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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
Renal Dose Adj Drug List
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
26
Drugs CI in CKD List
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
27
Monitoring in CKD-MBD
PTH, phosphorus (phosphate, PO4), Ca, and vitD levels
28
Hyperphosphatemia contributes to chronically elevated ___ levels (secondary ____) and must be treated to prevent bone disease and fractures
elevated PTH levels (secondary hyperparathyroidism)
29
3 types of phosphate binders
1) aluminum based, 2) calcium based, 3) aluminum calcium free
30
Aluminum-based phosphate binder examples and important notes
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
Calcium-based phosphate binder examples and important notes
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
Aluminum+Calcium-free phosphate binder examples and important notes
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
Aluminum+Calcium free phosphate binder that is NOT systemically absorbed and important notes
Sevelamer ADEs: N/V/D Can lower total cholesterol and LDL by 15-30%
34
Phosphate binder drug interactions: separate administration from ___, ___, and ___
levothyroxine, quinolones, and tetracyclines
35
Vit D deficiency occurs when the kidney is unable to hydroxylate vit D to its final active form, _____
1,25-dihydroxy vitamin D
36
Vitamin D3 (or ____) comes from ___
cholecalciferol, exposure to UV light from the skin
37
Vitamin D2 (or ____) comes from ____
ergocalciferol, plant sterols and it the primary dietary source of vitamin D
38
Calcitriol (Rocaltrol) is the active form of ___
vitamin D3
39
Cinacalcet (or ___) is a calcimimetic that mimics the actions of calcium on the ___ and causes a reduction in ___. Only used in ____ patients.
parathyroid gland and causes a reduction in PTH // dialysis patients
40
VitD analogs examples and notes
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
Calcifediol is prodrug of ___
calcitriol
42
Calcimimetics increase the sensitivity of calcium-sensing receptors on the parathyroid gland causing decrease in _____
PTH, Ca, and PO4
43
Calcimimetic examples and notes
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
As kidney function declines, EPO production ___
decreases
45
Eryhtropoiesis-stimulating agents (ESAs) have risks, including ___ and ___
elevated BP and thrombosis
46
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
< 10, exceeds 11
47
ESAs are only effective if adequate ___ is available
iron
48
Renal K excretion is increased by ______
hormone aldosterone, diuretics (loops > thiazides), high urine flow (via osmotic diuresis), and negatively charged ions in the distal tubule (e.g. bicarbonate)
49
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
Insulin
50
Hyperkalemia symptoms
Muscle weakness, bradycardia, fatal arrhythmias
51
Drugs that increase K levels
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
First step for treating severe hyperkalemia is to give _____ to stabilize the heart (prevent arrhythmias)
calcium gluconate (preferred) or calcium chloride Note: does not decrease potassium, just stabilized myocardial cells to prevent arrhythmias
53
Hyperkalemia treatment options: shift K intracellularly
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
Hyperkalemia treatment options: remove K
Furosemide Sodium polystyrene sulfonate Patiromer Sodium zirconium cyclosilicate Hemodialysis
55
____ (K binder) has higher risk of GI necrosis when administered with sorbitol. Do not use together.
Sodium polystyrene sulfonate (SPS, Kayexalate)
56
___ (K binder) has warning for hypomagnesemia
Patiromer (Veltassa)
57
___ is generally the preferred potassium binder d/t fastest onset of action
Sodium zirconium cyclosilicate (Lokelma)
58
Metabolic acidosis is a result of decreased ability of the kidney to reabsorb ___
bicarbonate
59
Bicarbonate replacement drug options
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
Factors affecting drug removal during dialysis
Molecular weight/size Vd Protein-binding Membrane Blood flow rate
61
Drugs with (smaller/larger) molecules are more readily removed in HD
Smaller
62
Drugs with a (large/smaller) Vd are less likely to be removed by dialysis
large
63
(high/low) protein-binding drugs are less likely to be removed by dialysis
High
64
(higher/lower) flux (pore size) and efficiency (surface area) HD filters remove more substances
High
65
(Higher/lower) HD blood flow rates increase drug removal
Higher

NAPLEX 2024 (74 decks)

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