Malnutrition Flashcards

(49 cards)

1
Q

define malnutrition

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

describe the prevalence of malnutrition by age, sex and hospital ward

A

more common in women than men especially in older age groups

most common in oldest and youngest age groups (18-19 and 90+)

most common in care of elderly and oncology

more common in those with gastrointestinal disease compared to cardio, resp and msk

generally - people over 65 especially if they have been admitted to hospital, people with chronic conditions (diabetes, lung disease, kidney disease) + chronic progressive diseases (cancer, dementia), people who abuse drugs or alcohol, people with any GI dysfunction

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3
Q

compared malnutrition in community vs in hospital

A

1 in 3 admitted to hospital were malnourished on admission → suggests that majority originates in community

but malnutrition is unrecognised and undiagnosed in the acute setting → 70% of patients lost weight (mainly muscle mass) at discharge and the most vulnerable are those who came in malnourished

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4
Q

what makes people in hospital particularly vulnerable to malnutrition

A

disease related anorexia - loss of appetite due to pathophysiological mechanisms + disruption of central regulation feeding behaviour

patients consume less than 80% of food on plate in hospital

belief that it is normal for appetite to decrease in hospital → held especially by older patients

belief by patient + staff that medical treatment is more important than food

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5
Q

what is the paradox of the body response to injury

A

metabolic response to breakdown particularly proteins into substrates necessary for survival e.g. for immune system + tissue repair

but this metabolic response can then threaten survival in extreme cases e.g. due malnutrition + loss of muscle mass it causes

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6
Q

how is malnutrition related to being acutely unwell

A

disease related anorexia - loss of appetite due to pathophysiological mechanisms + disruption of central regulation feeding behaviour

body’s response to stress → muscle breakdown into AA for gluconeogenesis + protein synthesis to supply immune response and tissue repair

increased demand for energy, protein + micronutrients → largest demand is for protein

patients who already are malnourished then become acutely unwell as they have less kilocalorie reserve to face illness

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7
Q

how does malnutrition affect clinical outcomes

A

causes physical and functional decline + worsens clinical outcomes

post operative mortality is 10x greater in people who have lost over 20% of bodyweight preoperatively

inadequate muscle tissue → unable to mobilise adequate amounts of endogenous nitrogen in response to stress → greater morbidity compared to those who have sufficient muscle tissue

people in england + wales still dying in hospital from malnutrition as the primary cause

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8
Q

how much does malnutrition cost the NHS

A

£19.6 billion per year

costs for malnourished patient x3 than well nourished

majority of cost is in secondary care

costs will rise in future as population ages

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9
Q

how is malnutrition diagnosed

A

screening → assess by dietician → diagnose

screen using MUST - used in community + hospital, based on BMI, unplanned weight loss + acute disease, categorises in low, medium + high risk of malnutrition
has to be done within 6 hours of hospital admission and every week thereafter
can miss malnourished clinical populations → especially where overhydration is common e.g. ascites

ASSESS:

dietician - defines nutrition status
anthropometry - physical measurements of body compartments e.g height, weight, mid arm muscle circumference

biochemistry → used to estimate nutrient availability in tissue and fluid to assess for deficiencies
testing for trace elements + micronutrients is expensive → needs justification
results can be skewed due to inflammatory response so not measure until CRP is below 10, results are monitored intensely in parenteral nutrition

history → drug + alcohol, diet, metabolic needs, nutritional loss, chronic disease, major surgery or illness, GI tract surgery, medication
nutrition history - anorexia, loss of taste or smell, excessive alcohol, poor fitting dentures, chewing or swallowing problems, fad diets, allergy, dietary restriction
dietary history - food intake
social history - socioeconomic status, living alone,

indirect calorimetry - most reliable measure of energy expenditure + guide energy prescription → measures resting metabolic rate using respirator gas exchange canopy (not used in clinical practice) so equations are used in clinical practice to determine estimated energy requirement

DIAGNOSE:

based on the dietitian assessment of nutritional status
create plan → implement it → monitor → evaluate

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10
Q

what are the limitations of BMI

what are the impacts of these

A

impact of gender, age ,e thnicity is ignored

cannot distinguish between fat mass and fat free mass

has minimal significance is dietetic assessment unless it is very low

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11
Q

what does recent unexplained weight loss specifically suggest in regards to body reserves

A

muscle loss and therefore protein loss

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12
Q

what are the anthropometric measurements carried out by dietician during malnutrition diagnosis

what do they indicate

A

anthropometry - measures body different compartments as they are affected differently by malnutrition

weight - recent unplanned weight loss reflects changes in energy protein status → impacts morbidity and mortality

BMI - has low significance due to its limitations unless very low

mid upper arm circumference and tricep skin fold thickness → used to calculate mid arm muscle circumference → used to assess lean body mass → associated with length of hospital stay and functional ability

multi-frequency bioelectrical impedance analysis - used in renal and haematology patients

CT - muscle distribution + composition, differentiate between visceral + subcutaneous fat, assess levels of fat and fat free mass very accurately (but expensive + radiation exposure so assess body composition mainly in research or when CT is part of clinical treatment pathway already)

hand grip strength → reflects upper extremity muscle strength → responds earlier to nutritional deprivation and repletion than other measurements e.g. muscle or body mass → the muscle strength can predict mortality and morbidity independent of muscle mass (reduced mortality for every 1kg increase in hand grip strength)

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13
Q

define estimated energy requirement

how is it determined

how is it used

A

average dietary energy intake predicted to maintain energy balance in an adult of defined age, gender, weight, height and level of physical activity

related to resting metabolic rate (but this is energy expended at rest)

using predictive equations - but have limited use in practice and have maximum accuracy of 70%

used as starting point to determine baseline set of energy requirements that patient has

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14
Q

what are the criteria for nutritional support

A
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15
Q

what is artificial nutrition support

A

provision of enteral or parenteral nutrients to treat or prevent malnutrition

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16
Q

what are the considerations when starting/stopping artificial support

A

feeding route:
oral is best → then enteral → parenteral

always need continued monitoring + evaluation of nutrition route
change or reconsider number of feeding routes if nutritional intake is sub optimal or long term feeding is required

starting and stopping requires ethical and legal considerations

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17
Q

what is enteral artificial feeding

how is it done

A

delivering directly nutrition to stomach or small intestine

naso-gastric tube is first line = NG tube

if naso-gsastric tube is contraindicated e.g. if gastric outlet is obstructed → so tube needs to be distal to stomach

then naso-duodenal (NDT) or jejunal tube (NJT) is used

long term >3 months = gastrostomy or jejunostomy (tube inserted into stomach or jejunum through abdomen)

nutritional feeds that can be used - renal, low sodium, respiratory, immune, elemental, peptide

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18
Q

how do the feeding routes for artificial nutrition compare to each other

A

oral is the best

enteral is superior to parenteral

when parenteral feeding is used, the aim is to move to enteral and then oral feeding as soon as clinically possible

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19
Q

what are the complications of enteral nutrition

A

mechanical - misplacement of tube, blockage of tube, buried bumper - part of gastronomy tube becomes lodged in gastric wall

metabolic - hyperglycaemia, deranged electrolytes

GI - aspiration, nasopharyngeal pain, laryngeal ulceration, vomiting, diarrhoea

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20
Q

what do you have to do to make sure NGT is in correct place

A

aspirate the contents

if the pH is <5.5 that indicates it is in the stomach as this pH is not found anywhere else in the body

if pH >5.5 then a chest x ray needs to be done and interpreted by professional

21
Q

what is parenteral nutrition

when is it used

A

delivering of fluids, electrolytes and nutrients directly into venous blood

when there is inadequate oral and or enteral nutritional intake

or

when there is a non-functioning, inaccessible or perforated GI tract

22
Q

where is parenteral nutrition inserted

A

using central venous catheter

centrally inserted into jugular, subclavian or femoral veins to reach the tip of of superior vena cava

or can be peripherally inserted via antecubital fossa to reach tip of superior vena cava

different central venous catheters are used depending on length of nutrition

23
Q

what are the contents of parenteral nutrition

A

will either use ready made/bespoke “scratch” bag

dietician liaises with MDT to determine fluid and electrolyte targets for each day

24
Q

what are the complications of parenteral nutrition

A

mechanical - occur when CVC is inserted, pneumothorax, haemothorax, thrombosis, cardiac arrhythmias, thrombus, catheter occlusion, thrombophlebitis (vein inflammation due to clot), extravasation (leakage of fluid around site)

metabolic - occur once feeding has started, deranged electrolytes, hyperglycaemia, abnormal LFTs, oedema hypertriglyceridemia

catheter related infections - intravascular catheters are one of the main sources of bacteraemia and septicaemia in hospitalised patients, need to keep monitoring to try and prevent these and also remember to switch to enteral when possible, assess patient using nutritional support MDT

25
does nutritional support actually benefit malnourished patients
strong evidence base for yes malnourished patients who receive nutritional support have lower mortality than ones who don't support decreases non-elective hospital admissions, increases energy+ protein intake and weight gain patients at risk of malnutrition who are given individualised nutrition support have better outcomes than those who are given standard hospital diet and no nutrition intervention
26
what is the most abundant circulating protein in healthy people
albumin 10-15g produced by hepatocytes everyday
27
what predictive effect does albumin have why
low plasma albumin = marker of poor prognosis albumin production is inhibited by pro-inflammatory cytokines e.g. IL-6, TNF → therefore is a negative acute phase protein → levels decrease as inflammation increases also in the acute inflammatory state there is increased degradation and transcapillary losses of albumin
28
how does albumin impact the nutrition status or nutritional support for patient
it doesn't → albumin is not valid marker of nutrition status nor is it an indication for nutritional support albumin is negative acute phase protein → its levels in plasma decrease in response to inflammation dietician will focus on the impact of the inflammatory state on the nutrition status evidence for this is hypoalbuminemia in obese trauma patients → they are not malnourished but their albumin is low due to the inflammation from their trauma
29
what is the body's response to starvation
starvation → reduced insulin secretion, increase in glucagon → gluconeogenesis from AA in muscle and glycogenolysis from liver stores → stores depleted within 24-72 hours → shift to produce energy from ketone production from FFA from lipid stores → FFAs used instead of AA to spare skeletal muscle breakdown → fat free mass is preserved to an extent → decrease in BMR → brain uses ketones over glucose → loss of fat mass action of cellular pumps is reduced to decrease energy expenditure → electrolytes can leak across cell membrane during starvation: increase in extracellular water, total body water and sodium depletion in total body potassium, magnesium and phosphate → serum concentrations of these are maintained but the intracellular stores are depleted Na+ and fluid leak into cells → Na+ and fluid intolerance micronutrient stores become depleted → thiamine deficiency is likely as its stores are limited + its water soluble
30
what effect does carbohydrate introduction have on the body during starvation
insulin secretion → stimulates action of Na+K+ ATPase pump which requires Mg2+ as a co-factor → drives K+ into cells and Na+ out carbohydrate + insulin drive phosphate into cells as it is need to make ATP there is increased cellular uptake of glucose, K+, Mg2+ and phosphate → therefore a decrease in the extracellular concs of glucose, K+ Mg2+ and phosphate thiamine is co enzyme needed for carbohydrate metabolism → therefore deficiency of thiamine can occur on refeeding in a vitamin B depleted patient carbohydrate also reduces Na+ and fluid excretion → expansion of extracellular fluid compartment → refeeding oedema and fluid overload therefore refeeding syndrome
31
what are the main features of refeeding syndrome
hypokalemia - low K+ hypomagnesaemia - low Mg2+ hypophosphatemia - low Phosphate thiamine deficiency Na+ and water retention → fluid overload and refeeding edema due to the shift from catabolic to anabolic reactions when carbohydrate is reintroduced after starvation
31
what are the main features of refeeding syndrome
hypokalemia - low K+ hypomagnesaemia - low Mg2+ hypophosphatemia - low Phosphate thiamine deficiency Na+ and water retention → fluid overload and refeeding edema due to the shift from catabolic to anabolic reactions when carbohydrate is reintroduced after starvation
32
what are the clinical consequences of refeeding syndrome
arrythmia, tachycardia, congestive heart failure → cardiac arrest and sudden death respiratory depression (hypoventilation) encephalopathy - dmage to brain rhabdomyolysis - breakdown of skeletal muscle coma seizures wernicke's encephalopathy - specific to thiamine deficiency, characteristic symptoms are ataxia, confusion, ophthalmoplegia (paralysis/weakness of extraocular muscles)
33
who is at risk of refeeding syndrome
34
what impact do drugs given on ICU have on nutrition
35
why would gastric residual volume be monitored in patient on ICU
to see if gastric motility is still effective → stomach is able to empty if secretions build up then patient is at risk of ulcers atracurium is paralysing agent given to patients on ventilator → but it often decreases gastric motility
36
what is given to patient with past alcohol or drug abuse why
IV pabrinex - corrects nutritional deficiencies, specifically replaces thiamine thiamine is likely to be low already in patients with history of drug and alcohol abuse
37
what route of feeding would be best for patient with acute pancreatitis being ventilated on ICU why
oral nutrition is not appropriate enteral nutrition as it is superior to parenteral because: maintains gut stability attenuates disease severity the feed will be peptide based and high ratio of medium chain triglycerides → not reliant on proteases or lipases for absorption
38
what happens if an acute pancreatitis patient is not tolerating enteral nutrition what would this look like
diarrhoea and steatorrhea (pancreatic enzymes could be added to feed to see if this improves) start parenteral nutrition and reduce enteral feeding to ta trophic minimal rate → maintains gut integrity as it stimulates the gut to prevent bacterial translocation and gut leakiness which can exacerbate the pancreatitis
39
what indicator would first suggest that patient is receiving adequate nutrition and is improving
better hand grip strength → indicates better muscle functioning → indicates adequate nutritional support
40
what is short bowel syndrome
intestinal failure where you are unable to maintain protein-energy, fluid, electrolyte or micronutrient balance on a conventionally accepted normal diet results from surgical resection, congenital defect or disease related loss of absorption defined as having less than 2m of bowel from the duodenal jejunal flexure
41
why do the effects of small bowel resection vary between patients
depends on the type, length and quality of small bowel left and whether or not they still have colon most absorption happens in jejunum, apart from vitamin B12 and bile salts which are absorbed in the ileum presence of colon is important because it can absorb , water, Na+ and fatty acids and slows intestinal transit → further aids absorption when colon + ileum is not present e.g. in jejunostomy → large amounts of fluid and electrolytes are lost and small bowel transit is very fast the length of jejunum left determines whether nutrition can be supported by diet alone: \<100 cm of jejunum left = long term IV fluid and electrolytes \<75cm jejunum = long term parenteral nutrition, fluid + electrolytes \<50cm jejunum + colon = long term parenteral nutrition, fluid + electrolytes
42
how do the losses between jejunostomy and jejunocolic anastomosis compare
jejunocolic lose much less fluid and electrolytes as they are able to resorb much more as colon is present and it slows down small intestinal transit to all further reabsorption in jejunum there are significant intestinal losses in jejunostomy and small bowel transit is very fast
43
how is high stomal loss managed
fluid restriction → hypotonic solutions e.g. water, alcohol, tea, coffee will cause net influx of Na+ from plasma into gut lumen due to the large concentration gradient between the lumen and the blood, water will follow Na+ → therefore a high stoma output also should reduce hypertonic fluids which contain sorbitol e.g. juice, coca cola and this high concentration induces secretions from enterocytes in order to dilute them give oral rehydration solution: Na+ concentration = 90mmol/l glucose concentration = 111mmol/l No K+ SGLT1 transport will co transport glucose and Na+ across apical membrane Na+ then actively pumped across basolateral membrane into blood via Na/K+ ATPAse H2O follows Na+ large amounts of Na+ and H2O reabsorbed → much lower stomal losses → prevents dehydration
44
if gastric residual volumes in patient on ventilator continue to increase what do you do
prescribe pro-kinetics to increase gastric motility if it doesn't start decreasing investigate where there is an obstruction or stenosis lower down if there is change from naso gastric to naso jejunal tube
45
how are the energy requirements for a patient in intensive care calculated
penn state equation gender, age, height specific includes clinical parameters specific to ICU e.g. temperature and ventilation settings
46
how would a increase in lean body mass be evidenced in patient
increase in hand grip strength increase mid arm muscle circumference
47
what urinary sodium indicates dehydration why would this be measured
\< 20mmol/l earlier indication of dehydration as it falls faster than plasma sodium
48
what are the key features of diet in jejunostomy patient
fluid restriction → to prevent dehydrated add Na+, higher content of fatty acids, higher calorific content than required by body → no colon so there is reduced absorption of Na+ and fatty acids and faster transit low fibre → anecdotally reduces intestinal secretions