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Nutrition - Intestinal Failure
PT4
21
Pharmacology
Graduate
03/04/2010

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Cards

Term
What is the difference between acute and chronic intestinal failure?
Definition

Intestinal failure is the impairment of absorptive capacity, needing prolonged fluid/nutrition support to maintain health

Acute - days-weeks; during chemo or radiation therapy

Chronic - Months to years

 

 

Short Bowel Syndrome:

Up to 50% of bowel can be removevd with no consequences, SBS usually occurs after surgical resections, thrombosis resulting in intestinal infarction, malignancy, or volvulus

Term
What are the most frequent disease states leading to chronic intestinal failure?
Definition
Term
What are the five factors that affect the severity of short bowel syndrome?
Definition

- Extent of the resection --> <80% is best

- Site --> Jejunum resection is best (Ileum can take over a lot of functions)

- Concomittant Disease --> No disease is best of course

- Duration --> > one year (what?)

- Antatomy of GI tract --> Presence of ileocecal valve and colon.  Valve stops food from moving backwards, and colon helps reabsorb electrolytes and fluids

Term
What is signficant regarding home parenteral nutrition for the management of gut failure?
Definition

- We want site to be at jejunem, so removing it doesn't affect too much, also want presence of ileocecal valve and colon, so bacteria doesn't infect GI tract.

- If jejunum was removed, and remaining length is <120cm and no colon, give TPN.  If jejunum removed and there IS colon, give TPN but <60cm is adequate. 

- Adaptation can occur as early as 1-2 days after resection, could take 1-2 YEARS, so keep giving nutrients

- Colon is needed for water/electrolyte exchange

Term
What are the strategies for the management of chronic intestinal failure (surgery and nutrition)?
Definition

- Long term/home nutrition support:  enteral, parenteral, or both

 

Surgery makes you shed a TEAR

- Transplantation

- End-end lengthening procedures

- Antiperistaltic segments

- Recirculating loops

Term
Which motility agents are available in the management of short bowel syndrome patients to reduce GI output?
Definition

Two types of individuals:  Absorbers and Secretors

Absorbers - Take in more nutrients/fluids than they lose, managed by po nutrient/electrolyte support

Secretors - Have more output than intake (usually <100cm intestine remaining), absorb only 35% of po, NEED IV SUPPORT

- Codeine and loperamide are motility agents

- 15-30mg of codeine 30 min.  before meals, reduces motility and secretions

- 4mg of loperamide 30 min. before meals, may need to break open capsules so they are absorbed

- H2 blockers or PPI's may also reduce gastric acid production and reduce overall fluid loss.

Term
Which is significant regarding octreotide, which is available in the management of short bowel syndrome patients to reduce GI output?
Definition

- Octreotide (Sandostatin)

- Octapeptide of endogenous somatostatin

- Blocks release of serotonin and other peptides like glucagon, gastrin, VIP, and insulin

- Increases Na and water reabsorption, so dec. diarrhea

- Start at 50mcg bid, then titrate upwards to 500mcg q8h

- IM sandostatin is NOT for this same indication

- Dose 10mcg/kg/dose or IV q12h

- ADR's: short term n/v, diarrhea, abd. pain, long term gallstones

- Suppresses tropic stimulation so avoid in early post-resection patients

- May reduce fat abs. messes with blood sugar, flushing, lightheadedness, headache

Term
Which is significant regarding cholestyramine, which is available in the management of short bowel syndrome patients to reduce GI output?
Definition

 

nAbsorbs bile salts which irritate colon
nMay be useful in choleretic (bile salt induced-green color) diarrhea if the ileal resection is <100cm and fecal fat <20g/d (Normal 6g/day).
nIf ileal resection is > 100cm, is usually ineffective and may worsen fat malabsorption(leading to steattorhea) if the bile salt pool is depleted
nDose: 4g qd or bid up to 24g/day before meals and at bedtime
 
nSide effects: constipation, nausea, vomiting, abdo distension and pain, malabsorption of fat soluble vitamins, blocks feeding tubes
nDrug interactions: avoid other meds 1h before and 4-6h after
nCommon interactions: digoxin, warfarin, thiazides, propranolol
Term
Which is significant regarding growth hormone, which is available in the management of short bowel syndrome patients to reduce GI output?
Definition

- Stimulates bowel adaption, may be combined with glutamine, enhances nutrient absorption

- Dose 0.1mg/kg/day sc for four weeks in PN patients who are stable and have optimal diet and medication therapy 6-24 months after bowel resection

- Timing and appropriateness remains controversial

Term
Which is significant regarding glutamine, which is available in the management of short bowel syndrome patients to reduce GI output?
Definition

- 2-4g/day

- may enhance GI mucosal integrity and improve the health of the enterocyte, thereby improving absorption

Term
What are the medication delivery issues in SBS patients?
Definition

- How do we know drug is being absorbed?

- need to know PK of the drug, part of intestine that needs to absorb it

- Rectal administration no good, as patient has diarrhea

- length of intestine, mucosal integrity, intestinal motility all plays a role

- Fat soluble or water soluble drug

- Physiological req. for abs.; Acidic (penicillin, ketoconazole), alkaline (procainamide, nitrofurantoin), bile acids needed (Cyclosporin A, D2, squinavir), ileal absorption (B12)

- Patient has low protein stores which can effect drug delivery

- No slow or timed release formulations, caution with EC, parenteral is an option, aerosol, topical.

Term
What pathophysiologic effects does SBS have on carbohydrates, fats, and proteins?
Definition

- Once nutrients are absorbed they are handled normally

- Carb malabsorption leads to diarrhea (lactose intolerance)

- For protein absorption, peptides are more easily absorbed than free amino acids

- Fat absorbption most affected in SBS

- Impaired bile salt recycling may lead to gallstones

- Fat can be provided as MCT, but needs LCT b/c we need essential fatty acids as well

Term
What pathophysiologic effects does SBS have on fluids and electrolytes?
Definition

- If dehydrated a patient will develop metabolic alkalosis and excrete more K+

- In jejunostomy patients with output of 1.5-21 (is this second number right?), give high NA solution (120meq/glucose 110mmol), low Na draw water out of people

- K+ replacement is only needed if jejunum <50cm and ostomy is present)

- Urine with Na <5meq/L is indicative of Na depletion

- Avoid tea, coffee, water

- Avoid liquids 30 min. before and after meals

- D2 can cure magnesium deficiency, 1-4g of calcium/day should fix this deficiency

Term
What pathophysiologic effects does SBS have on acid-base balance?
Definition

- Normal pH 7.4

- H+ and Cl- are lost in ostomy, diarrhea, urine losses

- If colon is present but diarrhea is still there, K+ and HcO3 will be lost, leading to metabolic acidosis

Term
What pathophysiologic effects does SBS have on trace element absorption in the Duodenum, Jejunum, Ileum, Terminal Ileum, Colon?
Definition

Duodenum - Calcium, Iron, CHO, fat, Mg, protein

Jejunum - CHO, fat, AA, Mg, copper, zinc, folate, Phosphorous

Ileum - Fat, Mg, Protein, Phosphorous

Terminal Ileum - B12, bile salts

Colon - Water and electrolytes

Term
What pathophysiologic effects does SBS have on vitamins?
Definition

- Most water soluble vitamins absorbed in the jejunum so not usually a problem

- If ileal resection >60cm, need B12

- If there is fat malabsorption then we need fat soluble vitamins (ADEK)

- Aqueous form of Vitamin E in PEG may have better absorption po in SBS

- Folate and B12 deficiency can lead to anemia

Term
What are some short term complications associated with SBS?
Definition

Hypovolemia  --> Increase fluids intake

Hypervolemia --> decrease fluids, diuretics

Hyponatremia --> Replace Na when indicated, diuresis prn

Hypernatremia - Rehydrate as needed, check for sources of Na

Hypokalemia --> Increase K+ intake

Hyperkalemia --> Check sources of K+, correct acidosis

Hypophosphotemia --> Increase P intake, d/c binders

Hyperphosphotemia --> Decrease P intake

Hypomagnesemia --> Increase Mg intake

Hypermagnesemia --> Decrease Mg intake

Hyperglycemia --> Reduce dextrose load, give insulin

Hypoglycemia --> Taper infusion, increase dextrose load

Resp. Acidosis --> Dec. dextrose, inc. fat kcal

Elevated chol. and triglycerides --> dec. fat or d/c if TG>300

Abnormal LFT, raised ALP, AST, Bili --> Decrease kcal, dex., provide essential FA's

Altered AA profile --> Change solution or decrease AA intake

Term
What are some altered nutritional requirements in patients with acute renal failure as well?
Definition

- Hyperglycemia and insulin resistance is common

- Hyperkalemia

- Increased serum P and Mg

- Zinc and Copper removed via dialysis, as well as WS vitamins

- Use concentrated macronutrient solutions, keep TG's below 300

Term
What are some altered nutritional requirements in patients with chronic renal failure as well?
Definition

- Less likely than ARF to develop glycemic problems

- Protein req. depend on dialysis

- Na is often low --> control with dialysis

- K+ usually high

- WS vits are decreased, FS are ok, vitamin A may be high

Term
What are some altered nutritional requirements in patients with hepatic failure as well?
Definition

- Insulin resis. is common

- TG are elevated

- Aromatic AA accumulate

- Branched AA decrease b/c of metabolism by skeletal muscle

- Na and water retention is common

- K+ and Mg is decreased

- Zinc --> lost in diarrhea

- Copper and Manganese not excreted --> should be held

Term
What are some altered nutritional requirements in patients with pulmonary failure as well?
Definition

- Hypermetabolism common in COPD

- Formula should be 60% fat, need to keep glucose load moderate to low as metabolism can lead to dioxide production which is difficult to excrete with lung issues

- Avoid over-feeding

- Keep patient slightly dry

- Make sure serum phosphate is adequate

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