
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21
Q

contrast loop and thiazide diuretics in terms of potency

A

loop diuretics more potent

22
Q

describe how loop and thiazide diuretics can be used to treat “edematous status”

A

both drugs can be used to lower edema caused by the two following conditions:

  • chronic heart failure (HF)
    • HF leads to edema because: lowered CO leads to –> renal hyperperfursion –> riggering RAAS activation –> causing Na+/water reabsorption –> f_luid retention_ –> edema
      • both drugs inhibit fluid rention, lowering edema as well as pulmonary and systemic congestion
    • loop vs thiazide:
      • ​loop diuretics best for severe HF and first choice for rapid relief of congestive symptoms
      • thiazide diruetics: best for mild HF
  • acute pulmonary edema
    • ​both durgs promote Na+ and water excretion –> lowering ventricular feeling pressure –> decreasing pulmonary edema
    • loop vs thiazide:
      • both drugs can be used, loop diuretics are better - “drug of choice” for acute pulmonary edema
23
Q

describe how loop and thiazide diuretics can be used to manage hypertension.

A
  • Thiazide diuretics: all patients with essential hypertension and normal renal function
  • Loop diuretics: hypertensive patients with renal insufficiency or heart failure
24
Q

discuss use of loop and thiazide diuretics in the treatment of diabetes

A

only thiazide diuretics are use dto treat diabetes. they can be used to treat

  • diabetes insipidus (DI):
    • diabetes inspidus is characterize by an inability of ADH to induce water reabsorption, either due to 1. impaired ADH synthesis (neurogenic DI) or 2. inadeuqate response of kidney to ADH
    • use of thiazides:
      • thiazides relieve polyuria and polydipsia secondary to DI by increasing urine flow (dont really get this, picture attached)
      • they are indicated in the treatment of lithium induced nephrogenic DI
        • ​they work by increasing expression of Na+ transporters in the DCT and CCT –> increasing water reabsorption
25
Q

discuss the clinical uses of thiazide diuretics pertaining to its effect on Ca++ movement

A
  • thiazide diuretics increase Ca++ reabsorption in the DCT and PCT, and can thus be used to treat:
    • nephrolithiasis (caused by a defect of Ca++ reaborption in PCT)
    • osteoporosis
    • hyperuricemia
26
Q

discuss the clinical use of loop diuretics pertaining to their effect on calcium reabsorption

A
  • loop diuretics decrease Ca++ reabsorption
    • they are combined with saline to treat hypercalcemia in patients with:
      • renal failure
      • HF
27
Q

thiazide-like duiretics

  • what are they?
  • what are their clinical uses and how do they work?
A
  • indapamide, metaolazone, chlorthalidone
  • can be combined with loop diuretics to treat patients with edema who:
    • have a GFR < 20 ml/min
    • are refractory to loop diuretics
  • how this works:
    • since these thiazide like diuretics decrease Na++ reabsorption in the PCT/DCT, they i_ncrease the load of Na++_ in the tubular filtrate in the thick ascending limb. this is Na++ that would have otherwise been reabsorbed, but will now be excreted due to loop diuretics
28
Q

adverse effects of both loop and thiazide diuretics

A

hypos:

  • hyponatremia
  • hypomagnesemia (especially loop diuretics)
  • hypokalemic metabolic acidosis: both diuretics increase tubular Na++ that arives to the collecting ducts
    • this may induce aldosterone mediated activativation of the Na/K exchanger, which would promote Na+ uptake in exchange for K+ secretion

hypers:

  • hyperuiciemia: this is because the diuretics themselves are secreted via an organic acid transporter that secretes uric acid.
    • the diuretics can compete for this transporter, leading to buildup or uric acid in the blood
  • hyperglycemia
    • ​hypokalemia can cause can decrease insulin secretion from pancreas B-cells
    • this doesn’t apply to thiazide-like diuretics
  • possibly hyperlipidemia
  • allergic reactions
29
Q

what are the unique AEs of loop diuetics?

A

otoxicity: reversible, stria vascularis edema that damages the ears

30
Q

what are the unique adverse effects of thiazide diuretics?

A

hypercalcemia

31
Q

drug drug interactions of loop & thiazide diuretics

A
  • dofelitide: prolonged QT interval
  • digoxin: hypokalemia
  • NSAIDS: decrease diuretic effect
  • anti-hypertensives: can cause hypotension
32
Q

what are the unique functions of the collecting tubule?

A
  • the collecting tubule is:
    • the final site of NaCl reabsorption
    • action site of ADH and aldosterone
    • site of K+ secretion
      • ​and thus the site of diruetic induced K+ changes
33
Q

discuss the movement of solutes at the collecting tubule

A
  • reabsorption of Na+ in principle cells causes a negative intraluminal charge that drives:
    • K+ secretion from principle cells
    • paracellular Cl- reabsorption
    • H+ secretion from adjacent intercalated cells
34
Q

what are the classes of K+ sparing diuretics and their MOAs?

A
  • they act on the collecting tubules to
    • increase excretion of Na+ and Cl-
    • decrease excretion of K+ and H+
  • classes: both block reabsorption at Na+ channel
    • aldosterone antagonists
    • Na+ blockers
35
Q

list the drugs in each class of K+ sparing diuretics.

A
  • aldosterone receptors antagonists
    • spironolactone
    • epleronone
  • Na+ channel blockers:
    • amiloride
    • triamterine
36
Q

what are the clinical uses shared by all K+ sparing diuretics?

A
  • both aldosterone antgonists and Na+ blockers: can be used to treat
    • edema and hypertension - in combo w/other diuretics
    • nephrogenic DI - in combination with thiazide diuretics
37
Q

what are the clinical uses of aldosterone receptor antagonists?

A

spironolactone, epleronone

  • hypertension, edema, nephrogenic DI (along with Na+ blockers)
  • specific to aldosterone antagonists:
    • hyperolderstonemia
      • ​primary hypersecretion: increased aldosterone secretion
      • secondary hypersecretion: caused by reduced intravascular volume
    • chronic heart failure with reduced ejection fraction
    • edema due to cirrhosis
38
Q

what are the adverse effects of both aldsterone antagonists and Na+ blocker potassium diuretics?

A
  • hyperkalemia
  • metabolic acidosis
39
Q

what are the adverse effects of aldosterone receptor antagonists?

A
  • hyperkalemia, metabolic acidosis (applies to all K+ sparing diuretics)
  • gynecomastia
  • mentstural irregularities
  • decreased libido

these AEs seen mostly in spironolactone

40
Q

AEs of triamterine

A

triamterine = Na+ channel blocke

  • hyperkalemia, metabolic acidosis (all k+ sparing diuretics)
  • megoblastic anemia
  • kidney stones
  • acute renal failure
41
Q

AEs of amiloride?

A

amiloride = Na+ channel blocker (potassium sparing diuretic)

  • hyperkalemia, metabolic acidosis (all K+ sparing diuretics)
  • nausea, vomitting, diarrhea
  • headache
42
Q

what are the contraindications of K+ sparing diuretics?

A
  • oral K+ administration
  • hyperkalemia
  • renal insufficiency
43
Q

what are the drug drug interactions of K+ sparing diuretics?

A
  • coadministration with the following drugs increases the risk of hyperkalemia:
    • _​_ACE inhibitors/ARBs:
      • block RAAS –> decrease aldosterone secretion and thus increase K+ retention
    • K+ supplements
    • trimethoprine - behaves like an Na+ blocker (sounds like triameterene)
    • cyclosporine & tacrolimus - impair K+ excretion
44
Q

potassium binding agents?

  • what are they?
  • what is their MOA?
  • what are their clinical uses?
  • drug drug interactions?
A
  • potassium binding agents:
    • paritromer (an oral suspension)
    • sodium polystyrene sulfonate
  • MOA: binds excess K+ in the intestinal lumen –> promotes its excretion
  • clinical uses: non life-threatening hyperkalemia
  • drug-drug interaction:
    • effects absorption of other drugs from the GI tract.
    • should be a 3 hr time gap between K+ binding agents and administration of other drugs
45
Q

mannitol

  • how does it work as a diuretic?
  • how is it admistered?
  • pharmokinetics
A
  • mannitol is an osmotic diuretic
  • MOA:
    • mannitol is easily filtered through the glomeruli
    • is restricted to the extracellular fluid compartment
    • thus, is NOT reabsorbed from the tubules
    • locally, by increasing osmolality of rental tubular fluid, mananitol
      • prevents water reabsorption in the PCT and the descending loop of Henle
      • opposes the action of ADH in the collecting tubule
  • pharmokinetics:
    • not metabolized
    • nontoxic
  • uses:
46
Q

clinical uses of mannitol as a diuretic.

A
  • CNS uses:
    • cerebral edema
    • intracranial hematoma
  • glaucoma
    • reduces intraocular pressure in patients requiring ocular surgery
      • administered pre-and post operation
  • prevents anuria (failure of the kidney to produced urine) caused by hemolysis (lysed RBCs) or ryabdomyolysis (muscle breakdown)
47
Q

adverse effects of mannitol

A
  • can expand the ECF volume to the point of:
    • worsening heart failure
    • producing pulmonary edema
    • causing
      • headache
      • nausea
      • vomitting
    • dehydration
    • hyperkalemia, hypernatrmia
48
Q

contraindications of osmotic diuretics

A
  • Pulmonary edema
  • Poor cardiac reserve
  • Severely dehydrated patient
  • Active cranial bleeding (though it can be used to treat intracrnial hemotoma)
  • Anuria (though it can be used to prevent anuria)
49
Q

summarize the drugs within each class of diuretics

S2B5 Pharmacology (3 decks)

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