Chapter 18: Renal Disease Flashcards

1
Q

Most common causes of CKD?

A

HTN and diabetes

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2
Q

Which diuretic works at the loop of henle?

A

loop diuretics

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3
Q

Which diuretic works at the distal convoluted tubule?

A

thiazide diuretics

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4
Q

Loop diuretics block which pump & where?

A

Na-K pump in the ascending limb of the loop of Henle

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5
Q

Thiazide diuretics block which pump?

A

Na-Cl

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6
Q

Loop diuretics cause (increased/decreased) Ca reabsorption back into the blood, while thiazide diuretics cause (increased/decreased) Ca reabsorption

A

Decreased; increased

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7
Q

Long-term use of loop diuretics can (increase/decrease) bone density, whereas long-term use of thiazide diuretics can (increase/decrease) bone density

A

Decrease; increase

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8
Q

When aldosterone antagonists like spironolactone and eplerenone block aldosterone, more ___ and ___ are excreted in the urine and serum ___ increases

A

Na, water

K

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9
Q

What is the normal range for Scr?

A

0.6-1.3 mg/dL

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10
Q

CKD is generally defined as GFR ____ and/or _____

A

<60 ml/min

albuminuria

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11
Q

What drugs are first-line in preventing progression of disease in pts with CKD, diabetes and/or HTN if albuminuria is present?

A

ACE-I and ARB

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12
Q

When starting treatment with an ACEi or ARB, the baseline SCr can increase by up to ___%. This is normal and treatment should not be stopped

A

30%

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13
Q

What should you counsel a patient on when taking an ACE-I or ARB?

A

Avoid potassium supplements and salt substitutes

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14
Q

Patients with advanced kidney disease require monitoring of

A

PTH, phosphorous, Ca and Vitamin D levels

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15
Q

What is the MOA of phosphate binders?

A

Block absorption of dietary PO4 by binding to it in the intestine

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16
Q

When are phosphate binders taken? What is the frequency?

A

TID with meals or right before a meal

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17
Q

Which phosphate binders are first line?

A

Calcium-based (i.e. Ca acetate, Ca carbonate)

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18
Q

What is a side effect of calcium-based phosphate binders?

A

hypercalcemia; especially when used with vitamin D due to increased Ca absorption

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19
Q

Which phosphate binders are non-Ca and non-aluminum

A

Sevelamer carbonate and sevelamer Hcl

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20
Q

What is unique about sevelamer?

A

Can lower total cholesterol and LDL by 15-30%

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21
Q

What are high levels of PTH treated with?

A

vitamin D

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22
Q

How does Vitamin D deficiency occur?

A

when the kidneys cannot hydroxylate vitamin D to the active form, 1,25-dihydroxy vitamin D

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23
Q

What is the difference between vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol)

A

D3 is synthesized in the skin after UV exposure and D2 is produced by plant sterols and is the primary source of dietary vitamin D

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24
Q

What is the MOA of vitamin D analogs?

A

increase intestinal absorption of Ca, raising serum calcium concentrations and inhibit PTH secretion

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25
Q

What is the MOA of calcimimetics?

A

increases sensitivity of Ca-sensing receptor on PT gland, causing decreased PTH, decreased Ca, and decreased phosphate

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26
Q

What is an ADE of cinacalcet?

A

hypocalcemia

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27
Q

A sudden loss of kidney function due to a non-renal condition (e.g., drugs)

A

Acute Kidney Injury (AKI)

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28
Q

Common cause of AKI

A

dehydration

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29
Q

How can AKI present

A

BUN:SCr ratio > 20:1 plus decreased urine output, dry mucous membranes, and tachycardia

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30
Q

What drug class works at the proximal tubule

A

SGLT2 inhibitors

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31
Q

Where does aldosterone work in the kidney

A

DCT and collecting duct

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32
Q

What does aldosterone do

A

Increases Na and water reabsorption and decrease K reabsorption

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33
Q

Which key drugs can cause kidney disease

A
Aminoglycosides
Amphotericin B
Cisplatin
Cyclosporine
Loop diuretics
NSAIDs
Polymyxins
Radiographic contrast dye
Tacrolimus
Vancomycin
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34
Q

Besides renal impairment, what else can cause increased BUN

A

dehydration

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35
Q

Low muscle mass = ____ SCr

A

low

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36
Q

When is the Cockcroft-Gault formula not preferred

A

Very young children, in ESRD or in unstable renal function

37
Q

Which two drugs use GFR instead of CrCl for dose adjustments

A

SGLT2 inhibitors and metformin

38
Q

Which key drugs require dose decrease or increase interval in CKD

A
  • Aminoglycosides (increase dosing interval)
  • BL antibiotics (except antistaphylococcal PCNs and ceftriaxone)
  • Fluconazole
  • Quinolones (except moxifloxacin)
  • Vancomycin
  • LMWHs (enoxaparin)
  • Rivaroxaban (for AFib)
  • Apixaban (for AFib)
  • Dabigatran (for AFib)
  • H2RAs (famotidine and ranitidine)
  • Metoclopramide
  • bisphosphonates
  • Lithium
39
Q

Key Drug(s) that are CI in CrCl < 60 mL/min

A

Nitrofurantoin

40
Q

Key Drug(s) that are CI in CrCl < 50 mL/min

A
  • Tenofovir disoproxil fumarate containing products (e.g., Stribild, Complera, Atripla, Symfi, Symfi Lo)
  • Voriconazole IV
41
Q

Key Drug(s) that are CI in CrCl < 30 mL/min

A
  • Tenofovir alafenamide containing products (e.g., Genvoya, Biktarvy, Descovy, Odefsey, Symtuza)
  • NSAIDs
  • Dabigatran (DVT/PE)
  • Rivaroxaban (DVT/PE)
42
Q

Key Drug(s) that are CI in GFR < 30 mL/min/1.73m2

A
  • SGLT2 inhibitors (canagliflozin, dapagliflozin, empagliflozin)
  • Metformin
43
Q

Treatment of hyperphosphatemia is initially focused on

A

Restricting dietary phosphate (e.g., avoid dairy products, cola, chocolate and nuts)

44
Q

If a dose of a phosphate binder is missed and a patient has already eaten, what should be done

A

The dose should be skipped

45
Q

What are the 3 types of phosphate binders

A
  1. aluminum based
  2. calcium based
  3. aluminum free, calcium free drugs
46
Q

What is a side effect of aluminum hydroxide

A

“dialysis dementia”

47
Q

Benefits of aluminum-free, calcium-free phosphate binders

A

No aluminum accumulation, less hypercalcemia

48
Q

Counseling point for lanthanum carbonate

A

Must chew tablet thoroughly to reduce risk of severe GI adverse effects

49
Q

Side effect of ferric citrate

A

Iron absorption - dose reduction of IV iron may be necessary

50
Q

Side effects of Lanthanum carbonate

A

Nausea/vomiting, diarrhea, constipation

51
Q

Side effects of sevelamer

A

N/V/D

52
Q

Phosphate binders must be separated from ____ and ___

A

levothyroxine and antibiotics that chelate (e.g., quinolones and tetracyclines)

53
Q

Calcium-based phosphate binders interact with many drugs, including

A

Quinolones, tetracyclines, oral bisphosphonates, and thyroid products

54
Q

What drug must be taken 1 hour before both Sucroferric oxyhydroxide and ferric citrate

A

Doxycycline

55
Q

What drug should be separated by 2 hours from ferric citrate

A

ciprofloxacin

56
Q

Which drug should not be used with sucroferric oxyhydroxide

A

levothyroxine

57
Q

Which drug class should be given 1 hour before or 2 hours after lanthanum

A

quinolone antibiotics

58
Q

Which drug should be separated by at least 2 hours from lanthanum

A

Levothyroxine

59
Q

Which drug class should be given 2 hours before or 6 hours after sevelamer

A

quinolone antibiotics

60
Q

____ serum concentrations can be decreased and doses of these medications should be given several hours before sevelamer

A

Levothyroxine

61
Q

What is the active form of vitamin D3

A

Calcitriol

62
Q

Which drug is a calcimimetic

A

Cinacalcet (Sensipar)

63
Q

Side effect of Vitamin D analogs

A

Hypercalcemia

64
Q

Cinacalcet brand name

A

Sensipar

65
Q

Side effects of etelcalcetide

A

Muscle spasms and paresthesia

66
Q

Which drug class can prevent the need for blood transfusions

A

Erythropoiesis-stimulating agents (ESAs)

67
Q

Which ESA is long-acting

A

darbepoetin alfa

68
Q

Brand names of epoetin alfa

A

Procrit, Epogen

69
Q

Brand name of darbepoetin alfa

A

Aranesp

70
Q

Risks of ESAs

A

elevated BP and thrombosis

71
Q

ESAs should only be used when Hgb is < ___ g/dL

The dose of ESAs should be held or d/c if the Hgb exceeds ___ g/dL

A

10

11 (risk of thromboembolic disease is increased with higher Hgb levels)

72
Q

ESAs are only effective if adequate ____ is available to make Hgb

A

iron

73
Q

What is the most abundant intracellular cation

A

Potassium

74
Q

Renal K excretion is increased by ___ & ___

A
aldosterone
diuretics (loops > thiazides)
75
Q

What causes K to shift into the cells

A

insulin

76
Q

Which patients are at a higher risk for hyperkalemia

A

Pts with diabetes - insulin deficiency reduces the ability to shift K into the cells, and many pts with diabetes take ACEi or ARBs

77
Q

Symptoms of hyperkalemia

A

Muscle weakness, bradycardia and fatal arrhythmias

78
Q

Key drugs that can increase K levels

A
ACEi
Aldosterone receptor antagonists
Aliskiren
ARBs
Canagliflozin
Drosperinon-containing COCs
Potassium-containing IV fluids (including PN)
K supplements
Trim-Sulfa
Transplant drugs (cyclosporine, everlomius, tacrolimus)
79
Q

What should be done to the pts meds if they have hyperkalemia

A

D/c all K sources

80
Q

What is done first if hyperkalemia is severe

A

There is an urgent need to stabilize the myocardial cells to prevent arrhythmias and to rapidly shift K intracellularly or induce elimination from the body

81
Q

Which med is used in hyperkalemia to stabilize the heart/prevent arrhythmias

A
Calcium gluconate (IV)
Onset: 1-2 min
82
Q

Which meds are used in hyperkalemia to shift K intracellularly

Include route and onset

A

Regular insulin (IV)
Dextrose (IV)
Sodium bicarb (IV)
Albuterol (nebulized)

Onset: all 30 min

83
Q

Which meds are used in hyperkalemia to eliminate K from the body

A

Furosemide (IV) Onset: 5 min
Sodium polystyrene sulfonate (oral) Onset: 1 hr
Patiromer (oral) Onset: 7 hrs
Sodium zirconium cyclosilicate (oral) Onset: 1 hr
Hemodialysis Onset: immediately

84
Q

sodium polystyrene sulfonate brand name

A

Kayexalate

85
Q

sodium polystyrene sulfonate warning

A

Can bind to other oral meds

86
Q

patiromer warnings/SE

A

WARNINGS
Hypomagnesemia
Binds to many oral drugs, separate by at least 3 hours before or 3 hours after

SE
Constipation

87
Q

sodium zirconium cyclosilicate warning

A

can bind other drugs, separate by at least 2 hours before or 2 hours after

88
Q

What is required if CKD progresses to failure (Stage 5 disease)

A

Dialysis

89
Q

Drug removal during dialysis depends primarily on which factors

A

Molecular weight/size
Vd
Protein-binding
High-flux and high-efficiency HD filters & higher dialysis blood flow rates