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Block 4b: Renal > Week 1: PHM-Diuretics > Flashcards

Week 1: PHM-Diuretics Flashcards

1
Q

Which 2 classes of diuretics combine at the thick descending & ascending limbs acting synergistically?

A

Loop and Thiazine; ex of how adding 2+ diuretics from different classes have synergistic action as long as sites of action differ

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2
Q

What is the site and MOA of carbonic anhydrase inhibitors?

A

Site: PCT MOA: Inhibit CA in lumen and in tubular cells. Decrease sodium bicarbonate reabsorption and causes HCO3 diuresis (may even lead to metabolic acidosis) *Normally, intraluminal/cellular mechanisms turn HCO3 into carbonic acid, which will dissociate into H2O and CO2 to be reabsorbed intracellularly by CA to regulate Na and H2O

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3
Q

How can CA inhibitors lead to Ca stones?

A

CA inhibitors alkalinize the urine; uric acid and cysteine and relatively insoluble in acidic urine and stones may form but their solubility can be enhanced by pH increase *excessive alkalization can lead to Ca stones*

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4
Q

Why are CA inhibitors used to treat alkalosis induced by excessive use of other diuretics?

A

CA inhibitors induce hyperchloremic metabolic acidosis

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5
Q

What diuretic class is used as prophylaxis/Tx of acute mountain sickness?

A

CA Inhibitors

In severe cases, rapidly progressive pulmonary and cerebral edema can occur.
But CSF formation and pH decrease so drugs like acetazolomide can ↑ ventilation and ↓ Sx

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6
Q

When are CA inhibitors contraindicated?

A

Liver Disease!

Urinary alkalinization->ammonia diversion in urine into systemic circulating, inducing worsening hepatic encephalopathy

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7
Q

What are 3 side effects/toxicities of CA Inhibitors?

A

1) Phosphaturia and Hypercalciuria
2) K Wasting: ↑ Na presented to CT (w/ HCO3) partially reabsorbed; lumen’s (-) electrical potential ↑ enhanced K secretion
3) Drowsiness and paresthesia: w/ higher doses from potential inhibition of CA in CNS

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8
Q

What are 3 ex’s of CA Inhibitors?
Which 2 are used for glaucoma Tx?*

A

1) Acetazolomide
2) Dichlorphenamide*
3) Methazolamide*

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9
Q

What is a PK consideration for CA Inhibitors?

A

efficacy ↓ after several days use

↓ HCO3 in glomerular filtrate; HCO3 depletion
->enhanced NaCl reabsorption by remainder of nephron

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10
Q

What is the site and MOA of loop diuretics?

A

Site: cortical and medullary thick ascending limb

MOA: inhibits NKCC2
↓ reabsorption of NaCl and ↓ lumen (+) potential that comes from K recycling
↓ in (+) potential also causes ↑ Mg and Ca excretion

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11
Q

What 2 things can loop diuretics stimulate?

A

1) Briefly stimulates RBP and ↓ peripheral venous compliance
2) Stimulates PGN synthesis in lung and kidney
*PG2 can enhance diuretic effect*

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12
Q

What drug class can interfere w/ loop activity especially in 2 comorbid conditions*?

A

NSAIDs ↓ PG synthesis in kidney

Interferes w/ loop activity’s diuretic effects for pts w/ nephrotic syndrome* and hepatic cirrhosis*

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13
Q

What are the 1st and 2nd line indications for loop diuretics?

A

1st: acute pulmonary edema; Tx for CHF to ↓ venous and pulmonary congestion
K, Mg, Ca excretion ↑ bc NKCC inhibited

2nd (or in combo w/ thiazide diuretics): HTN or severe HF in pts who are diuretic resistant

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14
Q

What class can help in acute and chronic renal failure patients but can’t prevent or shorten duration?

A

Loop Diuretics

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15
Q

What are 4 side effects of Loop Diuretics?

A

1) Hypochloremic metabolic alkalosis: ↑ Na delivery to distal tubule-> ↑ urinary excretion of K and H
2) Hypokalemia
3) Hypomagnesemia
4) Hyperuricemia: may precipitate gout attacks
*shouldn’t be used in pts w/ hx*

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16
Q

What is a possible dose related side effect of Loop Diuretics?

A

Hearing loss

From alts in electrolyte composition in inner ear fluid; usually reversible

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17
Q

What is a cross-reactivity risk w/ Loop Diuretics?

A

Pts w/ sulfonamide allergy

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18
Q

What are 4 ex’s of Loop Diuretics?
Which one can be used for sulfa allergic?*

A

1) Furosemide
2) Bumetanide
3) Torsemide
4) Ethacrynic Acid*

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19
Q

Why is the hypocalcemia generated w/ Loop Diuretics not a concern?

A

Bc Ca actively reabsorbed in DCT

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20
Q

What might loop diuretics enhance in hypercalcemic disorders? Does this offer Tx potential?

A

↑ Ca excretion

May be used to Tx mild hyperkalemia

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21
Q

What is the site and MOA of Thiazide diuretics?

A

Site: DCT

MOA: Inhibits NaCl reabsorption from luminal side of epithelial cells in DCT by blocking NaCl transporter

22
Q

Which class is a “ceiling diuretic?”

A

Thiazide Diuretics

↑ dose above normal doesn’t further diurese

23
Q

How do Thiazide Diuretics affect Ca levels?

A

↓ renal excretion of Ca
(+) in treating Ca containing urinary stones

24
Q

In what clinical condition are Thiazide diuretics indicated?

A

Diabetes Insipidus

25
Q

What are the primary indications and uses of Thiazide Diuretics?

A

Primarily results in contraction of ECF volume

  • (+) in HTN and mild CHF Tx
  • Edema assoc w/ liver and renal diseases

Adjunct to loop diuretics

26
Q 
Which class is 1st line Tx for Nephrogenic Diabetes Insipidus?
3 effects and clinical manifestations
A

Thiazide Diuretics

1) Paradoxically reduce polyuria
2) Plasma vol ↓, leading to enhanced proximal reabsorption of NaCl and H2O; ↓ fluid delivery to distal segments
3) ↑ expression of Na transporters in DCT and collecting tubules

Clinical: Excretion of large vols of dilute urine; hyponatremia, lethargy, anorexia, N/V, muscle cramps

27
Q

What are 2 rare side effects of Thiazide Diuretics?

A

Photosensitivity and generalized dermatitis

28
Q

What are 8 metabolic consequences of Thiazide Diuretics?

A

1) Metabolic alkalosis
2) Hyponatremia (from ↑ ADH and thirst)
3) Hypokalemia
4) Hypomagnesemia
5) Hypochloremia
6) Uric acid and Ca retention
7) Hyperglycemia
8) Hyperlipidemia

29
Q

What are 3 possible causes of hyperglycemia from Thiazide Diuretics?

A

1) Impaired pancreatic rel of insulin
2) ↓ tissue use of glucose
3) ↓ glucose tolerance, even unmasking DM

*Seen in doses > 50 mg, not in doses 12.5 mg

30
Q

What are 4 ex’s of Thiazide Diuretics?
What are 2 special indications?

A

1) Hydrochlorothiazide
2) Chlorothiazide
3) Chlorothalidone*
4) Metolazone*

*Chlorothalidone: ↓ stroke and heart attacks in HTN (over HCTZ)
*Metolazone: CHF pts resistant to loop diuretics, add-on to loop

31
Q

What is the site and MOA of ADH Antagonists?

A

Site: Collecting Duct

MOA: Inhibits ADH effects
can ↓ peripheral vascular resistance and ↑ CO

32
Q

When are ADH Antagonists not inidicated?

A

HTN or HF settings

33
Q

What are 2 ex’s of ADH Antagonists?
What is a special consideration for 1?

A

1) Conivaptan *must be infused IV
2) Tolvaptan

34
Q

What are 2 indications for ADH Antagonists?

A

1) Hypervolemic and euvolemic hyponatremia
(not corrected w/ fluid resuscitation)
2) SIADH mgmt when H2O restriction has failed

35
Q

What is a side effect and consideration for ADH Antagonists?

A

1) Severe hypernatremia

*Too rapid correction of Na can cause osmotic demyelination-> dysphagia, lethargy, seizures, even death

36
Q

What is an ex of an osmotic diuretic?

A

Mannitol

37
Q

What are 2 considerations for the osmotic diuretic Mannitol?

A

Rapid distribution in ECF and H2O extraction from cells

1) prior to diuresis, acute ↑ in ECF vol and hyponatremia can complicate HF and produce pulmonary edema
2) excessive use w/o adeq H2O replacement can lead to severe dehydration and hypernatremia

38
Q

What are 2 side effects of osmotic diuretics?

A

1) N/V, headache from initial hyponatremia
2) Hyperkalemia: H2O extracted from cells, intracellular K ↑ leading to cellular losses and ↑ in extracellular compartments

39
Q

What are 5 indications and responses for osmotic diuretics?

A

1) ↓ extracellular vol and pressure
2) ↑ H2O excretion rather than Na, compared to other classes
3) ↓ intraocular pressure
4) prevents acute renal failure after severe trauma or complicated surgical procedures, resulting in large pigment load on kidneys (from hemolysis/rhabdomyolysis)
5) promotes renal excretion of toxins

40
Q

When are osmotic diuretics not useful?

A

Conditions w/ Na retention

41
Q

What are 4 ex’s of K sparing Diuretics?

A

1) Spironolactone
2) Eplerenone
3) Triamterene
4) Amiloride

42
Q

What are 2 side effects of K Sparing Diuretics?

A

1) Hyperkalemia: esp in aldo receptor antagonists, risk ↑ w/ renal disease
2) Hyperchloremic metabolic acidosis by inhibiting H and K secretion

43
Q

What are side effects specific to the K sparing diuretic spironolactone (not eplerenone!)?

A

Endocrine abnormalities on steroid receptors: androgen and progesterone

1) Gynecomastia
2) Hirsutism
3) Impotence
4) Benign prostatic hyperplasia
5) Menstrual irregularities

44
Q

What is the site of action and 2 MOA’s for K sparing diuretics?

A

Site: Cortical collecting tubule

MOA 1: competitive aldosterone antagonist (↓ EF): Spironolactone and Eplerenone

MOA 2: interferes w/ Na influx through epithelial Na ion channels in luminal membrane of collecting ducts
Triamterene and Amiloride

45
Q

What are 2 general PD effects of K sparing diuretics?
What about for spironolactone and amiloride?

A

1) Na/K exchange sites are not stimulated
2) Prevents Na reabsorption and K/H secretion

Spironolactone: prevents protein synthesis that normally responds to aldo
Amiloride: directly blocks ENac

46
Q

When is the K sparing diuretic Spironolactone indicated?

A

Most effective in primary and secondary hyperaldosteronism
*Prevents aldosterone binding to its receptor*

Also cirrhotic edema (ascites) Tx

Vs. hypokalemia (in combo w/ Loop or Thiazide)

47
Q

What might evoke secondary hyperaldosteronism?

A

HF, Hepatic Cirrhosis, Nephrotic Syndrome

48
Q

What is the K sparing diuretic Eplerenone and its effects?

A

Spironolactone analogue w/ greater SP for aldo receptors and fewer AE

Interferes w/ fibrotic and inflammatory effects of aldosterone, slows progression of albumineria in diabetes

49
Q

How do Triamterene and Amiloride work and when are they indicated?

A

Directly interfere w/ Na entry

Can counteract K wasting of Thiazide
(all K sparing diuretics)

Used in combo w/ Thiazide for HTN Tx

50
Q

What are the 3 sites of action for osmotic diuretics?

A

1) Proximal Tubule: ↓ Na reabsorption by osmotic gradient, ↑ urine vol
2) Descending LOH: ↑ medullary blood flow, inhibits passive reabsorption of H2O
3) Collecting Duct: via osmotic effects, opposes ADH action

51
Q 
Which class of diuretics is indicated for Diabetes Insipidus?
How do the two types of DI compare?
In which one is administration of ADH or an analogue uniquely effective?\*
A

Thiazide Diuretics

  • Central DI*: deficient production of ADH (adjunct Tx)*
  • Nephrogenic DI*: inadequate responsiveness to ADH (1st line)

Block 4b: Renal (3 decks)

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