Nutrition & Diet Flashcards

1
Q

What is malnutrition?

A

A state of nutrition in which a deficiency or excess of energy, protein and other nutrients causes measurable adverse effects on tissue/body form and function and clinical outcome

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2
Q

What are some causes of malnutrition?

A

When intake is less than requirements:

  • increase in nutritional requirement
  • decrease in intake due to inadequate availability, quality or presentation of food
  • lack of recognition and treatment (may not realise they have higher requirements and need to eat more)
  • low intake even when food is available
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3
Q

Why may intake be low?

A
dysphagia
prolonged periods of nil by mouth (cancelled procedures for example)
treatment side effects
pain/constipation
psychological -e.g. depression
social -e.g. low income, isolation
poor dentition
reflux/feeding problems/food intolerance
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4
Q

Why may requirements increase?

A
  • infections
  • involuntary movements
  • wound healing
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5
Q

Why may losses increase?

A
  • gut malabsorption
  • diarrhoea and vomiting
  • high stoma output
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6
Q

What are the main consequences of malnutrition?

A
  • declining respiratory and cardiac function
  • reduced mobility
  • increased risk of pressure sores
  • increased risk of infection
  • reduced wound healing
  • apathy and depression
  • malabsorption increased risk
    all these can be triggers/causes for further malnutrition so get a viscous cycle
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7
Q

What is nutritional screening?

A
  • identify malnutrition/risk of malnutrition
  • completed for all adult patients on hospital admission and weekly thereafter if clinical concern
  • use MUST method
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8
Q

What is MUST?

A
Barts health method of nutritional screening:
BMI
Weight loss
acute disease effect
add scores
action plan
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9
Q

How is a nutritional assessment done?

A
  • anthropometrics (weight, height, BMI, weight history)
  • biochemistry (pre-existing malnutrition consider evidence of depletion/risk of risk factors)
  • clinical status (diagnosis, medication, will impact nutritional intervention)
  • dietary intake (routes available for feeding, pre-admission nutritional intake, allergies)
  • estimated requirements
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10
Q

How is height measured?

A

surrogate measures - knee height, demispan, ulna length
can be difficult if patient is ill
surrogate measures may overestimate height and so underestimate BMI

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11
Q

What is a demispan?

A

from a point on the midline at their sternal notch to the web between their middle and ring fingers

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12
Q

How is weight measured?

A

difficult to obtain if bedridden unless chair scales or hoist scales
surrogate measures - mid upper arm circumference (measure in supine position)
Can use BMI to estimate weight

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13
Q

What does BMI =?

A

BMI = weight/height^2

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14
Q

What are the ranges for mid upper arm circumference?

A

if <23.5 BMI likely to be <20 = underweight

if >32 BMI likely to be > 30 = overweight

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15
Q

How do you estimate dry weight?

A

Want to take out weight of ascites and peripheral oedema

These weights depend on whether the ascites is tense/moderate/minimal or severe/moderate/mild

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16
Q

What other anthropometric measures are there?

A

Fat mass -> skinfolds (indirectly estimate total adiposity, commonly use triceps site)
Fat free mass -> protein status (arm muscle circumference = mid upper arm circumference - (0.314 X Triceps site)

17
Q

What is the significance of handgrip dynamometry or grip strength?

A

measures muscles strength and endurance
predictor of mortality
can be measured supine or sitting, dominant or non-dominant side, repeated measures

18
Q

What is albumin?

A
large protein synthesised in the liver
most abundant protein in plasma 
trapped within capillaries usually
normal range is 35-50g/l
function is to maintain oncotic pressure (osmotic effect which helps to stop water leaking out through capillary walls)
19
Q

What are some causes of hypalbuminaemia?

A
  • low albumin arises because of inadequate protein intake
  • inflammation and sepsis associated with infection as increased C reactive protein, WBC = pyrexia
  • capillary walls become more porous and albumin drifts out = low plasma albumin
20
Q

How is albumin relevant to nutrition?

A

good prognostic indicator of mortality risk
albumin levels should normalise over a few weeks as inflammation falls
causes of low albumin should be sought and treated, don’t just assume poor protein intake
- low albumin often occurs in sick/malnourished patients but not caused by poor intake but infection and C reactive protein increase

21
Q

What is refeeding syndrome?

A

potentially fatal condition characterised by severe fluid and electrolyte shifts and related metabolic implications in malnourished patients undergoing refeeding

22
Q

What levels change during starvation?

A

glucagon levels rise
insulin falls
glycogen used up in first 24-72 hours
shift to protein for energy
fatty acids metabolised to produce ketone bodies which become a major source
loss of fat and lean body mass, water and minerals
intracellular stores of potassium, phosphate and magnesium become depleted

23
Q

How do levels change during refeeding?

A

change from fatty acids to carbohydrates
raised insulin secretion
stimulation of potassium, phosphate, magnesium to return to cells
intracellular stores replenished but at expense of plasma concentrations

24
Q

What are the clinical consequences of hypophosphatemia?

A

neurological - seizures, paraesthesia
musculoskeletal - rhabdomyolysis, weakness, osteomalacia
respiratory - impaired resp muscle function
cardiac - failure
renal - rhabdomyolysis, fluid and salt retention

25
What are the clinical consequences of hypomagnesaemia?
neurological - tetany, paraesthesia, seizures, ataxia, tremor cardiac - arrhythmias gastrointestinal - anorexia, abdominal pain
26
What are the clinical consequences of hypokalaemia?
``` neurological - paralysis, paraesthesia musculoskeletal - rhabdomyolysis respiratory - respiratory depression cardiac - arrhythmias, cardiac arrest gastrointestinal - constipation, paralytic ileus ```
27
Who is at risk of refeeding syndrome?
Risk - any patient with very little food intake > 5 days High risk - BMI <16, little/no nutritional intake for more than 10 days, low K/PO/Mg levels prior to feeding, unintentional weight loss >15% in last 3-6 months High risk if 2 of following - BMI <18.5, >10 unintentional weight loss in last 3-6 months, little/no nutrition for more than 5 days, history of alcohol abuse or drug use including chemotherapy, antacids or diuretics
28
Why should nutrition support be provided?
Maintain nutritional status and limit catabolism Preserve lean body mass maintain immune function preserve organ function and promote wound healing enhance recovery and improve patient outcomes
29
What are the 2 main routes for nutrition support?
Enteral - oral, nasogastric, orogastric, nasojejunal, gastrostomy, jejunostomy Parenteral - peripheral, central
30
When should enteral tube nutrition be used?
insufficient oral intake but gut function is fine
31
When should parenteral nutrition be used?
GIT unable to digest/absorb adequate amount of nutrients (short bowel syndrome, ileus, motility disorders, GI ischemia, bowel perforation, radiation enteritis, pancreatitis) GIT cannot be accessed (obstruction, enterocutaneous fistulae, severe inflammatory bowel disease)
32
What are the disadvantages of parenteral nutrition?
- risk associated with placement - risk of catheter related sepsis - disorder liver function - risk of gut atrophy - psychological - cost
33
What is the mechanism of refeeding syndrome?
Starvation/malnutrition -> glycogenolysis/gluconeogenesis and protein catabolism -> protein/fat/mineral/electrolyte/vitamin depletion = salt and water intolerance -> switch to anabolism (refeeding) -> fluid/salts/nutrients -> insulin secreted -> increase in protein and glycogen synthesis/glucose uptake/thiamine utilisation/potassium, magnesium, phosphate uptake and use -> hypokalaemia, hypomagnesaemia, hypophosphataemia, thiamine deficiency, salt and water retention (oedema) -> refeeding syndrome