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Renal Nutrition Mastery > Peritoneal Dialysis > Flashcards

Peritoneal Dialysis Flashcards

1
Q

How many % of cardiac output
circulates through the kidneys?
©Preventative

A

20%; filters 1600 L of blood per day

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2
Q

What is the glomerulus and what
does it do?

A

Kidney’s filtering unit; a network of capillaries
surrounded by a narrow wall of epithelial cells; forms
~125 ml/min of filtrate or 180 L of ultrafiltrate

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3
Q

How do solutes and fluid move across the
peritoneal membrane?

A

How do solutes and fluid move across the
peritoneal membrane?
1. Diffusion:
a. From blood into dialysate: uremic solutes and potassium
b. From dialysate into blood: glucose, lactate, bicarbonate, calcium
2. Ultrafiltration: removal of plasma water into dialysate
3. Fluid absorption: occurs through the lymphatics

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4
Q

What affects ultrafiltration rate in PD?

A

What affects ultrafiltration rate in PD?
- Concentration gradient for the osmotic agent (glucose, icodextrin, amino acids)
- Peritoneal membrane surface area & characteristics
- The ability for the osmotic agent to maintain gradient, hydrostatic & oncotic
pressure gradient, and sieving
- Sieving: when a solute is carried along with water across the membrane by
convection

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5
Q

Describe the composition of PD fluid/dialysate

A

Describe the composition of PD fluid/dialysate
- Bicarbonate / bicarbonate-lactate mixture, normal pH
- Osmotic agents → glucose monohydrate (1.5%, 2.5%, 4.25%), anhydrous glucose
(1.36%, 2.27%, 3.86%), amino acids (1-2%) and icodextrin (7.5%)
- Potassium-free
- Sodium 132-134 mEq/L → ↓ concentration to ↑ sodium removal, but may risk
hyponatremia
- Calcium 2-2.5 mEq/L or 3 mEq/L → personalized for bone mineral management
- Magnesium 0.6-1.2 mg/dL → may lead to magnesium depletion

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6
Q

What are the different peritoneal membrane
classifications based on the PET?

A

What are the different peritoneal membrane
classifications based on the PET?
- High transporters → achieve rapid & complete equilibrium d/t large effective surface area
& membrane permeability; lower ultrafiltration d/t glucose diffusion into blood and rapid
loss of osmotic gradient, higher protein losses
- Low transporters → have slower and less complete equilibration with lower membrane
permeability or small effective surface area, better ultrafiltration, lower protein losses
- High-/low-average transporters → intermediate clearances, ultrafiltration, protein losses

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7
Q

Which PD regimen may be recommended based
on pt’s peritoneal membrane classification?

A

Which PD regimen may be recommended based
on pt’s peritoneal membrane classification?
- High transporters → short duration dwells using APD, may benefit from nonglucose PD solution (d/t glucose diffusion into blood reducing osmotic
gradient)
- Low transporters → long-duration, high-volume dwells to maximize diffusion

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8
Q

How do you maximize clearance of solutes in PD?

A

How do you maximize clearance of solutes in PD?
- Clearance is highest at the start of a PD dwell when both blood urea
concentration and PD fluid glucose osmotic gradients are high
- Maximize total daily time on PD (no dry periods)
- Maximize the concentration gradient with more frequent exchanges
- Maximize effective peritoneal surface area with larger dwell volume (stretching
the membrane)
- Maximize ultrafiltration with higher glucose or osmotic agents

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9
Q

How often should you measure PD adequacy?

A

How often should you measure PD adequacy?
It is recommended that peritoneal dialysis Kt/V (effluent and urine) be
measured within 1 month of treatment initiation and at least one additional
time between month 2 and 6, and then once every 4 months thereafter.
Quarterly measurements may be more easily scheduled and tracked.

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10
Q

What are the adequacy targets for CAPD & APD?

A

Weekly Kt/V ≥ 1.7
- If the pt has >100 mL/d of residual urine volume and it is included as part of the total
weekly urea clearance goal, a 24-hr urine collection (urine V and urine urea) should
be obtained on a regular basis, usually quarterly.

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11
Q

How do you improve Kt/V in CAPD?

A

Increase exchange volume - but may increase fullness, cause back pain, abdominal
distention, potential leaks or hernia
- Increase exchange frequency - may decrease dwell time, interfere with lifestyle, add cost
- Increase tonicity of dialysate to increase clearance & ultrafiltration - but may lead to
obesity/hyperlipidemia from additional dextrose, compromise membrane integrity &
affect peritoneal transfer rates
- May use alternative osmotic agents (ie. colloid based icodextrin)

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12
Q

How do you improve Kt/V in APD?

A

Add daytime dwell in NIPD (>1 dwell or use alternate solutions to prevent fluid resorption)
- Increase dwell volumes on the cycler
- Increase time on cycler
- Increase cycle frequency to maximize concentration gradient - cycling waste dialysis time
- Increase tonicity of dialysate - may lead to obesity/hyperlipidemia from additional
dextrose, compromise membrane integrity & affect peritoneal transfer rates
- May use alternative osmotic agents (ie. colloid based icodextrin)

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13
Q

What are some indicators for increasing the
dialysis dose?

A

If pt is not thriving
- Neuropathy
- Pericarditis
- Decline in nutrition status /intake
- N & V
- Sleep disturbance
- Restless leg syndrome
- Pruritus
- Volume overload
- Metabolic acidosis unresponsive to oral bicarbonate tx
- Chronic hyperkalemia/hyperphosphatemia
- Unresolved anemia

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14
Q

How much protein is lost in PD & what affects
how much protein is lost?

A

5-15 g protein lost in a day, 50-80% of which is albumin
- 2-4 g amino acids lost per day (KDOQI for PD Adequacy 2006)
- Protein loss affected by size and molecular wt of protein, composition of dialysate,
permeability of peritoneal membrane, frequency and duration of dialysis, body
surface area, pt characteristics (clinical status / serum protein levels)
- Higher protein losses in pts with DM, acute peritonitis, and nighttime APD

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15
Q

What is the recommended protein intake for PD?

A

KDOQI 2020 3.0.3 - In adults with CKD 5D on MHD (1C) or PD (OPINION) who are
metabolically stable, we recommend prescribing a dietary protein intake of 1.0-1.2 g/kg body weight per day to maintain a stable nutritional status.
- Same protein range for pts with diabetes, but higher levels of dietary protein intake may need to be considered to maintain glycemic control (KDOQI 2020 - 3.0.4)
- 1.2 g/kg/d or more associated with neutral or positive nitrogen balance

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16
Q

What is the ideal nPNA for PD?

A

1.2 - 1.3 g/kg

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17
Q

What is the kcal recommendations for PD?

A

KDOQI 2020 Guideline 3.1.1 - In adults with CKD 1-5D (1C) or posttransplantation
(OPINION) who are metabolically stable, we recommend prescribing an energy intake of 25-35 kcal/kg body weight per day based on age, sex, level of physical activity, body composition, weight status goals, CKD stage, and concurrent illness or presence of inflammation to maintain normal nutritional status.
- Total kcal should include kcal absorbed from dialysate

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18
Q

How do you estimate kcal from monohydrate
glucose absorbed from dialysates?

A

Glucose monohydrate (on U.S. labels) come in 1.5%, 2.5%, 4.25% dextrose solutions
1. Calculate total grams infused: X% (g/dL) * 10 (dL/L) * total infusion volume (L)
2. Calculate total kcal: total grams infused (g) * 3.4 (kcal/g)
3. Calculate estimated kcal absorbed: total kcal * % absorption
- APD 40-50% estimated absorption
- CAPD 60-70% estimated absorption

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19
Q

What impacts how much kcal is absorbed from PD
dialysate?

A

Dextrose concentration (or use osmotic agents like icodextrin/amino
acids minimize kcal load)
● Membrane characteristics
● Volume
● Frequency of exchanges: fewer kcal absorbed with more frequent
exchanges
● Modality: APD 40-50% glucose absorption, CAPD 60-70% glucose absorption

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20
Q

What are some disadvantages to using glucose as
an osmotic agent?

A

Absorption of calories
- Potential for anorexia
- Rapid loss of ultrafiltration capabilities
- Metabolic abnormalities: hyperglycemia, hyperinsulinemia, hyperlipidemia, obesity

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21
Q

What are the main determinants of sodium
removal in PD?

A
  1. Ultrafiltration: alternative osmotic agents (icodextrin) offers more
    ultrafiltration and improves volume control
  2. PD modality: sodium clearance higher in CAPD than in APD
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22
Q

What is the fluid recommendation for PD?

A
  • KDOQI 2020 Guideline 6.5.3 In adults with CKD 3-5D, we suggest reduced
    dietary sodium intake as an adjunctive lifestyle modification strategy to
    achieve better volume control and a more desirable body weight (2B).
  • Pts can vary dextrose concentration in dialysate based on wt & volume
    status, but long-term use of hypertonic solutions can be detrimental to
    peritoneal membrane
  • 1-3 L/d depending on PD ultrafiltration & residual UOP
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23
Q

How is potassium managed in PD?

A
  • Potassium cleared by PD at similar rate to urea
  • 1400-1800 mg/day with 10 L of ultrafiltrate
  • Most pts tolerate intake of 3-4 g/d
  • Classic balance studies show fecal excretion of K increased in CAPD
    pts → hyperkalemia uncommon
  • If hypokalemia: increased dietary intake or supplementation
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24
Q

What are some causes of hypokalemia in PD?

A
  • Abnormal cellular redistribution after inadequate intake
  • Excessive restriction
  • Disproportionate dialysis clearance
  • GI losses (diarrhea, vomiting, gastric suction)
  • Diuretics
  • Diabetic acidosis → draws K into intracellular fluid
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25
Q

What is the calcium recommendation for PD?

A

KDOQI 2020 6.2.2 In adults with CKD 5D, it is reasonable to adjust
calcium intake (dietary calcium, calcium supplements, or
calcium-based binders) with consideration of concurrent use of
vitamin D analogs and calcimimetics in order to avoid hypercalcemia
or calcium overload (OPINION).
- KDOQI - BMD 2003 recommended to limit elemental calcium to 2000
mg/d, with no more than 1500 mg from calcium-based phos binders

26
Q

How is phosphorus managed in PD?

A
  • Clearance is ~300 mg/d with 4 x 2L exchanges
  • Most pts require phos binders & dietary restriction
  • Avoid phosphorus additives (almost entirely absorbed) in processed foods
  • Phos binders
27
Q

What are the phos recommendations for PD?

A
  • KDOQI 2020 6.3.1 - In adults with CKD 3-5D, we recommend adjusting dietary phosphorus intake to maintain serum phosphate levels in the normal range (1B).
  • KDOQI 2020 6.3.2 - In adults with CKD 1-5D or posttransplantation, it is
    reasonable when making decisions about phosphorus restriction treatment to consider the bioavailability of phosphorus sources (eg, animal, vegetable,
    additives) (OPINION).
  • KDOQI - BMD 2003 recommended to phos restriction to 800-1000 mg/d if serum phos is elevated
28
Q

Describe the lipid abnormalities often seen in PD

A
  • Low HDL, elevated VLDL, elevated TG
  • Potential causes: peritoneal protein loss & glucose absorption
  • High cholesterol (>250 mg/dL), but NOT low cholesterol, associated
    with increased mortality in PD pts
29
Q

What are the recommendations for lipid
management in PD?

A

KDIGO Lipids 2013 Guideline 5.1 - In adults with CKD (including those treated with chronic dialysis or kidney transplantation) and hypertriglyceridemia, we suggest that therapeutic lifestyle changes be advised.
- Dietary (weak evidence): a low-fat diet (<15% total calories), reduction of
monosaccharide and disaccharide intake, reducing the total amount of
dietary carbohydrates, and use of fish oils to replace some long-chain TGs
- Lifestyle: weight reduction, increased physical activity, reducing alcohol
intake, and treatment of hyperglycemia

30
Q

What are the n-3 PUFA recommendations in PD?

A

KDOQI 2020 4.3.2 & 4.3.4 - In adults with CKD 5D on PD (OPINION):
- Not to routinely prescribe LC n-3 PUFA, including those derived from
fish or flaxseed and other oils, to lower risk of mortality or
cardiovascular events
- Consider prescribing 1.3-4 g/d LC n-3 PUFA to improve the lipid profile

31
Q

Which vitamin and mineral recommendations in PD are
different than the RDA?

A

Vitamin US DRI PD
Folate 0.4 mg/day 1-10 mg/day
Pyridoxine (B6) 1.3-1.7 mg/day 10 mg/day
Iron 8-18 mg/day 10-15 mg/day, often need supplements
Zinc 8-11 mg/day 12-15 mg/day
Selenium 55 mcg/day 55-70 mcg/day

32
Q

How does PD compare to HD in pts with diabetes?

A
  • PD offers steadier biochemical state, fluid balance, lack of vascular
    compromise, absence of heparin therapy, and simplicity of technique with
    pts with vision or sensory limitations
  • PD offers equal or lower risk of death in pts with diabetes in the first 1-2
    years of dialysis compared to HD, possibly d/t lower prevalence of
    infections & CHF and better preservation of residual renal function
33
Q

How do you manage blood glucose in pts with DM
on PD?

A
  • Monitor blood glucose & need for increased insulin d/t glucose in
    dialysate diffusing into circulation
  • Use of alternative osmotic agents like icodextrin glucose polymer
    or amino acids may improve glycemic control
  • Nutrient modification, minimize use of hypertonic exchanges, wt
    control
34
Q

What are the pros and cons to intraperitoneal (IP)
administration of insulin compared with subcutaneous?

A

Pros:
- Provides direct delivery to liver via portal circulation rather than to
systemic circulation
- Prevents major BG fluctuations, rarely causes hypoglycemia
Cons:
- Need higher doses (dilutional effect)
- Potential for adherence to the plastic of the dialysis delivery system

35
Q

What is the rec. on using intraperitoneal nutrition
for tx of malnutrition in PD?

A

KDOQI 2020 Guideline 4.2.1 - In adults with CKD 5D on PD with
protein-energy wasting, we suggest not substituting conventional dextrose
dialysate with amino acid dialysate as a general strategy to improve
nutritional status, although it is reasonable to consider a trial of amino acid
dialysate to improve and maintain nutritional status if nutritional
requirements cannot be met with existing oral and enteral intake (OPINION).

36
Q

How would you manage wt gain, hyperglycemia,
and hypertriglyceridemia in PD?

A
  • Increase physical activity as tolerated
  • Limit sodium & fluid to minimize hypertonic exchanges
  • Use alternate non-glucose osmotic agents
  • Modify energy intake for wt goals
  • Modify intake of sugars and fats
37
Q

What is your intervention focus for malnutrition
management in PD?

A
  • Educate on protein goals & ways to meet those goals
  • Eat protein foods first, limit fluids at mealtimes
  • Frequent, smaller portions of easy-to-eat proteins (egg white, cottage cheese)
  • Increase protein intake slowly
  • Use oral nutrition supplement or intraperitoneal nutrition
  • Renal-specific water-soluble vitamin supplementation
  • Identify/avoid/treat sources of inflammation
38
Q

What are the 3 AKI etiology classifications?

A
  1. Prerenal
  2. Postrenal
  3. Intrinsic / Parenchymal
39
Q

Which of the 3 AKI classifications do not need
nutrition intervention?

A

Prerenal and postrenal are usually reversible with
quick/aggressive treatment & requires minimal MNT

40
Q

What conditions can cause decreased cardiac
output in prerenal AKI?

A
  • CHF / cardiomyopathy, valvular heart disease, pulmonary HTN
  • Sepsis, cirrhosis, hepatorenal syndrome
  • Drugs: NSAIDs, ACE-I, calcineurin inhibitors (cyclosporin /tacrolimus), radiocontrast agents, amphotericin B, cocaine, some herbs
41
Q

What are some diagnostic signs in prerenal
AKI?

A

Low urinary sodium < 10 mEq/L
High urine osmolality > 350-500 mOsm/kg
BUN:Cr ratio > 20:1

42
Q

What are some possible causes of postrenal AKI?

A

Prostate / gynecological / bladder / colorectal cancers
● Benign prostate hyperplasia
● Retroperitoneal disorders
● Neurogenic bladder
● Blood clot
● Urethral strictures
● Renal calculi or intratubular deposition/obstructions (uric
acid/oxalate, sulfonamides, acyclovir, methotrexate)

43
Q

What are some diagnostic signs of postrenal
AKI?

A

Severe sudden onset of oliguria/anuria
Urine osmolality >400 mOsm/kg early and 300
mOsm/kg later with BUN:Cr ratio of 10:1 to 20:1

44
Q

What are some treatment goals in postrenal AKI?

A

Correcting obstruction
2) Resuming normal hydration
Minimal nutrition intervention needed

45
Q

What are some treatment goals for prerenal AKI?

A

1) Early diagnosis
2) Restoration of renal perfusion / volume status
Prerenal azotemia should reverse within 1-2 days after, but
recovery depends on renal function decline / pre-existing CKD
Limited nutrition needed

46
Q

How is intrinsic / parenchymal AKI different from pre- and post-renal AKI?

A

intrinsic is 20-30% of AKI / postrenal is 5-15% of AKI/ prerenal is 50-60%
Intrinsic/parenchymal AKI involves tissue damage to the renal parenchyma; while pre-renal and post-renal AKI are the consequence of extra-renal diseases leading to the decreased GFR

47
Q

What are some diagnostic signs in intrinsic /
parenchymal AKI?

A

Azotemia, hyperkalemia, hyperphosphatemia Urine sodium > 30-40 mEq/L
Urine osmolality ~300 mOsm/kg (equivalent to serum d/t loss of urine dilution/concentrating function)
BUN:Cr ratio 10:1 to 20:1

48
Q

When would renal replacement therapy (RRT)
be initiated in AKI?

A
  • Worsening azotemia
  • High K
  • Volume overload
  • Severe acidosis that is resistant to conservative therapies
  • Significant symptoms of uremia present
    No consensus: used in 85% oliguric AKI; 30% of nonoliguric AKI
49
Q

What are the main purposes of initiating RRT in
AKI?

A
  • The need for large volume removal
  • High solute clearance
  • Recent abdominal surgery
50
Q

What nutrients are lost in each HD treatment?

A

2-5 g of peptides and 2-8 g of free amino acids

51
Q

What nutrients are lost in each PD treatment?

A

Average 10 g/day of protein lost, but can rise to 20 g/day or
more depending on peritoneal membrane permeability

52
Q

What nutrients are lost in each CRRT treatment?

A

Protein loss of 1.5 - 7.2 g/day,
Amino acid losses of 15-30 g/day, directly proportional to CRRT effluent flow
Glutamine losses of 2-4 g/day

53
Q

What factors contribute to hyperkalemia in AKI?

A

UOP <1L/day
- Metabolic acidosis exacerbates hyperkalemia d/t intracellular to
extracellular redistribution
- Rhabdomyolysis, tumor lysis syndrome, GI bleeding
- Potassium intake from diet, nutrition support, supplements, IV,
drugs, ACE inhibitors, potassium sparing diuretics (spironolactone)

54
Q

How is hyperkalemia in AKI managed?

A
  • Promote intracellular shift of potassium using:
  • Insulin & IV glucose
  • Correcting acidosis with bicarbonate
  • Beta-2 agonists
  • IV calcium gluconate
  • Potassium binding resins (sodium polystyrene sulfonate)
  • Diuretics
  • Dialysis
55
Q

What factors contribute to hypokalemia in AKI?

A
  • Extracellular to intracellular shifts with refeeding syndrome in
    the malnourished
  • May occur in the recovery/diuretic phase of AKI
  • Aggressive use of diuretic without sufficient K+ replacement
  • Magnesium deficiency may cause hypokalemia that is resistant
    to K+ supplementation
56
Q

What factors contribute to hypomagnesemia?

A
  • Refeeding syndrome in malnutrition (along with hypokalemia
    and/or hypophosphatemia)
  • Lost in CRRT effluent, may need frequent monitoring and
    replacement if serum Mg is low
57
Q

What are some vitamin considerations for
patients with AKI?

A
  • if on RRT: renal-specific vitamin including 1mg folate & 10mg pyridoxine per day
  • Vitamin C < 100 or 200 mg/day for oxalate management
  • Additional thiamin to replete losses during CRRT and to prevent lactic acidosis
  • Further study needed regarding vitamin D
  • Limit vitamin A to DRI dose of 700-900 mcg/day as in CKD
58
Q

What are some trace element considerations for
patients with AKI?

A
  • 100 mcg/d selenium to replete loses from CRRT
  • Supplement copper ONLY if copper is omitted from parenteral nutrition
    (ie. if total bilirubin >3 mg/dL) with long-term CRRT (>2 wks)
  • No zinc losses with RRT, but if omitted from PN in long-term CRRT,
    consider starting with 15 mg/d
59
Q

How do you determine energy needs in AKI?

A

Consider the underlying disease state/complication because AKI itself has limited effect on energy expenditure
- Indirect calorimetry
- 20-30 kcal/kg body weight or 130% basal energy expenditure during
hypermetabolic conditions (sepsis, MODS, use of CRRT)
- Composition: 3-5 g/kg of carbohydrates and 0.8-1 g/kg of fats

60
Q

What are the protein recommendations for AKI?

A

Recommendations per A Clinical Guide to Nutrition Care in Kidney Disease (2nd Edition)
1-1.3 g/kg in non-catabolic pts without dialysis
1.2-1.5 g/kg in catabolic and/or initiation of dialysis (up to 1.7 g/kg)
1.5-2 g/kg with maximum of 2.5 g/kg for critically ill adults on CRRT

Recommendations per KDIGO Clinical Practice Guideline for Acute Kidney Injury 2012
0.8-1.0 g/kg in non-catabolic pts without dialysis
1.0-1.5 g/kg in pts with AKI on RRT
Maximum of 1.7 g/kg in pts on CRRT and hypercatabolic pts

61
Q

What are the recommendations for sodium, potassium, and phosphorus in AKI?

A
  • Sodium: 2-3 g, or more with diuresis
  • Potassium: 2-3 g depending on labs (hyper-K), or more with dialysis,
    diuresis/return of kidney function, and anabolism
  • Phosphorus: 8-15 mg/kg, or more with CRRT/dialysis, return of kidney
    function, and anabolism
  • Consider need for phos binders depending on labs
62
Q

What are some considerations in providing nutrition
support in AKI?

A
  • EN preferred over PN
  • Assess risk for refeeding syndrome → K, Mg, Phos
  • AKI → nitrogenous wastes build up, metabolic acidosis, fluid retention,
    electrolyte/mineral imbalances (high K, Phos, Mg; low Na, Cl, Cal)
  • CRRT → uremia, solutes, fluids better managed; consider glycemic control
  • Intermittent RRT → may require stricter fluid/electrolyte limits
  • Recovery phase of ATN may involve diuresis → avoid concentrated formulas
  • Consider GI symptoms (GI bleed, GI motility, bowel edema) associated with AKI

Renal Nutrition Mastery (5 decks)

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