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Renal System > Diuretics > Flashcards

Diuretics Flashcards

1
Q

What are the four function regions of the nephron?

A

Glomerulus
PCT
Loop of Henle
DCT

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2
Q

What comprises the distal nephron?

A

Last portion of DCT along with the collecting duct

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3
Q

How are the nephrons oriented within the kidney?

A

Upper portion of Henle’s loop is in the cortex, and the lower part is in the medulla

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4
Q

What are the functions of the kidneys?

A

Cleansing the extracellular fluid
Maintainance of acid-base balance
Excretion of metabolic waste and foreign substances

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5
Q

What are the three basic renal processes?

A

Filtration
Reabsorption
Secretion

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6
Q

Where does filtration occur?

A

At the glomerulus

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7
Q

What is filtration?

A

Non-selective and passive process: virtually all small molecules are filtered, cells and large molecules remain in blood

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8
Q

What are the most abundant substances in the filtrate?

A

Na+ and Cl-
HCO3- and K+ are also present but in smaller amounts

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9
Q

Which substances undergo reabsorption?

A

> 99% of water, electrolytes, and nutrients that are filtered

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10
Q

How are solutes reabsorbed?

A

Active transport

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11
Q

How is water reabsorbed?

A

Follows solutes and is reabsorbed through passive diffusion

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12
Q

How do diuretics work?

A

Modulating the reabsorption

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13
Q

How many pumps do the kidneys have for active secretion?

A

Two: one for organic acids and one for organic bases

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14
Q

What is the role of the two major pumps on the kidneys?

A

Promote excretion of the molecules like waste, toxins and drugs

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15
Q

Where are the two major pumps of the kidneys located?

A

In the PCT

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16
Q

Why are Na+ and Cl- the ions of greatest interest when it comes to reabsorption?

A

They are the most abundant

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17
Q

What is the reabsorptive capacity of PCT?

A

Highly reabsorptive capacity
65% of Na+ and Cl- reabsorbed at the PCT
All of bicarbonate and potassium reabsorbed at PCT

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18
Q

How are substances reabsorbed at the PCT?

A

Sodium, chloride, and other solutes –> active reabsorption

Water follows through passive reabsorption

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19
Q

What is the descending loop of Henle like?

A

Freely permeable to H2O
H2O is drawn from the loop into the interstitial space

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20
Q

What is reabsorption in the ascending loop of Henle like?

A

20% of filtered Na and Cl is reabsorbed

It is NOT permeable to water; water remains in the loop as Na & Cl are reabsorbed

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21
Q

What is the reabsorption of the early segment of DCT like?

A

10% of filtered Na & Cl is reabsorbed, water follows passively

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22
Q

What is the distal nephron the site of?

A

Exchange of Na for K and is under the influence of aldosterone
Determination of the final concentration of urine and regulated by ADH

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23
Q

What stimulates the sodium-potassium exchange?

A

Aldosterone

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24
Q

What is the role of aldosterone in the sodium-potassim exchange process?

A

Aldosterone increases the expression of the pumps responsible for sodium and potassium transport

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25
Q
A
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26
Q

What is the purpose of diuretics?

A

They increase urine flow which is directly related to the amount of Na and Cl reabsorption which is blocked

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26
Q

How do diuretics work?

A

Most diuretics block Na & Cl reabsorption; they create an osmotic pressure within the nephron that prevents the passive reabsorption of water

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27
Q

What is the order of highest reabsorption to lowest, excluding PCT?

A

Highest in the loop, followed by early DCT, followed by late DCT and collecting duct (distal nephron)

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28
Q

Which drug would have a greater diuretic effect and why? Furosemide or Thiazides?

A

Furosemide because it blocks reabsorption in the loop, which is higher than the reabsorption in the early DCT, where Thiazides work

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29
Q

What is the adverse impact of diuretics on extracellular fluid?

A

Diuretics cause hypovolemia, acid-base imbalance, and altered electrolyte levels

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30
Q

How are the adverse effects of diuretics minimized?

A

By using short-acting diuretics and by timing drug administration such that the kidney is allowed to operate in a drug-free manner between periods of diuresis

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31
Q

What are the classifications of diuretics?

A

Loop diuretics
Thiazide diuretics
Potassium-sparing
Osmotic diuretics
Carbonic anhydrase inhibtors

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32
Q

What is the most effective kind of diuretic available?

A

Loop diuretics, they produce more loss of fluid and electrolytes than any other diuretic

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33
Q

What are examples of loop diuretics?

A

Furosemide
Butemanide
Torasemide
Ethacrynic acid

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34
Q

What cases is Furosemide used in?

A

HTN and edema caused by CHF

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35
Q

When is Bumetanide given/used?

A

Furosemide-unresponsive patients,
40 times more potent (rapid diuresis) than Furosemide

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36
Q

What is Torasemide?

A

More prolonged action than Furosemide, with less potassium loss

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37
Q

What is Ethacrynic acid? When is it used?

A

The only loop diuretic without a sulfonamide group; used with patients with sulfonamide intolerance

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38
Q

What is the MOA of Furosemide?

A

Inhibits the Na+ K+ 2Cl- cotransporter, if no Na+ transported, then no K+ which means no K+ in the blood (hypokalaemia)

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39
Q

Where does Furosemide act?

A

Thick ascending loop of Henle

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40
Q

What are the PK of Furosemide?

A

Oral administration, diuresis begins in 60 minutes and persists for about 8 hours

Furosemide undergoes hepatic metabolism followed by renal excretion

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41
Q

What are the therapeutic uses of Furosemide? (4)

A
  1. Pulmonary edema associated with CHF
  2. Edema (unresponsive to less efficacious diuretics)
  3. HTN that cannot be controlled with other diuretics
  4. Patients with severe renal impairment
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42
Q

What happens if Furosemide, on it own is insufficient?

A

Add a thiazide

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43
Q

What is the effect of adding another loop diuretic to Furosemide?

A

There is no added beneift

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44
Q

What are the adverse effects of Furosemide? (11)

A

Hyponatremia, hypochloremia and dehydration
Hypotension
Hypokalemia
Ototoxicity
Low Mg & Ca
Maternal death/abortion
Hyperuricemia
Hyperglycemia
Weakness/tiredness

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45
Q

What are signs of evolving dehydration with Furosemide?

A

Dry mouth, unusual thirst, and oliguria

46
Q

How can the risk of dehydration be minimized (Furosemide)?

A

Initiating therapy with low doses, adjusting the dosage carefully, and monitoring loss every day

47
Q

What causes hypotension (Furosemide)?

A
  1. Loss of volume
  2. Relaxation of venous smooth muscle
48
Q

What are the signs of hypotension?

A

Dizziness, lightheadedness, fainting

49
Q

What are the complications of Hypokalemia (Furosemide)?

A

Fatal dysrhythmias

50
Q

When is hypokalemia a special concern?

A

When patients are on digoxin, heart failure drug

51
Q

How is hypokalemia minimised?

A

Consuming potassium-rich foods, taking potassium supplements or using potassium-sparing diuretics

52
Q

What are the effects of ototoxicity due to Furosemide?

A

Rare hearing impairment, deafness is transient

53
Q

What is the concern wth hyperuricemia (Furosemide)?

A

Gout

54
Q

What are the drug interactions between Furosemide and Digoxin?

A

Increased risk of digoxin-induced toxicity
To reduce the risk: monitor K levels and when indicated K+ supplements or K+ sparing diuretc

55
Q

What are the drug interactions between Furosemide and Ototoxic drugs?

A

Increase risk of ototoxicity, especially aminoglycoside antibiotics (Gentamicin)

56
Q

What are the drug interactions between Furosemide and potassium-sparing diretics?

A

Helpful; reduce risk of hypokalemia

57
Q

What are the drug interactions between Furosemide and NSAIDs?

A

Attenuate effects of Furosemide

58
Q

What are the drug interactions between Furosemide and Antihypertensive drugs?

A

Excessive reduction in BP

59
Q

What are the drug interactions between Furosemide and Lithium?

A

Used in bipolar disorders
When Na levels are low, Li excretion is reduced

60
Q

What are examples of Thiazide diuretics?

A

Hydrocholorothiazie and chlororthalidone

61
Q

How do thiazide diuretics work?

A

They decrease reabsorption of NaCl by inhibiting Na+/Cl- co-transporter on the DCT

62
Q

Which membrane do thiazide diuretics act upon?

A

The luminal membrane, which means they must be present in the tubular fluid to have an effect on the Na+/Cl- transporter

63
Q

What is an example of patients that should not use thiazide diuretics?

A

Patients with inadequate kidney function should use loop diuretics

64
Q

What are the uses of thiazide diuretics?

A

Useful as initial therapy unless compelling issues prevent that

65
Q

What are the adverse effects of thiazide diuretics?

A

Hypokalemia
Hyperuricemia
Hyperglycemia

66
Q

What is the most widely used thiazide diuretic?

A

Hydrochlorothiazide

67
Q

What is the MOA of Hydrochlorothiazide?

A

Blocks reabsorption of Na & Cl in the early segment of the DCT

68
Q

What are the PK of Hydrochlorothiazide?

A

Diuresis begins 2 hours after oral administration; effects peak within 4 to 6 hours

69
Q

Where is Hydrochlorothiazide excreted?

A

Most of it excreted unchanged in the urine

70
Q

What are the therapeutic uses of Hydrochlorothiazide? (4)

A
  1. Essential HTN
  2. Edema
  3. Hyper-calciurea
  4. Diabetes inspidus
71
Q

What is the preferred drug for edema?

A

Thiazides; Hydrocholorothiazide

72
Q

How do Thiazides help with hyper-calciurea?

A

They promote the reabsorption of Ca (which is good for osteoporosis and recurrent stone formation in the kidneys)

73
Q

What are the adverse effects of Hydrochlorothiazide?

A

Similar to loop diuretics but no ototoxicity and hypocalcemia/hypomagnesemia

74
Q

What are the drug interactions of Hydrochlorothiazide?

A

Identical to loop diuretics
CAN be combined with ototoxic agents, though, without an increased risk of hearing loss

75
Q

What are other examples of thiazides?

A

Chlorothiazide & Methylclothiazide

76
Q

Where do the K+ sparing diuretics act?

A

Act on late DCT and collecting tube

77
Q

What are the two mechanisms of K+ sparing diuretics?

A

Non-aldosterone receptor blockers
Aldosterone receptor blockers

78
Q

Which K+ sparing diuretics are non-aldosterone receptor blockers?

A

Amiloride, Triamterene

79
Q

Which K+ sparing diuretics are aldosterone receptor blockers?

A

Spironolactone, Eplerenone

80
Q

How are K+ sparing diuretics sometimes used?

A

With loop/thiazide diuretics to reduce K+ loss

81
Q

What is the role of aldosterone?

A

Promotes Na uptake in exchange for K selection

82
Q

What is the MOA of Spironolactone?

A

Blocks aldosterone –> retention of K and increased secretion of Na

83
Q
A
84
Q

How long do Spironolactone effects take to develop?

A

They are delayed effects, take up to 48 hours to develop

85
Q

What are the therapeutic uses of Spironolactone? (6)

A
  1. HTN & Edema
  2. Heart Failure
  3. Primary Hyperaldosteronism
  4. PMS
  5. PCOS
  6. Acne in young women
86
Q

What are the adverse effects of Spironolactone?

A

Hyperkalemia
Endocrine effects

87
Q

What are examples of the endocrine effects that Spironolactone causes?

A

Gynecomastia
Menstrual irregularities
Impotence
Hirsutism
Deepening of the voice

88
Q

What are the drug interactions of Spironolactone?

A

Thiazide and loop diuretics
Agents that raise K+ levels (should be used ONLY when CLEARLY necessary)

89
Q

What are examples of agents that raise K+ levels?

A

ACE inhibitors
ARBs
Direct renin inhibitors

90
Q

What is the MOA of Triamterene?

A

Directly inhibits exchange protein (ENaC)
Results in a net decrease in Na reabsorption and a reduction in K secretion

91
Q

Does Triamterene act slowly or quickly? Why?

A

Quickly, because it directly blocks the exchange

92
Q

Why should you be careful if Triamterene is used with ACEi, ARBs, and direct renin inhibitors?

A

They suppress aldosterone secretion and thus can elevate K levels

93
Q

What are the therapeutic uses of Triamterene?

A

HTN & Edema (used in combination with loop/thiazide)

94
Q

What are the adverse effects of Triamterene?

A

Nausea, vomiting, leg cramps and dizziness

95
Q

Which drug is similar to Tramterene?

A

Amiloride

96
Q

Which diuretic categories does Mannitol fall under?

A

Osmotic diuretic

97
Q

What is the MOA of Mannitol?

A

Freely filtered in the glomerulus
Undergoes minimal reabsorption
Undergoes minimal metabolism
Pharmacologically inert

98
Q

Why must Mannitol be given parenterally?

A

It does not diffuse across GI and cannot be transported by carriers/receptors

99
Q
A
100
Q

What are the therapeutic uses of Mannitol?

A

Prophylaxis for renal failure
Reduction of intracranial pressure
Reduction of intraocular pressure

101
Q

What are the adverse effects of Mannitol?

A

Edema, careful with heart disease
Headache, nausea and vomiting

102
Q

What is an example of a carbonic anhydrase inhibitor?

A

Acetazolamide

103
Q

What tubule does Acetazolamide work on?

A

PCT

104
Q

What is the purpose of Acetazolamide?

A

Mostly used for their other pharmacologic effects rather than than diuretic effect because they are MUCH less efficacious than other diuretics

105
Q

What are the therapeutic uses of Acetazolamide?

A

Glaucoma and Altitude sickness

106
Q

How does Acetazolamide help with Glaucoma?

A

Oral acetazolamide decreases the production of aqueous humor and reduces IOP with chronic open-angle glaucoma

107
Q

What are the examples of topical carbonic anhydrase inhibitors that do not cause systemic effects?

A

Dorzolamide
Brinzolamide

108
Q

How does Acetazolamide help with altitude sickness?

A

It prevents weakness, breathlessness, dizziness, nausea, and cerebral as well as pulmonary edema

109
Q

What are the PK of Acetazolamide?

A

PO or IV
90% protein bound
Eliminated by kidney

110
Q

What are the adverse effects of Acetazolamide?

A

Metabolic acidosis
Potassium depletion
Renal stone formation

111
Q

What is the contraindication of Acetazolamide?

A

Liver cirrhosis because it could lead to decreased excretion of NH4+

112
Q
A

Renal System (13 decks)

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