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BRS 11 Gastroenterology > 1b Malnutrition > Flashcards

1b Malnutrition Flashcards

1
Q

What is meant by malnutrition?

A

A state in which deficiency, excess or imbalance, of energy, protein or other nutrients, results in a measurable adverse effect on body composition, function and clinical outcome.

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2
Q

Which demographic is malnutrition most common in?

A

Older females, white

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3
Q

Which groups are at the highest risk of malnutrition?

A

Over 65 over, alcohol or drug dependency or chronic progressive disease are at the highest risk of malnutrition

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4
Q

What are the three broad categories of causes of malnutrition?

A

Reduced intake
Maldigestion / malabsorption
Altered metabolism

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5
Q

What is disease related anorexia?

A

Disease = upregulation of pro-inflammatory cytokines which upregulate anorectic cytokines and reduce appetite

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6
Q

What are causes of maldigestion / malabsorption in the hospital?

A

Function
Length
Losses
Drug-nutrient interactions

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7
Q

Describe the changes in altered metabolism over the course of a hospital stay?

A

Initially = hypometabolism

Then increases to hypermetabolism

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8
Q

What is the impact of malnutrition ?

A

Physical and functional decline and poorer clinical outcomes

↑ Mortality, septic and post surgical complications, length of hospital-stay, pressure sores, re-admissions, dependency

↓ Wound healing, response to treatment, rehabilitation potential, quality of life

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9
Q

What is the MUST?

A

Malnutrition Universal Screening Tool - used to idenfity risk, not assessment or diagnosis

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10
Q

What are the three stages of diagnosing malnutrition?

A

Screen -> Assess (dietician collects information to determine the nature and cause of the nutrient imbalance) -> Diagnose

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11
Q

What are some of the factors which dieticians might assess?

A

Anthropometry
Body composition
Function
Biochemistry
Clinical
Dietary What a
Social Wat
Physical
Requirements

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12
Q

What are the factors which contribute to MUST?

A

Malnutrition universal screening tool (MUST) based on BMI, unplanned weight loss and presence of acute disease.
Categorises individuals as being at low, medium and high risk

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13
Q

What are the requirements for being malnourished?

A

BMI < 18.5 kg/m2 or

Unintentional weight loss >10 % past 3 - 6 / 12 or

BMI < 20 kg/m2 + unintentional weight loss > 5 % past 3 – 6 / 12.

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14
Q

What are the requirements for being at risk of malnourishment?

A

Have eaten little or nothing for > 5 days and / or are likely to eat little or nothing for the next 5 days or longer or

Have a poor absorptive capacity, and / or have high nutrient losses and/or have increased nutritional needs from causes such as catabolism.

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15
Q

How is the treatment of malnutrition established?

A

Ir oral nutrition safe and possible? - if yes then nutritional support, if no -> then artificial nutrition

If GI tract is functional and accessible, then Enteral tube feeding, if not, then parenteral nutrition

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16
Q

What are the nutritional options available via the oral route?

A

Fortification of meals and snacks
Altered meal patterns
Practical support
Oral nutritional supplements (ONS)
Tailored dietary counselling

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17
Q

Which patients are considered for oral nutritional support?

A

Consider for any patient with inadequate food and fluid intakes to meet requirements, unless they cannot swallow safely, have inadequate gastrointestinal function or if no benefit is anticipated e.g. end of life care.

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18
Q

Q. What is artificial nutrition support?

A

A. The provision of enteral or parenteral nutrients to treat or prevent malnutrition.

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19
Q

Which nutritional support is preferred, enteral nutrition and parenteral nutrition?

A

Enteral nutrition (EN) is superior to parenteral nutrition (PN)

20
Q

How to decide which enteral nutrition to use? Access

A

Is gastric feeding possible?

Yes = Naso-gastric tube (NGT)
No = Naso-duodenal (NDT) / naso-jejunal tube (NJT)

Long term (> 3 months) = Gastrostomy / jejunostomy

21
Q

What is in the nutritional feeds which are fed via the enteral route?

A

Nutritional feeds → renal, low sodium, respiratory, immune, elemental, peptide.

22
Q

What would you do with a patient who has a gastric outlet obstruction?

A

Gastric outlet obstruction = NGT feeding contraindicated → NJT

23
Q

What are the complications associated with enteral feeding?

A

Mechanical: misplacement, blockage, buried bumper

Metabolic: hypergylcaemia, deranged electrolytes

GI: Aspiration, nasopharyngeal pain, laryngeal ulceration, vomiting, diarrhoea.

24
Q

How to determine if NGT is misplaced?

A

Aspirate pH -> 5.5
If pH > 5.5 → chest x-ray, interpreted by trained professional following NPSA guidelines.

if pH if less than 5.5, then it means the tube is in the stomach

25
Q

What is parenteral nutrition?

A

Parenteral nutrition (PN): The delivery of nutrients, electrolytes and fluid directly into venous blood.

26
Q

What are the indications for parenteral?

A

Indications:

An inadequate or unsafe oral and/or enteral nutritional intake

OR

A non-functioning, inaccessible or perforated gastrointestinal tract

27
Q

What is the composition for parenteral?

A

Ready made / bespoke “scratch” bags.

MDT → fluid and electrolyte targets

28
Q

What is the access point for parenteral nutrition?

A

Central venous catheter (CVC): tip at superior vena cava and right atrium.

29
Q

What are the mechanical complications of parenteral nutrition?

A

Pneumothorax, haemothorax, thrombosis, cardiac arrhythmias, thrombus, catheter occlusion, thrombophlebitis, extravasion

30
Q

what are the metabolic complications associated with parenteral nutrition?

A

Deranged electrolytes, hyperglycaemia, abnormal liver enzymes, oedema, hypertriglyceridaemia

31
Q

What is the most common complication associated with parenteral nutrition?

A

Catheter related infections

32
Q

What is albumin and how does it relate to inflammation?

A

Albumin is synthesized in the liver, when it is low, there is a poor prognosis

Low albumin during inflammation

33
Q

What type of protein is albumin?

A

negative acute phase protein

34
Q

Outline the acute phase response and relate it to albumin.

A

The acute phase response.

Inflammatory stimulus → activation of monocytes & macrophages → release cytokines.

Cytokines act on liver to stimulate synthesis of some proteins e.g. c-reactive protein, whilst downregulating production of others e.g. albumin.

35
Q

Which cytokines are activated in the inflammatory state?

A

IL-1, IL-6, TNF-alpha, IFN-gamma, TGF-B

36
Q

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

A

No. Albumin synthesis ↓es in response to inflammation ∴ poor predictor of malnutrition during acute phase. However, do consider the aetiology / impact of the inflammatory response on nutrition status.

37
Q

What is refeeding syndrome?

A

A group of biochemical shifts & clinical symptoms that can occur in the malnourished or starved individual on the reintroduction of oral, enteral or parenteral nutrition.

38
Q

What are the consequences of refeeding syndrome?

A

Arrhythmia, tachycardia, CHF → Cardiac arrest, sudden death
Respiratory depression
Encephalopathy, coma, seizures, rhabdomyolysis,
Wernicke’s encephalopy

39
Q

Which patients are at risk of refeeding syndrome?

A
  • Little or no nutritional intake in recent past
  • Significant weight loss
  • Low BMI<18.5kg/m2
  • Electrolyte disturbance prior to feeding
  • History of alcohol or drug abuse
40
Q

Outline the pathogenesis of refeeding syndrome?

A
  1. Starving / malnutrition -> leads to glycogenolysis, gluconeogenesis and protein catabolism, downregulation of insulin
  2. This results in protein, fat and mineral depletion

(During starvation, there is an increase in extracellular water, total body water and sodium, and a depletion of total body potassium, magnesium and phosphate. Serum concentrations of these electrolytes are maintained whilst intracellular stores are depleted)

  1. Refeeding

The introduction of carbohydrate results in the secretion of insulin, stimulating the sodium-potassium ATPase pump, requiring magnesium as a co-factor. This drives potassium into cells and sodium and fluid out of cells into the extracellular space. The carbohydrate and insulin secretion drives phosphate into cells as it’s required for energy storage as ATP. This results in an increased cellular uptake of glucose, potassium, magnesium and phosphate, and a subsequent reduction in extracellular concentrations.

hence:

Hypokalaemia
Hypomagnesaemia
Thiamine deficiency
Salt and water retention = odema

41
Q

Who is at extremely high risk of refeeding syndrome?

A

BMI < 14 kg/m2
Negligible intake > 15 days

42
Q

Outline the management of refeeding syndrome?

A
  1. Start with 10-20 cals a kg
  2. Collect and monitor electrolytes daily following trust policy
  3. Administer thiamine from the onset of feeding
  4. Monitor fluid shifts and minimise risk of fluid and Na+ overload
43
Q

Outline feeding mode for patient with acute pancreatitis

A

ENTERAL- supports the functional and structural integrity of the gut, modulates immune system and attenuated disease severity

In pancreatitis, not only is enteral feeding possible but superior and preferred route of feeding

44
Q

If gastric residual volumes are trending upwards, how should feeding mode be changed?

A

Can start prokinetics

if duodenal stenosis—> NJT

45
Q

How are patients with dementia treated?

A

Parenteral - NG tube is contraindicated with severe dementia due to distress - they might pull it out due to being confused
Also patient is at risk of aspiration - refer to speech and language therapist

46
Q

What is the difference between clear and free fluids?

A

Clear = easy to digest and doesn’t leave bits in the digestive tract, water, tea, broth, and gelatin

free = any fluid which can be drunk through a straw,

BRS 11 Gastroenterology (25 decks)

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