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BRS Year 2 > malnutrition > Flashcards

malnutrition Flashcards

1
Q

when is oral feeding not advised

A

cognitive impairment

Dysphasia

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2
Q

Types of oral feeeing

A

By mouth

Normal food, softened food, thickened foods, puréed, fluids etc

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3
Q

What is first line enteral feeding

A

nasogastric tube

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4
Q

Complications of NG tubes

A 
Tube misplacement
Obstruction 
Electrolyte imbalance 
Hyperglycaemia 
Aspiration pneumonia!
Larynx ulceration, pharyngeal pain
Vomiting and diarrhoea
Line infections
Refeeding syndrome
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5
Q

How is parenteral nutrition done

A

Via central venous catheter

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6
Q

Difference between feeding or parenteral and enteral

A

Enteral made for patients needs

Parenteral from scratch bag

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7
Q

Indications for parenteral feeding

A

Where oral enteral unsafe

Or GI inaccessible or cannot function

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8
Q

How to testif enteral feed misplaced

A

pH shouldn’t be over 5.5

If over, immediate imaging to find it

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9
Q

What is refeeding syndrome

A

starvation for long time
if reintroduced to nutrients, surge in insulin
Encourages cells to take up potassium magnesium and phosphate which are already low in serum (and get lower) causing electrolyte imbalances
A causes arrhythmias, respiratory arrest, multi organ failure

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10
Q

definition of malnutrition

A

state resulting from lack of uptake/intake of nutrition leading to diminished physical and mental function and impaired clinical outcome from disease

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11
Q

rate of malnourishment upon admission to hospital

A

1 in 3 are manourished

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12
Q

what % of patients have lost weight at discharge

A

70%

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13
Q

factors that lead to malnutrition in hospitals

A 
co-morbidities e.g. dementia
inflexible mealtimes
quality of food
dysphagia, stomatitis, anaemia, poor dentition, ill fitting dentures
inactivity
low mood/depression
polypharmacy
excess nutritional losses
repeated NBM status
metabolic response to disease/injury
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14
Q

loss of what % of bodyweight preoperatively leads to 10x greater postop mortality?

A

> =20%

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15
Q

what increases with malnutrition?

A 
mortality
septic and post surgical complications
length of hospital stay
pressure sores
readmissions
dependency
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16
Q

what decreases with malnutrition?

A

wound healing
response to treatment
rehabilitation
QoL

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17
Q

CT advantages in formal nutrition assessment

A

provide info about body composition

-> however involves exposing patient to radiation

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18
Q

Why is BMI not used to assess malnutrition?

A

not representative of difference between fat and fat free mass

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19
Q

skin fold thicknesses used for malnutrition assessment

A
  • triceps skinfold thickness

- mid upper arm circumference use similarly to determine lean body mass (positive association)

20
Q

anthropometric analysis multifrequency bioelectrical impedance analysis used in which patients?

A

renal and haematology patients

21
Q

what type of fat can CT scans distinguish between?

A

visceral and subcutaneous fat

-> highly accurate for evaluating levels of fat and fat free mass

22
Q

problems with CT for nutritional assessment

A

expensive, expose individuals to small amounts of radiation
-> use for body comp restricted to research normally

-> being used more frequently in specialities where CTs are already part of the clinical treatment pathway

23
Q

why are micronutrient and trace elements tests not undertaken easily?

A

time consuming
expensive
results skewed as a result of the acute inflammatory response

24
Q

best way of obtaining dietary intake information

A

dietary history

25
Q

what is used to estimate energy requirement

A

predictive equations estimating resting MBR

-> generally no more accurate than 70%

26
Q

requirements to be malnourised

A
  • BMI < 18.5
  • unintentional weight loss >10% past 3-6/`1
  • BMI <20 + unintentional weight loss > 5% past 3-6/12
27
Q

people at risk of malnutrition

A

eaten little/nothing > 5 days and likely to have the same for the next 5
- poor absorptive capacity/high nutrient losses/increased nutritional needs

28
Q

Feeding options when oral nutrition isn’t safe

A 
enteral feeding (GI tract functional + accessible)
parenteral feeding (GI tract not functional/accessible)
29
Q

why is enteral nutritional superior to parentral?

A

it uses the gut

-> if parenteral used, aim to return to enteral then oral feeding as soon as/where clinically possible

30
Q

what is recommended from longer term enteral tube feeding (>3 months)

A

gastrostomy/jejunostomy

31
Q

what are the complications associated with enteral feeding?

A
  • misplaced NGTs cause death
  • mechanical (misplacement, blockage, buried bumper)
  • metabolic (hyperglycaemia), deranged electrolytes)
  • aspiration, nasopharyngeal pain, laryngeal ulceration, vomiting, diarrhoea
32
Q

indication for parenteral nutrition

A
  • inadequate or unsafe oral and/or enteral nutritional intake
    OR
  • non-functioning, inaccessible or perforated GI tract
33
Q

access points for CVCs?

A

tip at superior vena cava and right atrium-> different CVCs for short ad long term use

34
Q

complications associated with parenteral nutrition?

A

mechanical (pneumothorax, haemothorax, cardiac arrhythmias, thrombosis, catheter occlusion, extravasion)
metabolic (deranged electrolytes, hyperglycaemia, abnormal liver, enzymes, oedema, hypertriglyceridemia)

catheter-related infection

35
Q

low levels of what plasma proteins predicts poor prognosis?

A

albumin

36
Q

how does the acute phase response affect albumin production?

A

inflammatory stimulus -> activation of monocytes and macrophages -> release of cytokines

cytokines act on the liver to stimulate production of some proteins whilst downregulating production of others like albumin

37
Q

is albumin a valid marker of malnutrition in the acute hospital setting?

A

no
- though decreased in repsonse to inflammation, not marker of nutrition status nor indication for nutrition intervention in the acute setting

  • best evidence - hypoalbuminaemia in obese trauma patients
  • dietitian focused on the etiology/impact of the inflammatory state on nutrition status
38
Q

how does introduction of carbohydrate affect the response to starvation? refeeding

A

stimulates insulin production -> Na/K ATPase (Mg cofactor)
drives K into cells and Na out of cells
carbohydrate and insulin drives PO4 into cells
- increased cellular uptake of glucose, K, Mg and phosphate
- thiamine is coenzyme for carb digestion -> deficiency occur in refeeding of vit B depleted patient

39
Q

what can low concentrations of electrolytes from giving a starving person carbs cause?

A
  • less Na and fluid excretion = expansion extracellular fluid compartment –> this leads to refeeding oedema
40
Q

consequences of RFS?

A
  • arrhythmia
  • CHF -> cardiac arrest + sudden death
  • tachycardia
  • respiratory depression
  • encephalopathy, coma, seizures, rhabdomyolysis
  • Wernickes encephalopathy
41
Q

what are the the criteria for defining at risk of refeeding syndrome

A

very little or no food intake for > 5 days

42
Q

stages of RFS management

A
  1. start with 10/20kcal/kg
    CHO 40-50% energy and micronutrients
  2. correct + monitor electrolytes daily
  3. Administer thiamine from the onset of feeding
  4. Monitor fluid shifts + minimise risk of fluid/Na overload
43
Q

whole process of nutrition in hospital

A

screening
assessment
diagnosis
plan - implement, monitor, evaluate

44
Q

example of when NGT is contraindicated?

A

gastric outlet obstruction

go straight to ND/NJT

45
Q

composition of paraenteral nutrition feeds

A

ready made scratch bags

46
Q

what is short bowel syndrome

A

surgical resection or congenital defect/loss of absorption in bowel
characterised by inability to maintain energy, fluid, electrolyte or micronutrient balances when on a normal diet

BRS Year 2 (67 decks)

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