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NAPLEX 2024 > 18. Renal Disease > Flashcards

18. Renal Disease Flashcards

1
Q

Most common causes of renal disease

A

DM and HTN

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2
Q

Much of the Na, Cl, Ca, and water that are initially filtered out of the blood are reabsorbed in the ___

A

Proximal tubule

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3
Q

SGLT2 inhibitors work in this part of the nephron

A

Proximal tubule

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4
Q

In the descending limb of the loop of Henle, ___ is reabsorbed but not ____

A

Water is reabsorbed but Na and Cl ions

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5
Q

In the ascending limb of the loop of Henle, ___ is reabsorbed but not ____

A

Na and Cl ions are reabsorbed but not water

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6
Q

If ___ is present __ passes through the walls of the ascending limb and is reabsorbed

A

ADH, water

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7
Q

ADH is also called ____

A

Vasopressin

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8
Q

Loop diuretics inhibit ___ pump in the ____

A

Na-K pump, thick ascending limb of the loop of Henle

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9
Q

Effect of Loop Diuretics

A

Less Na reabsorption (increased Na conc in filtrate, less water reabsorbed)
Less Ca reabsorption (Ca depletion, long-term use can cause decreased bone density)

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10
Q

____ is involved in regulating K, Na, Ca, and pH

A

Distal convoluted tubule

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11
Q

Only ~5% of Na is reabsorbed in this part of the nephron

A

Distal convoluted tubule

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12
Q

Thiazides work in this part of the nephron

A

Distal convoluted tubule

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13
Q

Which is a stronger diuretic? Thiazide vs loop diuretic

A

Loop diuretic
Thiazides work in distal convoluted tubule which only reabsorbs 5% Na so diuretic effect is much less

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14
Q

~25% of Na is reabsorbed in this part of the nephron

A

Loop of Henle, ascending limb

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15
Q

Effect of thiazides diuretics

A

Increase Ca reabsorption at the Ca pump in the distal convoluted tubule – long-term use can have protective effect on bones unlike loop diuretics

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16
Q

Potassium sparing diuretics work in this part of the nephron

A

Distal convoluted tubule and collecting duct

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17
Q

Effect of potassium sparing diuretics

A

Decrease Na and water reabsorption, increase K retnetion

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18
Q

Nephrotoxic drugs list

A

Aminoglycosides, Amp B, cisplatin, cyclosporine, tacrolimus, vancomycin, loop diuretics, NSAIDs, polymixins, contrast dye

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19
Q

BUN measure nitrogen in urea, waste product of ____ metabolism

A

protein

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20
Q

Cr is the waste product of ___ metabolism

A

muscle

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21
Q

CrCl equation

A

(140-age) / (72 - Scr) * weight (*0.85 if female)

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22
Q

CKD criteria

A

eGFR < 60
Albuminuria (AER or UACR ≥30)
decreased eGFR or albuminuria for > 3 months

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23
Q

HTN in kidney disease - first-line treatment and notes

A

ACEi/ARBs, can increase SCr by 30% (d/c if > 30%), increase K (avoid K supplements and salt substitutions), monitor SCr and K

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24
Q

DM in kidney disease - therapies and notes

A

SGLT2i (cana, dapa, empagliflozin shown to decrease CV events and CKD)
Second line GLP1RA
Finerenone as add-on to SGLT2i and max tolerated ACEi/ARBs if eGFR ≥ 25

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25
Q

Renal Dose Adj Drug List

A

Aminoglycosides (increase dosing primarily)
Beta-lactam abx (except antistaphylococcal penicillins and CTX)
Fluconazole
Quinolones (except moxifloxacin)
Vancomycin
LMWHs (enoxaparin)
Rivaroxaban, Apixaban, Dabigatran (for AFib)
H2RAs (famotidine, ranitidine)
Metoclopramide
Bisphosphonates
Lithium

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26
Q

Drugs CI in CKD List

A

CrCl < 60: Nitrofurantoin
CrCl < 50: TDF (tenofovir disoproxil fumarate) containing products (e.g. Complera, Delstrigo, Stribild, Symfi) // Voriconazole IV (due to vehicle)
CrCl < 30: TAF (tenofovir alafenamide) containing products (e.g. Biktarvy, Descovy, Genvoya, Odefsey, Symtuza) // NSAIDs // Dabigatran and Rivaroxaban (DVT/PE)
GFR < 30: Metformin – do not start if GFR ≤ 45
Other: Meperidine, SGLT2i

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27
Q

Monitoring in CKD-MBD

A

PTH, phosphorus (phosphate, PO4), Ca, and vitD levels

28
Q

Hyperphosphatemia contributes to chronically elevated ___ levels (secondary ____) and must be treated to prevent bone disease and fractures

A

elevated PTH levels (secondary hyperparathyroidism)

29
Q

3 types of phosphate binders

A

1) aluminum based, 2) calcium based, 3) aluminum calcium free

30
Q

Aluminum-based phosphate binder examples and important notes

A

Aluminum hydroxide, rarely used d/t aluminum accumulation (nervous system and bone toxicity)
ADEs: aluminum intoxication, dialysis dementia, osteomalacia, constipation, nausea
Monitor: Ca, PO4, PTH, s/sx aluminum toxicity

31
Q

Calcium-based phosphate binder examples and important notes

A

Calcium acetate (Phoslyra), and calcium carbonate (Tums)
Use as first-line
ADEs: Hypercalcemia, constipiation, nausea
Monitor: Ca, PO4, PTH
Hypercalcemia can be problematic with concomitant use of VitD d/t increased calcium absorption

32
Q

Aluminum+Calcium-free phosphate binder examples and important notes

A

Sucroferric oxyhydroxide (Velphoro), Ferric citrate (Auryxia), Lanthanum carbonate (Fosrenol)
No aluminum accumulation, less hypercalcemia, but more expensive
Warnings: Iron absorption with ferric citrate, may require dose reduction of IV iron // GI perforation with lanthanum carbonate, contraindicated for GI obstruction, fecal impaction, ileus
ADEs: Velphoro/Auryxia - diarrhea, constipation, black feces // Lanthanum carbonate: N/V/D, constipation, abd pain

33
Q

Aluminum+Calcium free phosphate binder that is NOT systemically absorbed and important notes

A

Sevelamer
ADEs: N/V/D
Can lower total cholesterol and LDL by 15-30%

34
Q

Phosphate binder drug interactions: separate administration from ___, ___, and ___

A

levothyroxine, quinolones, and tetracyclines

35
Q

Vit D deficiency occurs when the kidney is unable to hydroxylate vit D to its final active form, _____

A

1,25-dihydroxy vitamin D

36
Q

Vitamin D3 (or ____) comes from ___

A

cholecalciferol, exposure to UV light from the skin

37
Q

Vitamin D2 (or ____) comes from ____

A

ergocalciferol, plant sterols and it the primary dietary source of vitamin D

38
Q

Calcitriol (Rocaltrol) is the active form of ___

A

vitamin D3

39
Q

Cinacalcet (or ___) is a calcimimetic that mimics the actions of calcium on the ___ and causes a reduction in ___. Only used in ____ patients.

A

parathyroid gland and causes a reduction in PTH // dialysis patients

40
Q

VitD analogs examples and notes

A

Calcitriol (Rocaltrol), Calcifediol (Rayaldee), Doxercalciferol (Hectorol), Paricalcitol (Zemplar)
Warnings: digitalis toxicity potentiated by hypercalcemia, contraindicated in hypercalcemia and vit D toxicity
ADEs: hypercalcemia, hyperphosphatemia, N/V/D (>10%)
Monitor Ca, PO4, PTH, 25-hydroxy vit D (calcifediol)
Take with food or shortly after meal to decrease GI upset

41
Q

Calcifediol is prodrug of ___

A

calcitriol

42
Q

Calcimimetics increase the sensitivity of calcium-sensing receptors on the parathyroid gland causing decrease in _____

A

PTH, Ca, and PO4

43
Q

Calcimimetic examples and notes

A

Cincalcet (Sensipar), Etelcalcetide (Parsabiv)
Warning: Cinacalcet - caution in pt with hx of seizures, contraindicated in hypocalcemia // Etelcalcetide - hypocalcemia, worsening HF, GI bleeding, decreased bone turnover
ADEs: Cinacalcet - hypocalcemia, N/V/D, paresthesia, HA, fatigue, depression, anorexia, constipation, bone fracture, weakness, arthralgia, myalgia, limb pain, URTIs // etelcalcetide - muscle spasms, paresthesia, N/V/D
Monitoring: Ca, PO4, PTH

44
Q

As kidney function declines, EPO production ___

A

decreases

45
Q

Eryhtropoiesis-stimulating agents (ESAs) have risks, including ___ and ___

A

elevated BP and thrombosis

46
Q

ESAs should only be used when Hgb is ___ and d/c if Hgb exceeds ___, as the risk for thromboembolic disease (DVT, PE, MI, stroke) is increased with higher Hgb levels

A

< 10, exceeds 11

47
Q

ESAs are only effective if adequate ___ is available

A

iron

48
Q

Renal K excretion is increased by ______

A

hormone aldosterone, diuretics (loops > thiazides), high urine flow (via osmotic diuresis), and negatively charged ions in the distal tubule (e.g. bicarbonate)

49
Q

With normal kidney function, acute rise in K from a meal would be offset by the release of ___, which causes K to shift into the cells

A

Insulin

50
Q

Hyperkalemia symptoms

A

Muscle weakness, bradycardia, fatal arrhythmias

51
Q

Drugs that increase K levels

A

ACEi, aldosterone receptor antagonists, aliskiren, ARBs, canagliflozin, drospirenone-containing COCs, K-containing IV fluids (including parenteral nutrition), K supplements, SMX/TMP, transplant drugs (cyclosporine, everolimus, tacrolimus)

52
Q

First step for treating severe hyperkalemia is to give _____ to stabilize the heart (prevent arrhythmias)

A

calcium gluconate (preferred) or calcium chloride
Note: does not decrease potassium, just stabilized myocardial cells to prevent arrhythmias

53
Q

Hyperkalemia treatment options: shift K intracellularly

A

Regular insulin+dextrose (dextrose given to prevent hypoglycemia, dextrose stimulates insulin secretion but does not shift K on its own)
Sodium bicarbonate (used when metabolic acidosis is present)
Albuterol (monitor for tachycardia and chest pain)

54
Q

Hyperkalemia treatment options: remove K

A

Furosemide
Sodium polystyrene sulfonate
Patiromer
Sodium zirconium cyclosilicate
Hemodialysis

55
Q

____ (K binder) has higher risk of GI necrosis when administered with sorbitol. Do not use together.

A

Sodium polystyrene sulfonate (SPS, Kayexalate)

56
Q

___ (K binder) has warning for hypomagnesemia

A

Patiromer (Veltassa)

57
Q

___ is generally the preferred potassium binder d/t fastest onset of action

A

Sodium zirconium cyclosilicate (Lokelma)

58
Q

Metabolic acidosis is a result of decreased ability of the kidney to reabsorb ___

A

bicarbonate

59
Q

Bicarbonate replacement drug options

A

Sodium bicarbonate, sodium citrate/citric acid solution (Cytra-2, Oracit)
Sodium citrate/citric acid solution is metabolized to bicarbonate by the liver (may not be effective in liver failure)
Monitor sodium levels

60
Q

Factors affecting drug removal during dialysis

A

Molecular weight/size
Vd
Protein-binding
Membrane
Blood flow rate

61
Q

Drugs with (smaller/larger) molecules are more readily removed in HD

A

Smaller

62
Q

Drugs with a (large/smaller) Vd are less likely to be removed by dialysis

A

large

63
Q

(high/low) protein-binding drugs are less likely to be removed by dialysis

A

High

64
Q

(higher/lower) flux (pore size) and efficiency (surface area) HD filters remove more substances

A

High

65
Q

(Higher/lower) HD blood flow rates increase drug removal

A

Higher

NAPLEX 2024 (74 decks)

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