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kidneyflashcards

1
Q

What cells in the glomerulus aid in filtration?

A

The podocytes

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2
Q

What cells in the glomerulus produce growth factors, matrix proteins, and contract?

A

Mesangial cells

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3
Q

What is azotemia?

A

Condition characterized by elevated BUN and SCr, due to decreased GFR

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4
Q

What is uremia?

A

Excess of urea and other nitrogenous waste in the blood – toxic! Many other metabolic/GI/CV/etc alterations involved in addition to renal of excretory function

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5
Q

What is proteinuria?

A

The presence of protein (albumin) in urine

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6
Q

What is hematuria?

A

The presence of blood in urine. If visible to naked eye, called gross hematuria.

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7
Q

What does edema lead to?

A

Circulatory congestion

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8
Q

True or false: CKD is classified with the RIFLE system which is based on the anatomical area of injury (prerenal/intrinsic/postrenal)

A

False – this system is used to classify acute kidney injury

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9
Q

What disease is characterized by progressive loss of kidney function due to parenchymal fibrosis (change of structure with increased fibroblasts)?

A

Chronic kidney disease

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10
Q

What three chronic conditions can be especially bad for the kidneys?

A

HTN, DM, and HLD

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11
Q

What two options do patients with ESRD have?

A

Hemodialysis or transplant

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12
Q

What must be present for dialysis to work?

A

A semipermeable membrane separating the blood and dialysate.

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13
Q

What is the semipermeable membrane in peritoneal dialysis?

A

The peritoneal membrane (peritoneum) that lines the abdominal viscera.

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14
Q

The stomach, liver, and kidneys can all be adversely affected by what class of drugs?

A

Analgesics and NSAIDS

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15
Q

What is the general term for kidney inflammation?

A

Nephritis

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16
Q

What body system has the greatest potential to harm the kidneys?

A

The immune system – immune pathogenesis, either antibody or cell mediated injury

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17
Q

In what three ways can antibodies harm the kidneys?

A
  1. Immune complex deposition as antibodies stuck in filtration membrane2. Anti-glomerular basement membrane (GBM) antibodies3. Antibody against another part of the glomerulus
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18
Q

Antibody and cell-mediated injury both lead to what end consequence?

A

Damage causes injury and detachment of epithelial cells in glomerulus, allowing protein leakage through GBM and filtration slits

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19
Q

What is the difference between NephrOTIC syndrome and NephRITIC syndrome?

A

Both lead to protein leakage, but only nephritic syndrome has RBC leakage too. Therefore, nephritic syndrome is more serious.

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20
Q

What is the general cause of primary glomerulonephritis?

A

Problems originating within the glomerulus.

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21
Q

Nephrosis is…

A

any disease of the kidney leading to degeneration of renal tubular epithelium

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22
Q

Nephritis is…

A

inflammation of the kidney.

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23
Q

Is azotemia associated with nephrotic syndrome or nephritic syndrome?

A

Nephritic syndrome

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24
Q

What is oliguria?

A

Low urine output

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25
Q

What are the two mechanisms for acute pyelonephritis?

A

Hematogenous (from blood) or ascending (due to bladder infection, vesicoureteral reflux, and internal reflux)

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26
Q

True or false: Cysts are precursors to tumors

A

False

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27
Q

What is the name of the autosomal dominant genetic cyst disease of the kidneys?

A

Adult Polycystic Kidney Disease (APKD) Eventually destroys structure of kidney and leads to intermittent gross hematuria

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28
Q

What is the name of the autosomal recessive genetic cyst disease of the kidneys?

A

Childhood Polycystic Kidney DiseaseSerious symptoms usually present at birthInfants may die from pulmonary or renal failure, if survive develop liver cirrhosis

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29
Q

Diuresis is…

A

an increase in urine volume

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30
Q

Natriuresis is…

A

an increase in renal sodium excretion

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31
Q

In addition to nephrotic syndrome and nephritic syndrome, what is the third important glomerular syndrome?

A

Chronic glomerulonephritisUsually associated with systemic chronic diseases like HTN, DM, SLE

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32
Q

Are kidney cysts always due to genetic mutations?

A

No, simple cysts seem to randomly happen and are more common

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33
Q

What cells in the nephron sense the rate of Na and Cl absorption, control GFR, and control renin release?

A

The cells in the macula densa

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34
Q

What portions of the nephron is the macula densa next to?

A

The distal convoluted tubule and the glomerulus (sense from DCT, signal to juxtaglomerular cells)

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35
Q

What cells are responsible for producing renin?

A

The juxtaglomerular cells

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36
Q

In which of the following is water more permeable? Thin limb of the loop of hence or thick limb of loop of henle

A

Water is more permeable in the thin limb.

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37
Q

What hormone controls calcium reabsorption?

A

Parathyroid hormone

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38
Q

Where in the nephron do loop diuretics act?

A

The thick ascending limb

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39
Q

Where in the nephron do osmotic diuretics act?

A

The thin descending limb

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40
Q

Where in the nephron do the thiazides act?

A

The distal convoluted tubule

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41
Q

Where in the nephron do potassium-sparing diuretics act?

A

The collecting duct

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42
Q

Where in the nephron do carbonic anhydrase inhibitors act?

A

The proximal tubule

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43
Q

What diuretic class acts on the distal convoluted tubule?

A

Thiazides

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44
Q

What diuretic class acts on the thick ascending limb?

A

Loop diuretics

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45
Q

What diuretic class acts on the proximal tubule?

A

Carbonic anhydrase inhibitors

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46
Q

What diuretic class acts on the collecting duct?

A

Potassium-sparing diuretics

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47
Q

What diuretic class acts on the thin descending limb?

A

Osmotic diuretics

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48
Q

What kind of diuretic is acetazolamide (Diamox)?

A

Carbonic anhydrase inhibitor

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49
Q

How do carbonic anhydrase inhibitors work?

A

They block carbonic anhydrase, which makes sodium and bicarbonate stay in the urine, so water stays with them.

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50
Q

Name four disadvantages of carbonic anhydrase inhibitors

A
  1. The kidney accommodates relatively quickly2. They are not as effective3. They cause loss of bicarbonate, risk of acidosis4. They destroy the proton gradient in the proximal tubule… less H+ secreted in exchange for sodium
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51
Q

In what situations would it be appropriate to use a CA inhibitor?

A

Metabolic alkalosis, altitude sickness (think respiratory alkalosis), glaucoma, and urinary alkalization to trap acidic drugs

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52
Q

What toxicities are associated with CA inhibitors (acetazolamide)?

A

Hyperchloremic metabolic acidosis, renal stones, potassium wasting, drowsiness/paresthesia

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53
Q

Under what stituations are CA inhibitors contraindicated?

A

Hepatic cirrhosis (CA inhibitor increases ammonium retention), sulfa allergies

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54
Q

What class of diuretics includes furosemide, bumetanide, torsemide, and ethacrynic acid?

A

Loop diuretics

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55
Q

What do loop diuretics block and how does this cause diuresis?

A

Loop diuretics block the NKCC transporter, which results in increased levels of Na, K, Cl, Mg, and Ca in the urine. Water follows.

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56
Q

What group on a CA inhibitor absolutely must be present for activity?

A

An unsubstituted sulfamoyl group (H2NO2S)

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57
Q

Substitution with an amine across from the sulfamoyl group has what effect on natriuretic activity? CA inhibitor activity?

A

Increases natriuretic activity but decreases CA inhibitor activity

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58
Q

Do Cl-, Br-, CF3-, and NO2- increase or decrease diuretic activity on a CA inhibitor?

A

Increase

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59
Q

The second sulfamoyl group on a CA inhibitor can be replaced with what kind of group to increase diuretic activity but decrease CA inhibitory activity?

A

An electrophilic group (aka carboxyl, etc.)

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60
Q

What is another name for loop diuretics?

A

High ceiling diuretics

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61
Q

What two chemical substituents must always be present on a loop diuretic?

A

A sulfamoyl and a carboxyl on 1 and 5 respectivelyA secondary amine must be in the 2 or 3 position

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62
Q

What is unique about ethacrynic acid?

A

It is a prodrug, becomes attached to either cysteine or glutathione in the body. Safe for those with sulfa allergies.

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63
Q

What toxicities are associated with loop diuretics?

A

Dehydration, hypokalemic metabolic alkalosis, ototoxicity, hyperuricemia (gout concern), hypomagnesemia

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64
Q

Furosemide and bumetanide should not be used in patients with…

A

sulfa allergies

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65
Q

Do loop diuretics act more rapidly or slowly?

A

Rapidly

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66
Q

List indications for loop diuretic therapy

A

Edema, acute hypercalcemia, hyperkalemia, acute renal failure, anion overdose

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67
Q

What transporter do thiazide diuretics target in the distal convoluted tubule?

A

The Na Cl symporter

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68
Q

What are chlorothiazide and and hydrochlorothiazide?

A

Thiazide diuretics

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69
Q

What is chlorthalidone (Hygroton)?

A

A thiazide-like diuretic

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70
Q

How do the thiazides affect Na, Cl, and Ca reabsorption?

A

The decrease sodium and chloride absorption, leaving them in the urine, and increase calcium reabsorption due to the presence of a Ca/Na antiporter

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71
Q

What are the clinical uses for thiazides?

A

HTN, CHF, kidney stones from idiopathic hypercalcuria, and nephrogenic diabetes insipidus

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72
Q

What toxicities are associated with the thiazides?

A

Hypokalemic metabolic alkalosis, hyperuricemia, impaired carbohydrate tolerance, hyperlipidemia, hyponatremia

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73
Q

What patients should absolutely not receive thiazides?

A

Patients with sulfa allergies

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74
Q

How do potassium-sparing diuretics function?

A

They block sodium reabsorption channels in the collecting duct

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75
Q

How do potassium-sparing diuretics spare potassium?

A

When they block sodium reabsorption, potassium is no longer excreted in exchange for sodium.

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76
Q

True or false: Potassium-sparing diuretics are highly effective at diuresis.

A

False. Often used in combination.

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77
Q

What are the clinical uses for amiloride (Midamor), a potassium-sparing diuretic?

A

CHR or hypertension in combination with a thiazide or loop diuretic.

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78
Q

What toxicities are associated with potassium sparing diuretics?

A

Hyperkalemia, hyperchloremic metabolic acidosis

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79
Q

Under what circumstances should amiloride not be given?

A

With potassium supplements or ACE inhibitors (which also retain potassium)

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80
Q

What are the clinical uses for triamtereme (Dyrenium)?

A

Edema associated with CHF, hepatic cirrhosis, nephrotic syndrome, or hyperaldosteronism

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81
Q

Under what circumstances should triamterene not be given?

A

Kidney stones, with potassium supplements, or with ace inhibitors

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82
Q

Where in the nephron do aldosterone antagonists act?

A

On nuclear receptors in the collecting duct cells

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83
Q

What is the net effect of aldosterone antagonists?

A

Decreased number of sodium channels, enhanced channel removal, inhibited transport of sodium to the blood

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84
Q

What additional action does spironolactone (Aldactone) have that eplerenone (Inspra) does not?

A

Inhibition of 5a-reductase, stopping metabolization of aldosterone to active metabolites

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85
Q

What are the clinical uses for spironolactone?

A

HTN or CHF in combination with other diuretics, mineralocorticoid excess, aldosteronism (primary or secondary resulting from CHR, cirrhosis, or nephrotic syndrome)

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86
Q

What toxicities are associated with spironolactone (Aldactone)?

A

Hyperkalemia, hyperchloremic metabolic acidosis, gynecomastia, impotence, BPH –> steroid!

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87
Q

Under what conditions should spironolactone not be used?

A

If chronic renal insufficiency or at the same time as potassium supplements, ACE inhibitors, or potassium sparing diuretics.

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88
Q

Which aldosterone antagonist is more selective–spironlactone or eplerenone?

A

Eplerenone (Inspra) – selective to receptors in kidney, heart, bv, brain

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89
Q

What are the clinical uses for eplerenone?

A

HTN. Will reach full effect in 4 weeks.

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90
Q

What toxicities are associated with eplerenone?

A

Hyperkalemia, hypertriglyceridemia

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91
Q

Under what conditions should you not use eplerenone?

A

With potassium supplementation, potassium sparing diuretics, ACE inhibitors, or CYP 3A4 inhibitors, chronic renal insufficiency, diabetes with microalbuminuria

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92
Q

How does mannitol work?

A

This sugar is excreted but cannot be reabsorbed, so it increases the osmotic pressure of the urine which draws more water into the urine to be excreted. Limits water reabsorption in the proximal tubule and descending limb

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93
Q

What effect does mannitol have on urine electrolytes?

A

Little to none. Mannitol causes diuresis without naturesis.

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94
Q

How is mannitol used clinically?

A

To increase urine volume or to reduce intracranial or intraocular pressure

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95
Q

What toxicities are associated with mannitol?

A

Extracellular volume expansion (peripheral swelling due to mannitol other tissues), dehydration, hypernatremia

96
Q

What is the name of the only ADH antagonist?

A

Demeclocycline (Declomycin)

97
Q

How does demeclocycline function?

A

It inhibits the effects of ADH at the collecting duct, stopping insertion of H20 channels and therefore reducing water reabsorption

98
Q

When should demeclocycline be used?

A

SIADH, elevated ADH

99
Q

What toxicities are associated with demeclocycline?

A

Nephrogenic diabetes insipidus, renal failure

100
Q

What is ESRD?

A

End stage renal disease–the point where the kidney function is so impaired that the patient must either get a transplant or go on dialysis

101
Q

What are the three major causes of CKD?

A

Diabetes mellitus, hypertension, and glomerulonephritis

102
Q

What equation estimates GFR and is used to stage CKD?

A

MDRD equation

103
Q

What albumin range is considered moderately increased?`

A

30-300mg/g

104
Q

What GFR stages are considered worrisome? What number is GFR under in these cases?

A

Stages 3a-5; Less than 60 mL/min/1.73m^2

105
Q

What are the breaks for staging GFR?

A

90, 60, 45, 30, 15

106
Q

What is the cockroft gault equation?

A

CrCl = (140-age)(IBW)/(SCr*72) x 0.85 if female

107
Q

What weight should you use in the cocroft gault equation if the patient is obese (>130% IBW)?

A

Adjusted body weight (=0.3(actual-ideal)+ideal)

108
Q

What five general complications can result from CKD?

A

Buildup of waste products in blood, fluid overload, metabolic acidosis, anemia, and mineral and bone disorder

109
Q

Name four symptoms that can result from uremia

A

Uremic fetor, uremic frost, metallic taste, encephalopathy

110
Q

Which cells hypertrophy in diuretic resistance?

A

DCT cells. Counteract by adding thiazides.

111
Q

What class of diuretics should be avoided in CKD patients?

A

Potassium sparing diuretics

112
Q

Which class of diuretics works better when CrCl <30mL/min – thiazides or loops?

A

Loops

113
Q

In CKD patients, does fluid restriction usually treat fluid overload sufficiently?

A

Trick question – fluid restriction not generally necessary if sodium intake controlled although free water intake should be avoided.

114
Q

In addition to sodium restriction, what other treatment can be used for fluid overloaded CKD patients?

A

Diuretics

115
Q

Which diuretics are permissible for a patient with sulfa allergies?

A

Ethacrinic acid, potassium sparing diuretics, aldosterone antagonists, ADH antagonists, mannitol

116
Q

What electrolyte dietary intake should be strictly restricted?

A

Potassium – limit to 3 gm/day

117
Q

What electrolyte imbalance are ESRD patients remarkably tolerant to?

A

Hyperkalemia – aim for 4.5 - 5.5 pre-dialysis

118
Q

What are the three major problems in mineral and bone disorder?

A

Hyperphosphatemia, hypocalcemia, and decreased vitamin D

119
Q

What do the three major problems in mineral and bone disorder (CKD-MBD) lead to?

A

Increased serum intact PTH (iPTH)

120
Q

True or false: Secondary hyperparathyroidism is largely asymptomatic until late stages, when it is not easy to treat

A

True

121
Q

What is the mechanism of action for phosphate binders?

A

They bind dietary phosphate ingested with food (so must be taken with food) and allow them to be eliminated in the feces

122
Q

What phosphate binder is cheaper – calcium carbonate or calcium acetate?

A

Calcium carbonate (Tums)

123
Q

What is the biggest disadvantage of calcium containing phosphate binders?

A

Possible absorption of calcium, which could cause more soft tissue calcification

124
Q

Which calcium containing phosphate binder is better if cost is not an issue?

A

Calcium acetate – binds twice as much phosphate, fewer hypercalcemic events

125
Q

Of the non-calcium phosphate binders, which is the best as far as low ADEs and other beneficial effects?

A

Sevelamer carbonate (Renvela)

126
Q

Which non-calcium containing phosphate binder has significant interactions with levothyroxine and other CKD drugs like paricalcitol and cinacalcet?

A

Sucroferric oxyhydroxide (Velphoro)

127
Q

Which phosphate binders are strongly affected by pH?

A

Calcium containing binders are almost 0% effective at low pH (such as the stomach)

128
Q

What two other positive effects does sevelamer carbonate have on the body?

A

It decreases LDL by 15-30% and decreases uric acid in the blood.

129
Q

What side effect of iron containing phosphate binders should patients be aware of?

A

They may darken or discolor stool.

130
Q

What non calcium containing phosphate binder has been almost entirely discontinued?

A

Amphojel (aluminum hydroxide) due to aluminum toxicity leading to anemia. Only for short term b/c cannot excrete aluminum.

131
Q

Which iron containing binder actually increases TSAT and ferritin?

A

Auryxia (ferric citrate).

132
Q

What foods are high in phosphorus?

A

Meat, dairy, beans, nuts, beer, pop

133
Q

What should daily dietary phosphorus be limited to?

A

800-1000mg

134
Q

Under what circumstances should phosphorus intake be limited?

A

If PTH > target range for stage 3, 4, or 5. ORPhos >4.6mg/dL for stage 3 and 4Phos >5.5mg/dL for stage 5

135
Q

What is the active form of vitamin D?

A

Calcitriol

136
Q

Where are the inactive forms of vitamin D converted?

A

Cholecalciferol (D3) and Ergocalciferol (D2) in the liver, 1,25-dihydroxyvitamin D in the kidney to active form

137
Q

What are the two inactive forms of Vitamin D that we administer to patients?

A

Ergocalciferol (Calciferol) and Cholecalciferol

138
Q

Which CKD patients should receive inactive vitamin D supplements?

A

Stage 3 and stage 4 or if iPTH is elevated but inactive vitamin D is normal or low.

139
Q

Which CKD patients should receive active vitamin D supplements?

A

Stage 5 or if both inactive vitamin D and iPTH are elevated (not being converted)

140
Q

What is the goal of vitamin D therapy in CKD patients?

A

To decrease the amount of iPTH by increasing the amount of vitamin D that the parathyroid gland senses.

141
Q

What is the undesired effect of active vitamin D products?

A

Elevation of blood calcium

142
Q

What is special about doxercalciferol (Hectorol)?

A

It is a pro-hormone that becomes activated in the liver at a more natural rate, maintaining more even serum concentrations.

143
Q

Which two activated vitamin D supplements lead to a >30% reduction in iPTH and have a lower calcemic activity?

A

Paricalcitol (Zemplar) and doxercalciferol (Hectorol)

144
Q

For what reasons would you choose paricalcitol over doxercalciferol?

A

Paricalcitol is approved for pediatric patients and has the most favorable ADE profile

145
Q

What activated vitamin D compound has higher incidence of hyperphosphatemia even though it more closely resembles body vitamin D kinetics?

A

Doxercalciferol

146
Q

For what reasons would you use calcitrol over doxercalciferol?

A

Calcitriol is cheaper and approved for pediatrics

147
Q

What activated vitamin D compound carries the greatest risk of hypercalcemia?

A

Calcitriol

148
Q

What is the name of the only calcimimetic drug?

A

Cinacalcet (Sensipar)

149
Q

How does cinacalcet work?

A

It mimics the action of calcium by binding the receptor and inducing conformational change, sending a signal to decrease iPTH secretion

150
Q

What notable drug does cinacalcet interact with?

A

Velphoro (sucroferric oxyhydroxide)

151
Q

What is the disadvantage inherent in cinacalcet’s mechanism of action?

A

When all calcium receptors are bound with cinacalcet, the body cannot sense or respond to a dangerous drop in blood calcium.

152
Q

What is the advantage of giving inactive vitamin D over active vitamin D?

A

The kidney will convert inactive vitamin D as needed, rather than dumping the activated form into the system.

153
Q

What four causes contribute to anemia in CKD patients?

A

Decreased erythropoietin, decreased RBC life from uremia, and vitamin/blood loss during dialysis

154
Q

What type of anemia do CKD patients tend to have?

A

Iron deficiency (microcytic) anemia

155
Q

What is a normal MCV?

A

80-96 um^3

156
Q

What is a normal RDW (red cell distribution width)?

A

11.5 - 14.5%

157
Q

What is the best assessment parameter for anemia?

A

Hemoglobin (Hb)

158
Q

At what lab value for hemoglobin should we do further workup or diagnose anemia?

A

Males – <12g/dL

159
Q

How often should hemoglobin be monitored for anemia?

A

Annually in CKD 3, biannually in CKD 4-5ND, and q3mos in CKD 5DIf PMH anemia, monitor CKD 3-5ND q3mos and CKD 5D q month

160
Q

What two general types of treatment are available for CKD patients with anemia?

A

Iron therapy and erythropoiesis stimulating agents

161
Q

When should you supplement with iron?

A

If TSAT <500ng/mLMonitor these every 3 months

162
Q

For which patients is oral iron appropriate for?

A

CKD stage 3-4 or peritoneal dialysis patients. NOT enough for hemodialysis patients

163
Q

What is the recommended daily dose of elemental iron?

A

At least 200mg

164
Q

What side effects are associated with oral iron?

A

Stomach upset

165
Q

What counseling tips should you tell patients on oral iron supplements?

A

Take with orange juice, separate from food, separate from Ca++ by 2hours, avoid meds that increase stomach pH

166
Q

What is different about heme iron vs elemental iron?

A

Heme iron is absorbed better and from a different site, so not subject to the 200mg daily iron rule.

167
Q

What is heme iron available as?

A

Proferrin ES, proferrin Forte

168
Q

IV iron supplementation is recommended for what patients?

A

CKD stage 5D

169
Q

Which IV iron supplement interferes with MRI for up to 3 months?

A

Feraheme (ferumoxytol)

170
Q

Which iron dextran brand should be avoided due to higher risk for anaphylaxis due to higher Mw iron?

A

Dexferrum

171
Q

Which IV iron supplement requires a test dose before it is administered with hemodialysis?

A

Iron dextran (InFed/Dexferrum)

172
Q

Which IV iron supplement is approved for non-CKD patients?

A

Iron sucrose (Venofer)

173
Q

What side effects may be caused by IV iron products?

A

Flushing, dizziness, and hypotension

174
Q

How often should ferritin and TSAT be monitored in IV iron + hemodialysis patients?

A

Every 1-3 months

175
Q

What can oxidative stress due to free iron in the blood lead to?

A

Atherosclerosis, proteinuria, renal tubular damage

176
Q

When is it appropriate to use an erythropoiesis stimulating agent?

A

After all other correctable causes of anemia have been addressed due to high price. CKD 3-5ND – if Hb <10g/dL, falling at rapid rate, needed to avoid transfusionCKD 5D – when Hb between 9 and 10 g/dL

177
Q

Why should ESAs not be used to increase Hb above 11.5 g/dL?

A

Although this would improve QOL, it also increases incidence of CVAs (strokes).

178
Q

What general hemoglobin range should be your goal with ESAs?

A

10 - 11 g/dL

179
Q

How do erythropoiesis stimulating agents (ESAs) work?

A

They stimulate erythroid progenitor cells.

180
Q

What are the two ESA drugs?

A

Recombinant human erythropoietin (Epogen, Procrit, EPO) and darbepoetin alfa (Aranesp)

181
Q

Which ESA has a longer half life and may be given less frequently?

A

Darbepoetin alfa (Aranesp)

182
Q

Which ESA is cheaper if given subcutaneously?

A

Epogen – because SC dose is 2/3 IV dose if target reached

183
Q

Which ESA is dosed in units? Which is dosed in mcg?

A

Units: EpogenMcg: Aranesp

184
Q

What adverse effects are associated with ESAs?

A

Pure red cell aplasia (PRCA) where antibodies develop to erythropoietin, HTN (23% patients) leading to increased cardiac arrest, seizure, stroke, exacerbations of HF, HTN, and MI

185
Q

How often should you monitor Hb during initiation of ESA therapy?

A

Weekly

186
Q

How often can you adjust the ESA dose?

A

No more than every 4 weeks

187
Q

What is the goal rate of increase in Hb?

A

1-2 g/dL increase per month

188
Q

By what percentage should you increase/decrease the dose if Hb has not increased at a fast enough rate/if Hb approaches 11?

A

25%

189
Q

What acid/base disorder are ESRD patients susceptible to? Why?

A

Metabolic acidosis because they cannot excrete H+ ions.

190
Q

When is metabolic acidosis secondary to ESRD treated?

A

When bicarb <20mEq/L

191
Q

How is metabolic acidosis secondary to ESRD treated?

A

Increased bicarbonate in dialysate, shohl’s solution OR sodium bicarbonate tablets

192
Q

What amount of protein should a CKD patient receive? How about an ESRD patient?

A

CKD (stage 3-5ND): 0.8 g/kg/day if GFR <30ml/minESRD: 1.2 g/kg/day due to protein loss through dialysis

193
Q

What types of vitamins need to be replaced in patients on dialysis?

A

Water soluble vitamins – B and C (Nephrocaps, Nephron FA)

194
Q

If a CKD patient is 60 yo?

A

60 yo: 30 - 35 kcal/kg/day

195
Q

True or false: CrCl is an accurate measure of acute kidney injury.

A

False because it may be changing rapidly and other waste products build up faster.

196
Q

List two examples of community acquired AKI

A

Prerenal azotemia (hypoperfusion) and postrenal obstruction (kidney stone)

197
Q

List three examples of hospital acquired AKI

A

Multiple organ failure, sepsis, bleeding, liver disease, mechanical ventilator

198
Q

What is functional acute renal failure?

A

A decrease in glomerular hydrostatic pressure which leads to decreased GFR (often caused by NSAIDs, ACE inhibitors)

199
Q

What is are helpful measures of acute renal function?

A

Urine output and FEna

200
Q

What UOP characterizes acute anuria?

A

<50mL / 24 hours

201
Q

What UOP characterizes oliguria?

A

<400 ml / 24 hours

202
Q

What UOP characterizes non-oliguria?

A

> 400 mL / 24 hours

203
Q

A FENa of <1% indicates what potential cause?

A

Prerenal or functional renal failure

204
Q

A FENa of >1% indicates what potential cause?

A

Renal injury

205
Q

What is the goal of acute renal injury treatment?

A

Remove cause then supportive therapy

206
Q

What are the most common nephrotoxic drug classes?

A

NSAIDs (and acetaminophen), ACE inhibitors, contrast media, and proton pump inhibitors

207
Q

What does the AEIOU abbreviation stand for when determining indications for renal replacement therapy?

A

Acid/base balance, Electrolytes, Intoxication, Overload, Uremia

208
Q

When should you initiate dialysis?

A

When BUN >100 and/or SCr >10. Look at S/Sx too.

209
Q

What kinds of molecules are you trying to pull out of the blood in dialysis?

A

BUN, creatinine, middle molecules like beta2microglobulin, uric acid

210
Q

Which dialysis vascular access has the longest survival rate?

A

AV fistula

211
Q

Which dialysis vascular access takes the shorter time to mature?

A

AV graft

212
Q

Which dialysis vascular access is associated with more complications?

A

AV graft

213
Q

Which dialysis vascular access might not be good for patients with poor circulation to extremities?

A

AV fistula

214
Q

What four types of substances are not removed from the blood during dialysis?

A
  1. High Vd (volume of distribution) – mostly in tissues2. High lipophilicity3. Large molecular weight4. Highly protein bound
215
Q

What two measures are used to analyze the effectiveness of a dialysis session?

A

Kt/V and URR

216
Q

What is Kt/V? What is your Kt/V goal?

A

Measure of the fraction of total body water that is cleared of urea. K is clearance, t is time, V is Vd. Goal = 1.4

217
Q

What is urea reduction ratio? What is a goal URR?

A

Measure of reduction of patient’s BUN. Goal is >70% reduction.

218
Q

What complications can arise during hemodialysis?

A

Hypotension, pruritus, muscle cramps

219
Q

What types of patients usually receive peritoneal dialysis?

A

Patients with bigger abdomens, residual kidney function, pediatric patients

220
Q

True or false: Peritoneal dialysis requires at least three sessions a week.

A

False – peritoneal dialysis is continuous

221
Q

What is the time between loading fluid into peritoneum and draining it out called?

A

Dwell time

222
Q

What is the reasoning for dwell times of different duration?

A

Different molecules take different times to equilibrate

223
Q

Describe the schedule of CAPD (continuous ambulatory peritoneal dialysis).

A

Patient switches waste out and puts new dialysate in three times during the day and dwells overnight.

224
Q

Describe the schedule of CCPD (continuous cyclic peritoneal dialysis).

A

Patient dwells during the day and a cycler drains and refills throughout the night.

225
Q

Describe the schedule of NIPD (nocturnal intermittent peritoneal dialysis).

A

Patient is “empty” throughout the day and cycler runs throughout the night. Unfortunately, no long dwell.

226
Q

Describe the schedule of NTPD (nocturnal tidal peritoneal dialysis).

A

Patient is “empty” throughout the day and cycler runs throughout the night, but does not fully drain the fluid, leaving a reserve volume in the entire time.

227
Q

What signs and symptoms can indicate peritonitis?

A

Cloudy effluent, abdominal pain, fever, N/V, chills, tenderness

228
Q

What should you use to treat peritonitis?

A

Empiric therapy (covers gram + and -) before organism identified, then modify once cultures obtained.

229
Q

What is unique about treatment of peritonitis?

A

Antibiotics can be administered intraperitoneally, directly to the infection site. Especially good when PO not an option or poor vascular access.

230
Q

What is the primary use for continuous renal replacement therapies?

A

Acute renal failure, especially if pt critically ill or hemodynamically unstable.

231
Q

What drug should be used in conjunction with CAVH (continuous arteriovenous hemofiltration)? Why?

A

Heparin. Because the heart is pumping the blood through at a slow rate that can lead to clotting.

232
Q

What force is removing waste in CVVH (continuous venovenous hemofiltration)? How?

A

Convection – addition of ultrafiltrate fluid before dialyzer increases blood volume, which must be forced out through dialysis.

233
Q

Do continuous renal replacement therapies work at slower or faster rates than hemodialysis?

A

Slower – they can work on the blood 24/7 but hemodialysis must happen over 4 hours per session.

234
Q

What force is removing waste from the blood in CVVHD (continuous venovenous hemodialysis)? How?

A

Diffusion. In this method, dialysate is being run opposite the blood so substances can diffuse from the blood to dialysate just like regular hemodialysis except longer period of time/slower rate.

235
Q

What force is removing waste from the blood in CVVHDF (continuous venovenous hemodiafiltration)? How?

A

Convection AND diffusion. This is done by running the blood opposite dialysate just like hemodialysis, but there is also ultrafiltrate added to the blood before it reaches the dialyzer so that excess volume is also spilling over into the dialysate and waste.

GI MEds for pup (2 decks)

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