malnutrition & disorders Flashcards

1
Q

What is malnutrition?

A

-State resulting from lack of uptake or intake of nutrition, leading to altered body composition & body cell mass, leading to diminished physical & mental function & impaired clinical outcome from disease

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2
Q

Where do we see highest prevalence of malnutrition?

A

In youngest and oldest age groups. More in women. High prevalence in oncology and care of elderly, and those with GI illness. Risk >65 years hospital admission, those with long term disease and chronic progressive disease, alcohol abuse.

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3
Q

When is greatest weight loss seen and what is problem with malnutrition in acute settings?

A

Greatest weight loss seen in those underweight already. Malnutrition often unrecognised & undiagnosed in acute settings

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4
Q

What are some reasons for malnutrition in hospital?

A

Disease related anorexia, response to stress (muscle breakdown), paradox of metabolic response to injury can lead to tissue loss, reduced food intake (poor appetite, GI symptoms, inactivity, depression, inflexible hospital symptoms, quality of food, belief medical treatment is priority)

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5
Q

What is impact of malnutrition in a hospital setting?

A

Greater mortality post-op, septic complications, increased hospital stay, pressure sores, re-admission, dependency, decreased wound healing, worse response to treatment, rehabilitation & quality of life.

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6
Q

What does screening for malnutrition do? Limitations?

A

Simple tool to identify risk, not assessment or diagnosis. Limitation - can miss malnourished population (eg. Overhydration for oedema)

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7
Q

What is included in an assessment of malnutrition by a dietician?

A
  • Collecting & interpreting info to determine cause and nature of imbalance
    1. anthropometric measurements - scale, BMI (rarely), mid-arm muscle circumference)
    2. CT scan to distinguish types of fat
    3. biochemistry - nutrient availability, deficiencies, trace elements)
    4. history - clinical, dietary, nutrition requirements (RMR-BMR - predictive equations to maintain energy balance), social, physical history
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8
Q

After diagnosis what is done for malnutrition?

A

Diagnose, implement, monitor, evaluate

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9
Q

When is nutrition support considered?

A
  1. malnourished - BMI<18.5, unintentional weight loss >10% past 3-6 months, or BMI<20 + unintentional weight loss >5% past 3-6 months
  2. at risk of malnutrition - have eaten little/nothing for >5 days or wont for next 5 days or have poor absorptive capacity &/or have high nutrient losses &/or increased nutritional needs due to things like catabolism
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10
Q

What is artificial nutrition?

A

Provision of enteral or parenteral nutrients to treat or prevent malnutrition

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11
Q

What are types of artificial nutrition and when do you use each?

A
  1. enteral uses gut. Better than parenteral.
  2. parenteral - uses blood, aim to return to enteral and then oral feeding asap. Assess considered: if gastric feeding possible naso-gastric tube (NGT). If not naso-duodenal NDT or naso-jejunal NJT.
    If long term > 3 months = gastrostomy/jejunostomy.
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12
Q

What do nutritional needs depend on?

A

Many factors - renal, low sodium, respiratory, immune, elemental, peptide.

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13
Q

When is NGT feeding contraindicated and what do you use instead?

A

NGT contraindicated in gastric outlet obstruction, use NJT

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14
Q

What are complications of enteral feeding?

A
  1. mechanical: misplacement (aspirate pH <5.5. if greater x-ray needed to make sure tube is in stomach), blockage, buried bumper.
  2. metabolic - hyperglycaemia, deranged electrolytes
  3. GI: aspiration, nasopharyngeal pain, laryngeal ulceration, vomiting, diarrhoea
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15
Q

What is parenteral nutrition and when is it used? How is it used?

A
  • Parenteral nutrition is delivery of nutrients, electrolytes and fluids directly by venous blood access via central venous catheter at SVC and right atrium.
  • Different CVC for short/long term use.
  • Composition ready made or scratch bag with fluid/electrolyte target for the day.
  • Done when inadequate or unsafe oral or enteral nutrition intake or non functioning, inaccessible, perforated GI tract
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16
Q

What are complications of parenteral nutrition?

A
  1. mechanical: line inserted - pneumothorax, haemothroax, thrombosis, cardiac arrhythmia, catheter occlusion, thrombophlebitis, extraversion
  2. metabolic: deranged electrolytes, hyperglycaemia, abnormal liver enzymes oedema, hypertriglyciredaemia
  3. catheter related infections
17
Q

What is effect of receiving nutrition support on morality and readmissions?

A

Decreased mortality and readmissions

18
Q

What is albumin? When is it made? What stimulates production and inhibits production?

A

Protein made in liver. Stimulated by insulin, cortisol, GH. Inhibited by pro-inflammatory cytokines - IL-6, TNF.

19
Q

Why is albumin not a valid marker of malnutrition in acute hospital setting?

A

Pro-inflammatory cytokines In inflammation act on liver to stimulate production of some proteins and down-regulate others like albumin.
-Negative acute phase protein albumin decreases due to inflammation so not valid marker of malnutrition.

20
Q

When does re-feeding syndrome happen?

A

When malnourished/starved people are reintroduced to oral/enteral/parenteral nutrition

21
Q

in re-feeding syndrome, what happens during prolonged fasting ?

A
  • Hormonal/metabolic changes to prevent muscle breakdown.
  • Muscle decreases ketone body use, uses fatty acids.
  • Brain uses ketones instead of glucose.
  • Liver decreases gluconeogenesis to preserve muscle.
  • Intracellular ions become depleted but serum concentrations normal because intracellular compartment affected
22
Q

In re-feeding syndrome what happens when food is reintroduced? What can this cause?

A
  • Glycaemia leads to increased insulin which stimulates glycogen, fat & protein synthesis, and stimulates absorption of potassium, magnesium and phosphate into cells depleting serum phosphate, magnesium, potassium.
  • Hypokalaemia leads to deranged membrane potential so arrhythmias & cardiac arrest.
  • Hyperglycaemia leads to fatty liver, hypercapnoea, respiratory failure.
  • Magnesium deficiency leads to cardiac dysfunction & neuromuscular complications.
  • Thiamine deficiency (co-enzyme in carb metabolism) (vit B1) leads to wernicke’s encephalopathy (ocular abnormalities, ataxia, confusion, hypothermia), or korsakoff’s syndrome (amnesia).
  • Rapid decrease in renal excretion of water and sodium, if fluid repletion to maintain urine output may get fluid overload leading to congestive heart failure, pulmonary oedema, cardiac arrhythmia
23
Q

Who is at risk of refeeding syndrome? High risk? Very high risk of refeeding syndrome?

A
  • At risk: very little/no food intake for >5 days.
  • High risk: 1 of following –> BMI <16, unintentional weight loss <15% in 3-6 months, very little/no nutrition >10 days, history of alcohol abuse or drugs (insulin, chemo, antacids, diuretics).
  • Really high risk –> BMI <15, negligible intake >15 days.
24
Q

How is risk of refeeding syndrome managed?

A
  • Give no more than 10-20kcal/kg of nutrition (40-50% from carbs), micronutrients from onset of feeding, thiamine from onset of feeding.
  • Correct & monitor electrolyte daily.
  • Monitor fluid shifts & minimise risk of fluid & sodium overload.
25
Q

In pancreatitis what type of feeding is preferred?

A

Enteral over parenteral. Eg. Naso-gastric tube NGT

26
Q

What should you prescribe before feeding if at risk of refeeding syndrome?

A

30 minutes before feeding IV pabrinex (contains thiamine)

27
Q

Duodenal stenosis, what type of feeding should you try?

A

Naso-jejunal tube NJT feeding distal to stenosis

28
Q

How would you know patient isnt absorbing enteral nutrient? What would you do?

A

Steatorrhea & diarrhoea. Start parenteral nutrition & reduce NJT feeding to minimal rate

29
Q

What is short bowel syndrome and what can it be due to?

A

From surgical resection, congenital defect or disease associated loss of absorption. Cant maintain protein energy, fluid electrolyte and micronutrient balance on normal diet.

30
Q

What do you need in each type of short bowel syndrome?

A

Short bowel syndrome <2 m from duodeno-jejunal flexure.
Critical lengths: <100cm of jejunum = long term IV fluid + electrolytes.
<75cm of jejunum = long term PN, fluid + electrolytes. <50cm of jejunum + colon = long term PN, fluid + electrolytes

31
Q

What are surgical options for short bowel syndrome?

A

Ileocolic anastamosis. Jejunocolic anastamosis. End-jejunostomy.

32
Q

What is end-jejunostomy?

A
  • This surgery involves removal of the colon, ileum, and some of the jejunum.
  • The remaining jejunum is then connected to a surgical opening (stoma) created in the belly.
33
Q

What is stoma output target and what does higher stoma output risk?

A

Stoma target <1.5L/day.

High stoma output risk of dehydration & electrolyte imbalance.

34
Q

How do you prevent further dehydration & electrolyte imbalance? (high stoma output)

A

Limit all fluids.
-Restrict hypotonic fluids & certain hypertonic fluids containing sorbitol & glucose. Encourage them to drink 1L of glucose saline solution a day

35
Q

What value of urinary sodium indicates dehydration?

A

<20mmol/L. early measure.