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Pharm 2 > Diuretics, Renal meds, and Lytes > Flashcards

Diuretics, Renal meds, and Lytes Flashcards

1
Q

Where does NaCl reabsorption primarily occur?

A

Proximal tubule

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2
Q

What diuretics work primarily on the proximal tubule?

A

CAI’s and Osmotics

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3
Q

What is the role of the loop of henle?

A

Concentration of urine

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4
Q

What is the difference b/w the descending and ascending loop of henle?

A

Descending: water is reabsorbed and NaCl diffuses in

Ascending: water stays in and NaCl ACTIVELY reabsorbed

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5
Q

What diuretics work primarily on the loop of henle?

A

Loop diurectics

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6
Q

What is the role of distal convoluted tubule?

A

Reabsorption

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7
Q

What diuretics work primarily on the DCT?

A

Thiazides

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8
Q

What is the role of the collecting duct?

A

Final concentraient of urine

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9
Q

What meds work on the collecting duct?

A

Potassium-sparing diuretics

Vasopressin

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10
Q

2 definitions of Chronic kidney disease

A

Kidney damage > 3 months defined by structural or functional abnormalities with or without decreased GFR

Or

GFR <60ml/min for > 3 months with or without kidney damage

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11
Q

difference b/w acute and chronic kidney damage

A

Acute is < 3 months

Chronic is > 3 months

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12
Q

Stage I kidney disease

A

GRF > 90ml/min

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13
Q

Stage II Kidney disease

A

GFR 60-89 ml/min

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14
Q

Stage III Kidney disease

A

GFR 30-59 ml/min (Moderate)

Its less than 60, so its where CKD begins

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15
Q

Stage IV kidney disease

A

GFR 15-29 ml/min (severe)

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16
Q

Stage V kidney disease

A

GFR < 15 ml/min (Kidney failure)

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17
Q

Stage VI kidney disease

A

Dialysis

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18
Q

At what stage of CKD are meds starting to be renally adjusted?

A

Stage 3

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19
Q

What criteria is use to diagnose acute kidney disease

A

RIFLE criteria

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20
Q

RIFLE criteria is based on ___

A

GFR

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21
Q

Pre-renal injury is usually due to ____

A

dehydration (occurs before the kidney)

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22
Q

Intrinisic renal injury is usually due to ___

A

medications (large molecules)

causes damage along the nephron

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23
Q

Post-renal injury is usually due to ____

A

obstruction (kidney stone, growth)

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24
Q

What is FENa?

A

Fractional Excretion of Na

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25
Q

FENa levels for pre-renal, intrinsic, and post-renal

A

Pre-renal: <1%
Instrinic: <1.3%
Post-renal: <1.5%

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26
Q

What is the most common carbonic anhydrase inhibitor?

A

Diamox (Acetazolamide)

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27
Q

What are carbonic anhydrase inhibitors primarily used for?

A

Glaucoma and altitude sickness

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28
Q

MOA of carbonic anhydrase inhibitors?

A

Inhibit CA, which inhibits H+ secretion in the proximal tubule. Bicarb and sodium are blocked from reabsorption.

Effect is short lived due to compensation at loop of Henle.

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29
Q

CAI’s cause a loss of Bicarb, which leads to ____

A

Hypokalemic metabolic ACIDOSIS

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30
Q

Tolerance to CAI’s usually develops after ____

A

2-3days

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31
Q

Main SE’s of CAI’s

A
  1. PONV/GI upset
  2. Blurred vision leading to confusion and agaitation

Not too worried about fluid shifts

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32
Q

Examples of osmotic diuretics

A

Mannitol

Urea

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33
Q

MOA of osmotic diuretics

A

large molecules result it movement of water through osmosis

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34
Q

What major electrolyte abnormality can occur with osmotic diuretics?

A

hypernatremia

due to loss of water an reduced intracellular volume

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35
Q

Giving mannitol to a a patient with poor myocardial function can results in ___

A

CHF

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36
Q

What diuretics can be given to for differential diagnosis of acute oliguria?

A

Mannitol

Loops

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37
Q

Mannitol is only nephroprotective for which patients?

A

Renal transplant surgery, less incidence of ARF

no evidence it prevents ARF in other cases (CV surgery, trauma, other transplants, surgery in the presence of liver dz/jaundice)

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38
Q

T/F

Mannitol requires the presence of intact BBB

A

true

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39
Q

T/F

Mannitol can initially increase ICP if given too rapidly

A

True

due to vasodilation of intracranial and extra cranial vessels simutaneously

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40
Q

How long should Mannitol be administered to decrease ICP?

A

Over 10 mins

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41
Q

SE’s of mannitol

A

pulmonary edema
hypovolemia
electrolyte disturbances
plasma hyperosmolarity

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42
Q

Is urea small/large molecule size

A

small

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43
Q

T/F

urea can cross BBB

A

True

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44
Q

What has a greater rebound increase in ICP after administration, mannitol or urea?

A

Urea

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45
Q

What are two major drawbacks to urea?

A

high incidence of VTE

Tissue necrosis (not seen with mannitol)

46
Q

What lab value will change when giving urea?

A

Increase BUN (due to fluid shifts, NOT ARF)

47
Q

T/F

Compared to mannitol, urea has more SE and is less effective

48
Q

Examples of Loop diuretics

A
  • Furosemide (Lasix)
  • Bumetanide (Bumex)
  • Torsemide (Demedex)
  • Ethacrynic acid (Edecrin)
49
Q

MOA of loop diurectics

A

Inhibits Na and Cl reabsorption in the ascending loop and to a lesser extent in the proximal tubule.

50
Q

T/F

loop diuretics are the best meds for chronic edema (form CHF and liver dz)

51
Q

DOA of loop diuretics

52
Q

what loop diuretic has the worst oral bioavailability?

53
Q

Loop diuretics are contraindicated in patients with ___ allergy

A

sulfa

except Ethacrynic acid (Edecrin)

54
Q

The only difference b/w loop diuretics is _____

A

oral bioavailability (no difference IV)

55
Q

Which loop diuretic is safe in patients with a sulfa allergy?

A

Ethacrynic acid (Edecrin)

56
Q

Loop diuretics can lead to what 3 things

A

Loss of Na and water

Hypokalemic metabolic alkalosis

divalent loss (both K+ and Mg+)

Hypocalcemia

57
Q

carbonic anhydrase inhibitors can cause hypokalemic metabolic _____, loop diuretics can cause hypokalemic metabolic _____

A

acidosis

alkalosis

58
Q

What other med should be ordered along with loop diuretics?

59
Q

Which loop diuretic has the highest risk of electrolyte abnormalities?

60
Q

Clinical uses of loop diuretics

A
  1. mobilizaiton of edema fluid due to renal, hepatic, or cardiac dysfunction.
  2. Treatment of increased ICP.
  3. Treatment of hypercalcemia.
  4. Differential diagnosis of acute oliguria.
61
Q

Lasix produces diuresis within __

62
Q

Furosemide induced production of prostaglandins (E4) results in renal vaso____ and increased ____.

A

renal vasodilation and increased RBF

63
Q

What med can inhibit Furosemide-induced increases in RBF?

64
Q

What 3 classes of antibiotics can interact with lasix?

A

Cephlasporins (nephrotoxicity)
Aminoglycosides (nephrotoxicity)
PCN (higher risk of allergic interstitial nephritis)

65
Q

T/F

Combination of Furosemide and Mannitol is more effective in decreasing ICP then either drug alone.

66
Q

T/F

Effects of lasix on ICP is affected by intact BBB

A

FALSE

not affected by alterations in BBB. Mannitol requires a intact BBB

67
Q

What is more effective in decreasing ICP, mannitol or lasix?

68
Q

What effect is seen if mannitol is given to someone with a disruption in BBB?

A

rebound intracranial HTN

69
Q

SE’s of loop diuretics

A
  1. fluid/electroly abnormalities (can cause arrhythmias and seizures)
  2. Acute tolerance (braking phenomenon)
  3. Deafness/Tinnitus (esp if used with ASA)
  4. cross-sensitivity with sulfa allergies
  5. Drug interactions
70
Q

use caution if giving loop diuretic with what 2 other nephrotoxic drugs

A

NSAID’s and ACE inhibitors (eps if already hypotensive)

71
Q

What 5 electrolyte abnormalities can occur with loop diuretics?

A 
Hypokalemia
Hypochloremia
Hyponatremia
Hypomagnesemia
Metabolic alkalosis
72
Q

What is the “braking phenomenon”?

A

Once the electrolytes get depleted so far, the fluid will stop following the electrolytes (because it would than cause a reverse osmosis)
urine is less concentrated because your peeing everything out, the fluid will start going back into the body because it is so electrolyte dependent

73
Q

Examples of thiazide diuretics

A 
Chlorothiazide (Diuril)
Hydorchlorothiazide (Hydrodiuril)
Indapamide (Lozol)
Metolazone (Zaroxolyn)
Chlorthalidone (Hygroton)
74
Q

MOA of thiazide diuretics

A

Compete for the Na-Cl cotransporter in the distal tubule to inhibit reabsorption.

Inhibit only urinary diluting capacity, not concentrating capacity.

75
Q

Thiazide diuretics lead to what 3 things

A
  1. Loss of Na and water
  2. Hypokalemic metabolic alkalosis
  3. Increased Ca reabsorption (Hypercalcemia)
76
Q

What is the difference b/w loop diuretics an thiazide diuretics in regards to calcium?

A

Thiazides = hypercalcemia

loops = hypocalcemia

77
Q

What class of diuretics is 1st line treatment for HTN?

A

Thiazides

loops have too many electrolyte abnormalities

78
Q

2 specific SE’s seen with thiazide diuretics

A

Hyperglycemia and hyperuricemia (gout)

79
Q

Examples of potassium-sparing diuretics

A

K+ sparing:
Amiloride (Midamor)
Triamterene (Dyrenium)

Aldosterone antagonist:
Spironolactone (Aldactone)
Eplerenone (Inspra)

80
Q

MOA of K+ sparing potassium diuretics

A

Amiloride and Triamterene:

Inhibit Na reabsoprtion induced by aldosterone. Inhibit active counter transport of Na and K in the collecting duct

81
Q

MOA of aldosterone antagonist potassium spring diuretics

A

Spironolactone and Eplerenone: C
Competes for aldosterone receptor sites in the distal tubule to block Na reabsorption and K secretion

can cause HYPERKALEMIA (esp with spironolactone)

82
Q

Clinical uses of potassium sparing diuretics

A

Used for the treatment of refractory edematous states due to:
CHF and Cirrhosis of the liver.

83
Q

Main SE of potassium-sparing diuretics

A

Hyperkalemia (esp if used in combo with NSAID’s, ACE inhibitors, and beta blockers)

does not produce hyperglycemia and hyperuremias like thiazides

84
Q

What form of calcium is preferred to treat hyperkalmia, gluconate or chloride?

A

Gluconate

chloride is an option if central line is in place

85
Q

What combo of meds is the quickest way to treat hyperkalmia?

A

Insulin and dextrose (works in 15-30mins, last 2-6hrs)

86
Q

When treating hyperkalemia with insulin, when would you not need to dextrose along with it?

A

If BG >200/250

87
Q

What is drawback to using kayexalate for hyperkalemia?

A

takes 4 to 6 hrs to reach the colon where it exerts its actions

88
Q

Patiromer (Veltassa) and Sodium zirconium cyclosilicate (Lokelma) are newer agents to treat hyperkalemia. Which one is used for acute treatment?

A

Sodium zirconium cyclosilicate (Lokelma)

onset = 1hr, but takes 48 to mainly see a benefit

89
Q

What is a draw back to Patiromer (Veltassa)?

A

give separate from other meds by 3 hours (before and after)

90
Q

What is a draw back to Sodium zirconium cyclosilicate (Lokelma)?

A

sustained action up to 12 months

91
Q

What other med be given to stabilize the cardiac membrane besides calcium?

A

Magnesium

caution using calcium in patients who are also on dig….can worsen dig toxicity

92
Q

Calcium levels are dependent on ____

A

albumin

if low albumin, ca+ will look falsely low

93
Q

what is a drawback to using albuterol to treat hyperkamlemia?

A

absorbs systemically

94
Q

Thiazide diuretics increase the likelihood of ___ toxicity

A

digoxin

think increased Ca+

95
Q

Thiazide diuretics can potentiate the effects of ___

A

non-depolarizing NMB’s

96
Q

What electrolyte also needs to be corrected along with potassium?

97
Q

IV calcium lowers/increases the threshold potential of the myocardium

98
Q

Should you give bicarb to treat hyperkalemia?

A

No. Unless they are severely acidotic

99
Q

What can occur if you treat hyponatremia too quickly?

A

central pontine demylinosis

permanent

100
Q

What meds are assoc. with hyponatremia?

A 
Thiazides diuretics
Loop diuretics
Carbamazepine
lithium
SSRI's
101
Q

Hyponatremia should be corrected no faster than ___ in the 1st 24 hours and _____ in 48 hours

A

6-12 mEq/L

18 mEq/L or less

102
Q

Presentation of hyponatremia

A
  1. Neurologic depression
  2. Seizures
  3. Respiratory depression
  4. Coma
103
Q

VAPTAN’s (vasopressin receptor blockers) are indicated for ___ and ___ hyponatremia

A

euvolemic and hypervolemic

104
Q

When would not want to give a VAPTAN to treat hyponatremia?

A

If hypovolemic, don’t have the fluid volume to remove….would do more harm

remember vasopressin causes you to hold onto water.

105
Q

Treatment for hypernatremia

106
Q

causes of hypercalcemia

A

Hyperparathyroidism, cancer, thiazides

107
Q

causes of hypocalcemia

A

Hypoparathyroidism, renal disease, loop diuretics

108
Q

If someone has low albumin, how do you calculate their corrected calcium level

A

Normal albumin level (4) - current albumin level (ex. 2.5) = 1.5

take 80% of that and add it to the Ca+ value that is measured on your BMP and that will give you the corrected calcium level

109
Q

T/F

If a patient has liver or renal disease, you want to measure their calcium level of the BMP

A

FALSE

need to use ionized calcium levels (free form of calcium)

110
Q

Treatment for hypercalcemia

A

Give fluids to try and dilute out, you can use diuretics (NOT a thiazide diuretic) you can use a loop diuretic

can used meds to treat to osteoporosis (Zoledronic acid, Denosumab and Myocalcin )…..slow down osteoblasts and start holding more Ca+ in the bones

Nasal myocalcin or IV Zoledronic acid à to store it away and get it out of the blood stream

Corticosteroids if start to get symptomatic

111
Q

Antihypertensive effects from Thiazides is from ______

A

vasodilation

Emily harped on that is not from fluid movement. Initially there is decreased ECF and decreased CO, but the sustained antihypertensive effect is from vasodilation (takes weeks to months to develop)

112
Q

T/F

Thiazide diuretics inhibit only urinary diluting capacity, not concentrating capacity

A

True

be careful bc its easy to think to affects the concentrating capacity bc its site of action is the DCT

Pharm 2 (19 decks)

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