Term
| What is the most common complication associated with PN administration? |
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Definition
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Term
| What are some different causes of hyperglycemia in PN patients? |
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Definition
- Stress-associated hyperglycemia in acutely ill and septic patients
- Excess carbohydrate administration
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Term
| What causes stress-induced hyperglycemia? |
|
Definition
- Insulin resistance
- Increased gluconeogenesis and glycogenolysis
- Suppressed insulin secretion
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Term
| What are symptoms of excess carbohydrate administration? |
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Definition
- Hyperglycemia
- Hepatic steatosis
- Increased CO2 production
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Term
| How should PN be initiated? |
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Definition
| PN should be initiated at 50% of estimated energy needs or approximately 150 to 200 grams of dextrose for the first 24 hours |
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Term
| How should PN be modified for patients who are hyperglycemic and requiring insulin therapy or a hypoglycemic agent? |
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Definition
| Less dextrose should be delivered (approximately 100 grams) in hyperglycemic patients requiring insulin therapy or on a hypoglycemic agent |
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Term
| What is the recommended GIR and kcal/kg/d from carbohydrates? |
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Definition
| Carbohydrate administration should not exceed 4 to 5 mg/kg/min or 20 to 25 kcal/kg/day |
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Term
| How should patients be monitored relative to glucose control in PN? |
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Definition
| Capillary blood glucose concentrations should be monitored every 6 hours and more frequently in hyperglycemic patients |
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Term
| How can insulin be administered in PN patients? |
|
Definition
- Subcutaneously
- Intravenously via insulin infusion
- Directly through PN infusion
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Term
| What is a normal initial dose of insulin for normal and hyperlgycemic PN patients? |
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Definition
| An initial dose of 0.05 to 0.1 units of insulin per gram of dextrose in PN is common, or 0.15 to 0.2 units of insulin per gram dextrose in patients who are already hyperglycemic |
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Term
| How should the PN infusion be altered based on sliding scale insulin requirements? |
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Definition
| Two-thirds of the total amount of sliding scale insulin required over 24 hours may be added to the next day's PN formulation |
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Term
| How should dextrose content of PN be advanced relative to glycemic control? |
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Definition
| Increases in dextrose concentration in PN should not be implemented until glucose concentrations are controlled |
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Term
| How should insulin in PN be adjusted if the dextrose concentration is altered? |
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Definition
| Insulin should be adjusted proportionally with respect to PN glucose concentration |
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Term
| What type of deficiency can cause hyperglycemia? How should it be handled? |
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Definition
| Chromium deficiency (rare). Increasing chromium dose in PN formulation beyond the standard amount may be necessary, as increasing insulin will have no effect. |
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Term
| What are some possible consequences of uncontrolled hyperglycemia? |
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Definition
| Uncontrolled hyperglycemia may result in hyperosmolar hyperglycemia, nonketotic dehydration, coma, and death secondary to osmotic diuresis |
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Term
| What is PN-induced hypoglycemia generally caused by? |
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Definition
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Term
| How should PN-induced hypoglycemia be handled? |
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Definition
| Treatment includes initiation of D10, administration of an ampule of D50, and/or stopping any source of insulin administration |
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Term
| Which patients are at greatest risk of rebound hypoglycemia after stopping PN? |
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Definition
| Patients requiring large doses of insulin have a greater propensity for rebound hypoglycemia |
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Term
| How should glucose control be measured after discontinuation of PN? |
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Definition
| Capillary blood glucose concentration should be measured 30 minutes to 1 hour after PN solution is discontinued to help identify rebound hypoglycemia |
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Term
| Which are the two essential fatty acids? |
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Definition
| Linoleic acid and alpha-linolenic acid |
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Term
| What are symptoms of EFAD? |
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Definition
- Scaly dermatitis
- Alopecia
- Hepatomegaly
- Thrombocytopenia
- Fatty liver
- Anemia
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Term
| What lab test can be done to identify EFAD? |
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Definition
| EFAD is determined by a triene/tetraene ratio of more than 0.2 |
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Term
| How long does it take for EFAD to develop in adults receiving EFA-free PN? |
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Definition
| EFAD can develop in 1 to 3 weeks in adults receiving EFA-free PN |
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Term
| How much of each type of IVFE must be given in order to avoid EFAD? |
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Definition
- 250 mL of 20% IVFE twice a week
- 500 mL of 10% IVFE twice a week
- 500 mL of 20% IVFE once a week
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Term
| What can be done to prevent EFAD in patients who are intolerant to IVFEs? |
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Definition
In patients intolerant to IVFEs, a trial of topical skin application or oral ingestion of oils (safflower or sunflower) to alleviate biochemical deficiency may be given
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Term
| What are causes of hypertriglyceridemia? |
|
Definition
- Dextrose overfeeding
- Rapid administration rates of IVFE (>110 mg/kg/hr)
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Term
| What are potential complications of hyperlipidemia? |
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Definition
| HLD may impair immune response, alter pulmonary hemodynamics, and increase risk of pancreatitis |
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Term
| What can be done to reduce risk of complications from hyperlipidemia? |
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Definition
| Reducing dose or lengthening infusion time of IVFE can help reduce complications |
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Term
| How much IVFE should patients receive at maximum? How quickly should it be infused if administered separately? |
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Definition
| IVFE intake should be restricted to less than 30% of total calories or 1 g/kg/d and be provided slowly over no less than 8 to 10 hours if administered separately |
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Term
| What are acceptable serum triglyceride concentrations for PN patients? |
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Definition
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Term
| What is a potential symptom of fat intolerance in PN patients? What should be done if this symptom occurs? |
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Definition
| Occasionally serum triglyceride concentrations will rise in a patient who is fat-intolerant. In such patients, IVFE infusions should be reduced or discontinued. |
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Term
| Can IVFE-induced hyperlipidemia cause pancreatitis? |
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Definition
| IVFE-induced hyperlipidemia rarely causes pancreatitis unless serum triglyceride concentrations exceed 1000 mg/dL |
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Term
| Are IVFE safe for use in patients with pancreatitis? |
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Definition
| IVFE are safe for use in patients with pancreatitis WITHOUT hypertriglyceridemia |
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Term
| What should be done if serum triglycerides exceed maximum allowable levels in PN patients? |
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Definition
| IVFE should be witheld from PN regimen if serum triglyceride concentrations exceed 400 mg/dL |
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Term
| Which patients are at risk of allergic reaction to IVFE? |
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Definition
| Allergic reactions to IVFE can occur in patients with egg allergy due to the egg phospholipid that is used as an emulsifier |
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Term
| How should PN patients who develop amino acid intolerance such as prerenal azotemia, hepatic encephalopathy, or hyperammonemia be treated? |
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Definition
| A reduction in amount of amino acids provided may be beneficial |
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Term
| Should vitamin administration be delayed in PN patients until signs of vitamin deficiency develop? |
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Definition
| No, they should receive daily multivitamin infusion |
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Term
| How should PN be altered for patients with a history of alcohol abuse? |
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Definition
| They should receive supplemental thiamine (25 to 100 mg/d), especially if they did not receive thiamine upon admission |
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Term
| How should PN be handled in patients on warfarin? |
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Definition
| Patients on warfarin and TPN require close monitoring due to vitamin K in regimen |
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Term
| How should thiamine be handled in PN patients at risk of refeeding syndrome? |
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Definition
| Thiamine supplementation is recommended during PN initiation in patients at risk of refeeding syndrome |
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Term
| What is the clinical manifestation of thiamine deficiency for PN patients? |
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Definition
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Term
| What are the recommended practices during periods of short vitamin supply? |
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Definition
- Use oral or enterally administered multivitamins whenever possible
- Ration IV multivitamin dose by 50% of give one dose 3x/week
- If IV multivitamins are no longer available, administer thiamine, ascorbic acid, pyridoxine, and folic acid daily and B12 at least once per month
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Term
| How should vitamin administration be altered in PN patients with renal failure? Why? |
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Definition
| Vitamin A toxicity is a potential complication of renal failure patients on PN. However, there are no multivitamin formulations that exclude fat-soluble vitamins and hemodialysis patients need MORE water-soluble vitamins. |
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Term
| How does vitamin degradation affect PN administration? |
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Definition
| Vitamin degradation is not much of an issue in the acute-care setting. However, degradation must be considered in home PN patients. |
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Term
| How should vitamins be administered in home PN patients? Why? |
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Definition
| Daily addition of vitamins to PN before infusion has been recommended d/t risk of degradation |
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Term
| PN patients with high intestinal losses are at risk of which mineral deficiency? |
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Definition
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Term
| How should PN be altered in patients with hepatobiliary disease, and why? |
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Definition
| Patients with hepatobiliary disease should have consideration of reduction of copper and manganese due to impaired excretion |
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Term
| How should manganese and copper be handled in long-term PN patients? |
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Definition
| Removal of supplemental manganese and reduction of copper dose may be necessary in long-term PN patients |
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Term
| How is iron handled in PN patients? |
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Definition
| Iron is not a component of PN formulations due to compatibility issues. PN iron supplementation can be administered separately as repletion dose when necessary. Delivery of maintenance iron on a monthly basis has been suggested. When PN iron is provided, monitoring of iron status (ferritin) should be conducted to avoid overload. |
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Term
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Definition
| PN-associated liver disease |
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Term
| What are the three types of hepatobiliary disorders associated with PN therapy? |
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Definition
| Steatosis, cholestasis, and gallbladder sludge/stones |
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|
Term
|
Definition
| Hepatic fat accumulation. It is predominant in adults and generally benign. |
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Term
| How does steatosis present in PN patients? |
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Definition
| Steatosis generally presents as modest elevations of serum aminotransferase concentrations that occur within 2 weeks of PN therapy initiation, and may return to normal even as PN therapy is continued. Most patients are asymptomatic. |
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Term
| What are the concerns of steatosis with patients on long-term PN? |
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Definition
| There is concern that it may lead to fibrosis or cirrhosis in patients on long-term PN |
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Term
| What is PN-associated cholestasis, and in what populations is it generally found? |
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Definition
| PN-associated cholestasis is a condition of impaired secretion of bile or frank biliary obstruction that occurs predominantly in children, but which may also become an issue in patients receiving long-term PN |
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Term
| How does PN-associated cholestasis generally present? |
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Definition
| PNAC generally presents as an elevation of alk phos, gamma-glutamyl transpeptidase, and conjugated bilirubin with or without jaundice |
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Term
| What is the prime indicator for cholestasis, and why? |
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Definition
| Elevated serum conjugated bilirubin (>2 mg/dL) is the prime indicator for PNAC because other markers are not sensitive or specific |
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Term
| What risks are associated with PN-associated cholestasis? |
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Definition
| PNAC is a serious complication because it may progress to cirrhosis and liver failure |
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Term
| What causes gallbladder sludge/stones in PN patients? |
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Definition
| Gallbladder sludge/stones in PN patients is related more to lack of enteral stimulation (and thus decreased bile flow/gallbladder contractility) than the PN infusion itself |
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Term
| What is the greatest risk factor for development of biliary sludge in PN patients? |
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Definition
| Overall duration of PN therapy |
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Term
| What can biliary sludge result in? |
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Definition
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Term
| How is risk of PN-associated liver disease affected by factors unrelated to PN? |
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Definition
| There are quite a few factors that affect risk of PN-associated liver disease other than the PN itself including sepsis, intestinal bacterial overgrowth, and massive intestinal resection |
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Term
| What is the primary cause of steatosis during PN administration? |
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Definition
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|
Term
| How do dextrose-based PN formulations with little or no fat affect development of steatosis? |
|
Definition
- Excess carbohydrates are deposited in liver as fat
- EFAD can result in steatosis
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Term
| What percentage of nonprotein calories should be provided as carbohydrate in PN formulatons? |
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Definition
| 70 to 85% of nonprotein calories should be provided as calories in PN patients |
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Term
| What is the maximum amount of carbohydrates that should be provided via PN to adults in g/kg/d? |
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Definition
| Carbs should not exceed 7 g/kg/d in adults |
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Term
| How does phyosterol content of IVFEs affect risk of biliary sludge/stones? |
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Definition
| Phytosterols in IVFEs (such as in soybean oil-based emulsions) may impair bile flow and cause biliary sludge and stones |
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Term
| How does excessive IVFE infusion rate affect risk of steatosis? |
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Definition
| Excessive IVFE rate exceeds the liver's ability to clear the phospholipids and fatty acids, leading to direct deposition in the liver |
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Term
| How does carnitine affect risk of steatosis? |
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Definition
| Primary carnitine deficiency has been associated with the development of steatosis |
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|
Term
| How is carnitine handled in PN? |
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Definition
| Carnitine is not routinely added to PN. However, the role of carnitine in the prevention and treatment of PN-associated liver complications has been inconsistent. |
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|
Term
| How is choline handled in PN patients? |
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Definition
| Cholene is not a component of PN formulations because endogenous synthesis is hypothetically adequate for meeting needs. However, steatosis in some PN patients resolves after choline supplementation. Unfortunately there is no commercially available injectable choline preparation. |
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|
Term
| What is the best strategy for handling PN-associated liver complications? |
|
Definition
- Rule out non-PN factors
- Consider PN modifications
- Maximize enteral intake
- Prevent/treat bacterial overgrowth
- Pharmacotherapy
- Intestinal transplantation (for patients with PN failure)
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|
Term
| What non-PN factors are associated with liver complications? |
|
Definition
- Hepatotoxic medications
- Herbal supplements
- Biliary obstruction
- Hepatitis
- Sepsis
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Term
| What modifications can be made to PN to treat liver complications? |
|
Definition
- Decrease dextrose
- Decrease IVFE (<1 g/kg/day)
- Provide a balance of dextrose and IVFE
- Cyclic PN infusion
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|
|
Term
| What is a typical cyclic infusion time? |
|
Definition
|
|
Term
| What medication can be used to stimulate bile flow and maintain gallbladder contractility? |
|
Definition
|
|
Term
| What are the bone mineral density measurements that indicate osteoporosis/osteopenia? |
|
Definition
- Osteoporosis: T score <-2.5
- Osteopenia: -1 to -2.5
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|
|
Term
|
Definition
| Osteomalacia is softening and bending of the bones that occurs because the bones fail to calcify. Identification requires bone biopsy and is therefore difficult to obtain. |
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|
Term
| How is the body affected by higher than recommended doses of calcium provided parenterally? |
|
Definition
| Doses in excess of the recommendations are offset by higher urinary calcium losses and therefore not recommended |
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|
Term
| How does inadequate phos affect calcium metabolism? |
|
Definition
| Inadequate phos can increase urinary calcium losses |
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|
Term
| How does PN protein intake affect calcium levels? |
|
Definition
| Higher protein doses have been associated with increased urinary calcium excretion, so reducing to maintenance levels is recommended |
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|
Term
| How does chronic metabolic acidosis affect risk of hypercalciuria/metabolic bone disease? How should it be treated in PN patients? |
|
Definition
| Chronic metabolic acidosis has been associated with hypercalciuria/metabolic bone disease. Correction of acidosis w/ acetate in PN formulation reduces calcium excretion. |
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|
Term
| How does cyclic vs. continuous PN infusion affect calcium excretion? |
|
Definition
| Cyclic PN infusion increases urinary calcium losses, so benefits must be weighed when determining cyclic vs. continuous |
|
|
Term
| How does PN vitamin D affect risk of bone disease? |
|
Definition
| Inadequate or excessive vitamin D can cause bone disease |
|
|
Term
| What's the deal with aluminum toxicity and PN? |
|
Definition
| The protein hydrolysates that used to be used for PN infusions contained significantly more aluminum than the current crystalline AA formulations and toxicity sometimes occured. However, aluminum intake remains a concern |
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|
Term
| What is the relationship between magnesium and calcium deficiencies? How should this be treated? |
|
Definition
| Magnesium deficiency can cause calcium deficiency? Hypomagnesemic hypocalcemia should be treated with magnesium because calcium supplementation alone is ineffective |
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|
Term
| How should be bone disease be monitored in long-term PN patients? |
|
Definition
| They should receive DEXA at baseline and every 2-3 years if normal or 1-2 years if osteopenia is present |
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|
Term
| What modifications should be made to PN in order to prevent and treat osteoporosis in long-term PN patients? |
|
Definition
- Avoid high doses of protein
- Avoid excessive doses of sodium
- Calcium and phos at recommended amounts
- Treat metabolic acidosis
- Maintain adequate magnesium and copper intake
- Minimize aluminum contamination
- Avoid adding heparin
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