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1B Gastroenterology > Malnutrition > Flashcards

Malnutrition Flashcards

1
Q

what is malnutrition?

A

a state resulting from lack of uptake or intake of nutrition

leading to altered body composition and body cell mass

leading to diminished physical and mental function and impaired clinical outcome from disease

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2
Q

where is the highest prevalence of malnutrition?

A
  • Chronic, progressive conditions
  • Elderly >65 or young
  • 1 in 3 malnourished on admission
  • 70% lost weight at discharge
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3
Q

what are the impacts of malnutrition?

A
  • Increased:
    • Mortality
    • Septic and post-surgical complications
    • Length hospital stay
    • Pressure sores
    • Readmission
    • Dependency
    • cost
  • Decreased:
    • Wound healing
    • Response to treatment
    • Rehabilitation potential
    • Quality of life
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4
Q

who should nutrition support be considered in?

A
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5
Q

what is considered as malnourished?

A
  1. BMI <18.5
  2. Unintentional weight loss >10% past 3-6/12
  3. BMI< 20 with unintentional weight loss >5% in past 3-6/12
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6
Q

who is at risk of malnutrition?

A
  1. 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
  2. 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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7
Q

what is artificial nutrition support?

A

provision of enteral or parenteral nutrients to treat or prevent malnutrition

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8
Q

when is parenteral nutrition support used?

A

Oral nutrition not possible/safe and GI tract not functional/accessible

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9
Q

what is the first line of nutrition support if oral not posisble?

A

enteral nutrition-> superior to parenteral

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10
Q

what is the aim with parenteral nutrition?

A

return to enteral -> oral feeding as soon as posisble

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11
Q

what are the options for gastric feeding?

A

if enteral feeding possible:

  • Yes = Naso-gastric tube (NGT)
    • Contraindicated in gastric outlet obstruction.
  • No = Naso-duodenal (NDT) / naso-jejunal tube (NJT)
  • Long term (> 3 months) = Gastrostomy/jejunstomy
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12
Q

what are the complications of gastric feeding?

A

misplaced NGTs

mechanical

metabolic

GI

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13
Q

how do you confirm an NGT is in correct location?

A
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14
Q

what are the mechanical complications of gastric feeding?

A

misplacement

blockage

buried bumper

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15
Q

what are the metabolic complications of gastric feeding?

A

hyperglycemia

deranged electrolytes

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16
Q

what are the GI complications of gastric feeding?

A
  • Aspiration
  • Nasopharyngeal pain
  • Laryngeal ulceration
  • Vomiting
  • Diarrhoea
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17
Q

what is parenteral nutrition?

A

The delivery of nutrients, electrolytes and fluid directly into venous blood

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18
Q

what are the indications for parenteral support?

A
  • An inadequate or unsafe oral and/or enteral nutritional intake
  • OR
  • A non-functioning, inaccessible or perforated gastrointestinal tract
19
Q

how is access obtained for PS?

A
  • Central venous catheter (CVC): tip at superior vena cava and right atrium.
  • Usually through jugular, subclavian or femoral veins or peripherally inserted central catheters inserted from antecubital fossa into central vein (done at bedside)
  • Different CVCs for short / long term use
20
Q

what is the composition for parenteral support?

A
  • Ready made / bespoke “scratch” bags.
  • MDT → fluid and electrolyte targets for the day
21
Q

what are the general categories for complications from PS?

A

mechanical (usually from entering supply)

metabolic (From feed)

catheter-related infection

22
Q

what are the mechanical complications from PS?

A
23
Q

what are the metabolic complications from PS?

A
  • Deranged electrolytes
  • Hyperglycemia
  • Abnormal liver enzymes
  • Oedema
  • Hypertriglyceridemia
24
Q

what are the effects of parenteral nutrition on mortality and readmisison?

A

decreases

25
Q

where is albumin synthesised?

A

liver

26
Q

what is the correlation between albumin and prognosis?

A
  • low plasma albumin = poor prognosis.
  • A negative acute phase protein = ↓ plasma albumin when ↑ inflammation.
27
Q

what is albumin synthesis stimulated by?

A
  • stimulated by hormones such as insulin, cortisol and GH and inhibited by pro-inflammatory such as IL-6 and TNF-alpha
28
Q

what happens in the acute phase response to albumin?

A
  • Inflammatory stimulus → activation of monocytes & macrophages → release cytokines.
  • Cytokines act on liver to stimulate production of some proteins whilst downregulating production of others e.g. albumin.
  • Degradation and transcapillary losses of albumin increase in this state
29
Q

why is albumin not a valid marked of malnutrition in hospital?

A
30
Q

what happens to CRP, SAA, haptoglobin, albumin, transferrin and fibrinogen after an inflammatory stimulus?

A
31
Q

what is refeeding syndrome?

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.
32
Q

what happens during starvation?

A
  • Reduction in insulin secretion
  • Increase in glucagon secretion to produce glucose
  • Glycogen stores in liver and amino acids in skeletal muscle are metabolised into glucose
  • Once stores are depleted (24-72hrs) metabolism shifts to ketone production due to free fatty acids being released from fat stores
  • These are used instead of amino acids
  • This spares skeletal muscle breakdown and fat free mass is preserved
  • Decrease in basal metabolic rate
  • Brain adapts to using ketones
  • Reduction in action of cellular pumps to reduce energy expenditure
  • Electrolytes leak across cell membrane
  • Increase extracellular water, total body water and sodium
  • Decrease in total body potassium, magnesium, phosphate
  • Serum concs maintained while intracellular stores depleted
  • Sodium and fluid lead into cells = sodium and fluid intolerance
  • Micronutrient stores depleted and thiamine deficiency likely as it is water soluble and limited stores
33
Q

what happens on the introduction of carbohydrates during starvation?

A
  • = secretion of insulin stimulated Na/K+ ATPase pump- requiring magnesium as a cofactor
  • This drives K+ into cells and sodium + fluid out of cells into extracellular space
  • Carbohydrate and insulin secretion drives phosphate into cells (required for energy storage as ATP)
  • Increase cellular uptake glucose, K+, magnesium, phosphate = reduction extracellular concs
  • Thiamine is coenzyme in carbohydrate metabolism
    • Deficiency can occur on refeeding in a vit B depleted patient
  • Low conc electrolytes and thiamine= clinical manefestations
  • Carbohydrate reduces Na + fluid excretion = expansion extracellular fluid compartment à refeeding oedema & fluid overload
34
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
35
Q
  • At risk:
    • Very little or no food intake for >5 days
  • High risk
    • >1 of following:
      • BMI<18.5
      • Unintentional weight loss >15% 3-6/12
      • Very little/ no nutrition >10days
      • Low K+, Mg2+, PO4 prior to feeding
    • Or >2 of following
      • BMI<18.5
      • Unintentional weight loss >10% 3-6/12
      • Very little/ no nutrition >5 days
      • PMHx alcohol or drugs (insulin, chemo, antacids, diuretics)
  • Extremely high risk
    • BMI <14
    • Negligible intake >15 days
A
36
Q

what is the management of refeeding syndrome?

A
37
Q

what is atracurium?

A

paralysing agent

decreased energy expenditure and gut motility

38
Q

what is propofol and side effects?

A

sedation/analgesia

risk fat overload

39
Q

what is fentanyl and side effects?

A

analgesia/sedation

constipation, decreased gut motility, gastric emptying

40
Q

what is noradrenaline and side effects?

A

vasoconstrictor/ vasopressor

reduce hepatic, renal and splachnic blood flow= enteral intolerance + gut ischaemia

41
Q

what is insulin and side effects?

A

insulin resistance and hyperglycemia-caution in enteral to avoid hypoglycaemia

42
Q

what is sodium docusate used to treat and cautions?

A

treat constipation

enteral nutrition often causes diarrhoea

43
Q

what is lansoprazole used for and cautions in nutrition support?

A

PPI- stress ulcer prophylaxis

alters pH- NG tube confirmation by pH unreliable

44
Q

what is phenytoin used for and cautions in nutrition support?

A

anticonvulsant

request break from feed for drug absorption enterally

1B Gastroenterology (12 decks)

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