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Drug Action I > Block 2 - Diuretic Pharm > Flashcards

Block 2 - Diuretic Pharm Flashcards

1
Q

How are diuretics classified?

A
  1. Site of action (loop)
  2. Efficacy (high-ceiling)
  3. Chemical structure (thiazide)
  4. Similarity of action with other diuretics (thiazide-like)
  5. Effects on K+ excretion (K+ sparing)
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2
Q

What is a nephron?

A

Single epithelium lined by a single layer of cells which can generically be referred to as tubular epithelial cells

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3
Q

Describe the efficacy of diuretics working in the PCT?

A

PCT reabsorbs 65% of filtered Na+, however diuretics have limited effect

thick ascending limb has a great re-absorpative capacity -> reabsorbs most of the rejective from the PCT

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4
Q

What is the MOA of CA-I?

A

NaHCO3 is poorly reabsorbed from the lumen -> needs to be converted to CO2 and H2O by CA that is inhibited by CAI located in the PCT

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5
Q

How does CA-I effect renal system?

A

CAI decreases NaHCO3 reabsorption by increasing HCO3 excretion -> Increased urine pH -> Metabolic acidosis

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6
Q

How does CA-I effect extra-renal system?

A

CA increases HCO3 in aqueous humor-> CAI decreases aqueous humor formation and intraocular pressure

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7
Q

What are the therapeuti uses of CAIs?

A

Glaucoma, edema (low efficacy)

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8
Q

What is an example of CAI? Its characteristics?

A

Diamox (Acetazolamide)
F: 100%
t1/2: 6-9 h
Can cause sulfa-like toxicities due to sulfonamide

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9
Q

What is important about the thick ascending loop of henle (TAL)?

A
  1. Site for reabsorption of Na, K, Cl but nearly impermeable to water
  2. Major site of Ca2+ and Mg2+ reabsorption
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10
Q

Why are loops considered high ceiling?

A

Highly efficacious diuretics

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11
Q

How much Na+ does TAL reabsorb?

A

20%

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12
Q

What is the NKCC2 and how do loops affect it?

A
  1. NKCC2 carriers mediate reabsorption of Na, K, and 2Cl
  2. Loops inhibit this carrier
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13
Q

What are the loop diuretics?

A
  1. Lasix (Furosemide)
  2. Demadex (Torsemide)
  3. Ethacrynic acid
  4. Bumex (Bumetanide)
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14
Q

PK properties of Lasix?

A

F ~ 60%
t½ ~ 1.5 h
CL (~65% renal ~35% hepatic)].

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15
Q

PK properties of Demadex

A

F ~ 80%
t½ ~ 3.5 h
CL (~20% renal ~80% hepatic)].

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16
Q

PK properties of Ethacrynic acid?

A

F ~ 100%
t½ ~ 1 h
CL (~67% renal ~37% hepatic

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17
Q

PK properties of Bumex?

A

F ~ 80%
t½ ~ 0.8 h
CL (~62% renal ~38% hepatic)

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18
Q

How do loops cause hyponatremia? Along with other ADRs?

A

↑ excretion of Na+, K+, Ca2+, Mg2+ with fluid volume depletion, hypokalemia, hypomagnesemia, and hypocalcemia

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19
Q

How do loops cause hyperuricemia?

A

Decrease uric acid excretion that may result to gout like symptoms

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20
Q

What are some non-renal loop actions?

A

Direct vascular effects, increasing systemic venous capacitance and decreases left ventricular filing pressure

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21
Q

What loop diuretics have weak CAI activity?

A

Lasix and Ethacrynic acid

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22
Q

What are loop diuretic indications?

A
  1. CHF
  2. HTN
  3. Edema of CKD
  4. Nephrotic syndrome
  5. Ascites of liver cirrhosis
  6. Acute pulmonary edema
23
Q

What are the ADR of loops?

A
  1. Fluid and electrolyte imbalance
  2. Gouty attacks
  3. Hyperglycemia
  4. Ototoxicity (hearing impairment/deafness)
24
Q

How much NaCl is reabsorbed in DCT? Water

A

10%
Impermeable to water

25
Q

What is the MOA of thiazides?

A

NCC (Na/Cl carrier) pumps Na+ and Cl- into DCT and benzothiadiazides inhibits this process located in the DCT

26
Q

What are the thiazide drugs?

A
  1. Hydrochlorothiazide
  2. Hygroton, Thalitone (Chlorthalidone)
  3. Chlorothiazide
  4. indapamide
  5. Metolazone
27
Q

PK of hydrochlorothiazide?

A

F ~ 70%
t½ ~ 2.5 h
cleared renally

28
Q

PK of chlorthalidone?

A

F ~ 65%
t½ ~ 47 h
CL (~65% renal, ~ 10% biliary, ~25% unknown pathway

29
Q

PK of chlorothiazide?

A

F = 9 – 56%
t½ ~ 1.5 h
cleared renally

30
Q

PK of indapamide?

A

F ~ 93%
t½ ~ 14 h
cleared hepatically

31
Q

PK of metolazone?

A

F ~ 60%
CL (~80% renal, ~10% hepatic, ~10% biliary

32
Q

What are some of the pharmacological actions of thiazides and how does that contribute to its ADRs?

A
  1. Increased Na+ and Cl- excretion with volume depletion -> hyponatermia, hypochloremia, hypotension
  2. Increase excretion of K+ -> hypokalemia
  3. Decreased Ca+ and uric acid excretion -> hypercalcemia and hyperuricemia
  4. Can cause weak CAI action
33
Q

What are the indications of thiazides?

A
  1. HTN
  2. Edema with CHF
  3. Hepatic cirrhosis
  4. Renal (nephrotic syndrome and chronic renal failure)
34
Q

What are common ADRs of thiazides?

A
  1. Fluid and electrolyte balance
  2. hypotension
  3. hypokalemia, hyponatremia, hypochloremia
  4. metabolic alkalosis
  5. hypomagnesemia
  6. hypercalcemia, and hyperuricemia
35
Q

How much of NaCl is reabsorbed in the CT?

A

2-5%

36
Q

What is important about the CT?

A
  1. Site where aldosterone exerts a significant influence
  2. Major site of potassium secretion
37
Q

What drug class is active in the CT?

A

K+ sparing

38
Q

What is the MOA of K+ sparing

A

Na+ is reabsorbed by epithelial Na+ channels (ENaC) with the loss of K+ and H+

Diuretic inhibits ENaC -> increased Na+ and Cl- excretion

39
Q

What are potassium sparing drugs?

A
  1. Amiloride
  2. Triamterene
40
Q

PK of amiloride?

A

F = 12 - 25%
t½ ~ 9 h
cleared renally

41
Q

PK of triamterene?

A

F ~ 50%
t½ ~ 4 h
extensively metabolized to an active metabolite which is cleared hepatically

42
Q

What is aldosterone antagonists site of action?

A

CT

43
Q

What are the aldosterone antagonists?

A
  1. Spironolactone (Aldactone, CaroSpir)
  2. Eplerenone
44
Q

PK of aldactone?

A

Some affinity toward progesterone and androgen receptors
F ~ 65%
t½ ~ 1.6 h
cleared hepatically

45
Q

PK of eplerenone?

A

Very low affinity for progesterone and androgen receptors
t½ ~ 5 h
cleared hepatically

46
Q

ADRs of diuretics in the CT? Spironolactone?

A

Hyperkalemia

Gynecomastia, impotence, menstrual irregularities

47
Q

In what ways are thiazides administered? Names?

A

Coadministered with thiazides and loops

Dyazide, Maxzide (Triamterene + HCTZ)
K+ sparing/thiazide

48
Q

How do loops and thiazide induce hyperuricemia?

A
  1. Urate is poorly soluble and is transported across cell membranes
  2. Diuretics increase rate reabsorption at the PCT and inhibit secretion into tubules by competing with irate for the efflux transporters
49
Q

According to the highlighted number which drugs correspond to hyper uricemia

A
  1. Furosemide, bumetanide
  2. Furosemide, thiazides
  3. HCTZ, torasemide
  4. Torasemide
50
Q

What is the BBW of loop diuretics?

A

Potent
High doses may need to profound diuresisw with water and electrolyte depletion

51
Q

What is the BBW of HCTZ? Counseling points?

A
  1. Increased risk of non-melanoma skin cancer

Requires protection of skin from sun and undergo skin cancer screenings

52
Q

What is are the outcomes of chronic diuretic use?

A

Sustained deficit in total-body Na+ which is not compatible with life

53
Q

What is diuretic braking?

A

Renal compensatory mechanisms try to bring the balance of Na+ excretion with Na+ intake

54
Q

What is the mechanism of braking?

A
  1. Activation of sympathetic nervous system
  2. Activation of RAAS
  3. Decreased arterial BP, renal epithelial cell hypertrophy
  4. Increased renal epithelial transporter expression and alterations in natriuretic hormone (ANP)

Drug Action I (32 decks)

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