Treatments Quiz 2

Question 1

Plasma Creatinine

Answer 1

Simple but innacurate esp. w/ mild renal impairment.

Reduced w/ low muscle mass

Raised w/ high protein meal.

Question 2

Cystatin C

Answer 2

Low mol. wt protein produced by all nucleated cells

Not affected by diet, gender, age, muscle mass

Affected by steroids

Great test –> Mayo uses this

Question 3

Creatinine Clearance

Answer 3

Urine collections unreliable

Overstimates GFR (tubular secretion of creatine)

Question 4

Cockroft Gault Formula

Answer 4

Used to estimate creatinine clearance

140-age x wt / 72 x S cr

More accurate than plasma creatinine especially w/ mild renal impairment.

Overestimates in obesity and low protein diet.

Question 5

Modification of Diet in Renal Disease (MDRD)

Answer 5

186 x (serum creatinine) ^-1.154 x (age)^-.203 x .742 (f) x 1.210 (AA)

More accurate than Cockroft Gault (not according to Muster)

Question 6

CKD-EPI Equation

Answer 6

Most accurate

Variables for age, sex, race, and serum creatinine levels

Question 7

Plasma clearance

Answer 7

Best approximation of true GFR

Invasive, may use radioisotopes.

Question 8

Management of CKD

Answer 8

1. ) Treat reversible causes of renal dysfunction (pre-renal - dehydration, hypotension; Renal - nephrotoxic drugs; Post-renal - stone, BPH)
2. ) Preventing or slowing the progression of renal disease (ACEi or ARBs, HTN, Protein restriction), hyperlipidemia, glycemic control, weight control, and smoking)
3. ) Treatment of complications of renal dysfunction (volume overload, hyperkalemia, metabolic acidosis, hyperphosphatemia, hyperparathyroidism - consequence of PO4 increase, anemia)
4. ) Preparation and initiation of renal replacement therapy

Question 9

ACEi and ARB

Answer 9

Indicated in diabetic and non-diabetic renal diseases

Up to 25% increase in creatinine can occur within 4 weeks –> not a reason to change unless large jump.

Must recheck levels –> most common cause of large jump = dehydration from diuretics.

Higher increases in heart failure, volume depleted state, and bilateral stenosis (contraindication)

Monitor creatinine and potassium

Start w/ small dose and gradually increase the dose

Question 10

Phosphate Binders

Answer 10

Used to treat hyperphosphatemia in CKD

First line is limiting phosphorous restriction (big one is dairy)

First line binders: Calcium Carbonate (TUMS); Calcium Acetate (Acetate) –> cheap and effective, but only works at low levels–> hypercalcemia

Second line binders: Lanthanum carbonate, Sevalamer, and Sucroferric Oxyhydroxide –> expensive, effective, no calcium toxicity issus

Question 11

Calcitrol

Answer 11

Vitamin D analog used to treat secondary hyperparathyrodism.

Decrease PTH, but increase PO4- –> must treat high PO4- first w/ binders.

Question 12

Doxecalciferol

Answer 12

Vitamin D analog used to treat secondary hyperparathyrodism.

Decrease PTH, but increase PO4- –> must treat high PO4- first w/ binders.

Question 13

Paricalcitol

Answer 13

Vitamin D analog used to treat secondary hyperparathyrodism.

Decrease PTH, but increase PO4- –> must treat high PO4- first w/ binders.

Question 14

Cinacalcet

Answer 14

Calcimimetic - secondary treatment for hyperparathyroidism.

Used when PO4- is high

Very expensive

Question 15

Erythropoetin (Procrit)

Answer 15

Short acting EPO used when Hg is below 10 in CKD

Question 16

Darbepoetin

Answer 16

Long acting EPO used when Hg is below 10 in CKD

Question 17

Acetazolamide

Answer 17

MOA: Carbonic Anhydrase inhibitor that acts in the proximal tubule. Not used for diuretics clinically for diuresis –> too many side effects.

Uses: glaucoma, urinary alkilinization, metabolic alkalosis, acute altitude sickness

Side effects: hyperchloremic metabolic acidosis, renal stones, renal potassium wasting

Question 18

Furosemide

Answer 18

Lasix

Class: Loop diuretic

MOA: Inhibits NKCC in thick ascending limb (normally 25% of sodium reabsorption). Normally tubular fluid becomes hypo-osmolar here (no aquaporins), but loop diuretics block this resulting in increased retention of ions and water later in nephron.

Increase NaCl and K excretion.

Major uses: pulmonary edema, edema, hyperkalemia, acute renal failure, anion overdose (bromide, fluoride, iodide)

Active for 6 hours (laSIX)

Question 19

Bumetanide

Answer 19

Class: Loop diuretic

MOA: Inhibits NKCC in thick ascending limb (normally 25% of sodium reabsorption). Normally tubular fluid becomes hypo-osmolar here (no aquaporins), but loop diuretics block this resulting in increased retention of ions and water later in nephron.

Increase NaCl and K excretion.

Major uses: pulmonary edema, edema, hyperkalemia, acute renal failure, anion overdose (bromide, fluoride, iodide)

Question 20

Clorthalidone

Answer 20

Class: Thiazide diuretics

MOA: Block NaCl transporter in DCT (normally accounts for 8% of NaCl reabsorption. Block results in increased excretion of Na, Cl, and K (Na/K exchange in collecting tubule)

*thiazides are sulfonylureas –> bind to SUR( sulfonyl urea receptor) on potassium channel controlling inuslin release –> suppress insulin release.

Uses: HTN (decreased rate of stroke, DM, CHF, and CAD complications), HF, nephrolithiasis caused by hypercalcemia, nephrogenic diabetes insipidus.

Side effects: Hyperglycemia, hyperuricemia (gout), hypokalemia, hyperlipidemia, hyponatremia

Question 21

Hydrochlorothiazide

Answer 21

Class: Thiazide diuretics

MOA: Block NaCl transporter in DCT (normally accounts for 8% of NaCl reabsorption. Block results in increased excretion of Na, Cl, and K (Na/K exchange in collecting tubule)

*thiazides are sulfonylureas –> bind to SUR( sulfonyl urea receptor) on potassium channel controlling inuslin release –> suppress insulin release.

Shown to vasodilate as well due to action on K+ channels –> dual mechanism.

Best evidence of drugs from this class.

Uses: HTN (decreased rate of stroke, DM, CHF, and CAD complications), HF, nephrolithiasis caused by hypercalcemia, nephrogenic diabetes insipidus.

Side effects: Hyperglycemia, hyperuricemia (gout), hypokalemia, hyperlipidemia, hyponatremia

Question 22

Metalozone

Answer 22

Class: Thiazide diuretics

MOA: Block NaCl transporter in DCT (normally accounts for 8% of NaCl reabsorption. Block results in increased excretion of Na, Cl, and K (Na/K exchange in collecting tubule)

*thiazides are sulfonylureas –> bind to SUR( sulfonyl urea receptor) on potassium channel controlling inuslin release –> suppress insulin release.

Uses: HTN (decreased rate of stroke, DM, CHF, and CAD complications), HF, nephrolithiasis caused by hypercalcemia, nephrogenic diabetes insipidus.

Side effects: Hyperglycemia, hyperuricemia (gout), hypokalemia, hyperlipidemia, hyponatremia

Question 23

Spironolactone

Answer 23

Class: Potassium Sparing Diuretic/ Aldosterone Antagonit

MOA: Inhibit aldosterone receptor –> blocks exhcange of intraluminal Na for extraluminal K, less potassium secreted.

Major use: hyperaldosteronism, CHF

Side effects: hyperkalemia, gynecomastia, hypercholemic metabolic acidosis, acute renal failure, kidney stones

Question 24

Eplerone

Answer 24

Class: Potassium Sparing Diuretic/ Aldosterone Antagonit

MOA: Inhibit aldosterone receptor –> blocks exhcange of intraluminal Na for extraluminal K, less potassium secreted.

Prevents fribrotic changes in kidneys and heart caused by aldosterone.

Major use: hyperaldosteronism, CHF

Side effects: hyperkalemia, hypercholemic metabolic acidosis, acute renal failure, kidney stones

Question 25

Desmopressin

Answer 25

ADH analog

Used to treat diabetes insibidus and bedwetting.

Question 26

Demecocycline

Answer 26

Antibitic w/ some activity as an ADH antagoinst

Question 27

Mannitol

Answer 27

Osmotic diuretic

MOA: Not absorbed in the nephron; therefore, it exerts and osmotic effect to retain water.

Uses: Reduce body water or to reduce ICP or intraocular pressure.

Toxicities: extracellular volume expansion, dehydration, hyperkalemia, hypernatremia, hyponatremia when renal function is impaired.

Question 28

Canigliflozin

Answer 28

SGLT-2 Inhibitors

Reduce reabsorption of glucose –> loss of glucose in urine.

Helps reduce blood sugar in DM; causes weight loss (loss of energy)

Many side effects: ketoacidosis, UTI, yeast infections, hypoglycemia.

Question 29

Dapagliflozin

Answer 29

SGLT-2 Inhibitors

Reduce reabsorption of glucose –> loss of glucose in urine.

Helps reduce blood sugar in DM; causes weight loss (loss of energy)

Many side effects: ketoacidosis, UTI, yeast infections, hypoglycemia.

Question 30

Gliflozin

Answer 30

SGLT-2 Inhibitors

Reduce reabsorption of glucose –> loss of glucose in urine.

Helps reduce blood sugar in DM; causes weight loss (loss of energy)

Many side effects: ketoacidosis, UTI, yeast infections, hypoglycemia.

Question 31

Probenicid

Answer 31

Inhibit renal organic acid transporters of urate to facilitate excretion (normally 90% or urate is reabsorbed in proximal tubule).

Prevents reabsorbtion or Uric Acid (Gout treatment)

Also used to prolong the action of penicillins.

Question 32

Amilioride

Answer 32

Class: Potassium Sparing Diuretic

MOA: Block Enac in DCT –> decreased Na exchange for K.

Mild diuretec –> primarily prevent excessive K wasting.

Question 33

Triamterene

Answer 33

Class: Potassium Sparing Diuretic

MOA: Block Enac in DCT –> decreased Na exchange for K.

Mild diuretec –> primarily prevent excessive K wasting.

Question 34

Ammonium Chloride

Answer 34

Used to acidify urine

Question 35

Sulfinpyrazone

Answer 35

Inhibit renal organic acid transporters of urate to facilitate excretion (normally 90% or urate is reabsorbed in proximal tubule).

Prevents reabsorbtion or Uric Acid (Gout treatment)

Also used to prolong the action of penicillins.