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Y2 S&P - Water & Electrolytes, Cardiovascular, Nutrition, Physiology of infection > Nutrition > Flashcards

Nutrition Flashcards

1
Q

What are the functions of the kidneys?

A

EPO, calcitriol, renin

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2
Q

What happens in CKD?

A
  • Reduced activation of 25-OH vitamin D3 by OHase to calcitriol which regulates calcium intestinal absorption so low Ca levels
  • Potassium is normally excreted in the urine = amount ingested to keep a balance so hyperkalaemia
  • The kidney contributes to maintenance of the blood pH by excreting H+ and reabsorbing HCO3- in the PCT to keep blood pH at 7.4, leading to acidosis
  • EPO production is a glycoprotein hormone produced in the kidney which regulates the red blood cell production
  • anaemia
  • The production of urine controls fluid balance and salt balance is maintained both contributing to blood pressure maintenance. The amount of salt excreted roughly equals salt ingested.
  • HTN/ Fluid restricton
  • Renin secretion: enzyme released in response to low blood volume or decreased sodium chloride concentration.

It activates the renin-angiotensin system by cleaving angiotensinogen to yield angiotensin 1 which is converted to angiotensin 2 by angiotensin converting enzyme. This constricts blood vessels and activates the thirst reflex leading to increased blood pressure.

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3
Q

What are the causes of CKD?

A

Diabetes, glomerulonephritis, polycystic kidney disease, polynephrittis, HTN, renovascular, uncertain aetiology/other

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4
Q

What are the stages of CKD?

A

x

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5
Q

What are the stages of disease and nutritional issues?

A

x

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6
Q

Which nutritional interventions are used in CKD?

A

Delay progression of CKD, minimise sx of uraemia, minimise effect of renal disease on blood biochem and fluid status, Id and treat malnutrition

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7
Q

What are the different routes of feeding?

A

Oral, NGT, jejunostomy tube (if aspirating or vomiting a lot), gastrostomy tube

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8
Q

What is an NGT?

A

Risk of aspiration in ICU _> ensure upright 30-45 degress; don’t place at night; high aspirates and inadequate calories common in ICU (RIG/PEG/ gestrostomy feeding for long term); can give higher rates/volumes into stomach

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9
Q

How do you delay the progression of renal disease?

A

Diabetic control which reduces nephropathy (HbA1c of 48mmol/mol); HTN (aim for 120-139/90mmHg; 120-129/80mmHg in diabetes/albumin:creatinine ratio of 70mg/mmol or more; strong evidence that CV risk reduced, as HTN can be contributory or causative); obesity aim for adequate glycaemic control and BP, morbid obesity linked to 2.3 RR developing CKD

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10
Q

How do you minimise uraemic Sx?

A

Sx before starting dialysis: tiring easily, weakness, anorexia/nausea, muscle cramps, bad taste in mouth -> protein restriction diet: 0.75g/kg ideal body weight/day for pts with stage 4-5 not on dialysis

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11
Q

How do you manage a low protein diet?

A

Start with high bio value proteins to reduce overall protein intake (Meat, fish, dairy, eggs), then consider low bio values of protein (Rice/paste/bread/cereals).

Complex and restrictive -> to meet kcal req may need to add in low protein high kcal snacks often high in fat/sugar; reducing protein also reduces K and PO4 intake

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12
Q

How do you minimise the effect of renal disease on blood biochem and fluid status?

A

Oedema (peripheral and pulmonary) = salt (recommendation <6g/d) and fluid restriction (CKD 5), controlling this improves BP, and salt reduces kidney injury as ^ salt intake = worsening albuminuria and kidney tissue injury; hyperphosphataemia: PO4 intake and PO4 binding medication - elevated sPO4 increases mortality risk; hyperkalaemia: reducing K intake and considering non dietary factors

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13
Q

What are the 2 types of renal bone disease due to CKD?

A

Bones become thin and weak;

deformities in joints in fingers and in rib cage;

sPO4 main factor determining the Ca/PO4 product and prevalence of metastatic calcifaction including vascular calcification and heart valve calcification

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14
Q

What is calciphylaxis?

A

Syndrome of vascular calcification and thrombosis and skin necrosis -> chronic non-healing wounds; rare but serious

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15
Q

Which foods are good for phosphate?

A

x

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16
Q

Which foods are bad for salt restricted diets?

A

x

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17
Q

What are the different types of phosphate binders?

A

x

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18
Q

What is the effect of hyperkalaemia?

A

Can be present in CKD, HD, PD pts; can lead to sudden death by arrhythmia; difficult to Dx -> K = 3.5-6 mmol/l HD, 3.5-5.5 in PD, 3.5-5.3 CKD

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19
Q

What are the non-dietary causes of hyperkalaemia?

A

Acidosis, low HCO3 level, constipation, medicines (K sparing diuretics), blood transfusions, poor blood sugar control, dietary high K foods

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20
Q

What are the foods with high potassium?

A

To cook low K, need to boil NOT fry, steam

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21
Q

What do you do to reduce K?

A

Reduce spinach and other high K foods and drinks; suggest alternative veg; boil instead of steaming/frying

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22
Q

What are the causes of malnutrition in renal disease?

A

Uraemia, anorexia, acidosis, infections, dietary restrictions, tiredness due to Tx, nutrient losses, hypercatabolism, depression, family support

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23
Q

What are the calorie requirements for CKD HD, PD?

A

CKD/HD = 35kcal/kg/d, 30 >60y; PD = 35 kcal/kg/d or 30 kcal/kg/d >60y including kcals from dialysate

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24
Q

How do you treat malnutrition?

A

Enteral nutrition support: oral nutrition supplements/tube feeding; parenteral nutrition support: intra dialytic parenteral nutrition/total parenteral nutrition

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25
Q

What are the renal considerations when supporting nutrition?

A

Fluid restriction necessary?, electrolytes (PO4/K necessary); protein

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26
Q

What is the overall nutritional support for renal patients?

A

x

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27
Q

Which tumours have high, medium and low risk of weight loss?

A

High: head/neck, oesophago-gastric and pancreatic cancers; medium risk: prostate, colorectal, lung; low risk: breast, sarcomas and NHL; unintentional weight loss is associated with low QOL, poor treatment tolerance and poorer prognosis

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28
Q

What makes up weight?

A

Fat (subcut and visceral), muscle (skeletal and appendicular), bone, organs, fluid

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29
Q

What weight assessment do we do in clinical practice?

A

Weight, BMI, BSA, nutrition screening, visible signs of fat loss (orbital/triceps), visible signs of muscle loss (clavicle/temporal); fluid (oedema/ascites)

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30
Q

Why does weight loss matter?

A

Treatment toxicity, fatigue, sarcopenia, wound healing, skin integrity, dose reduction, reduced QOL, radiotherapy replanning, increased mortality

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31
Q

Why are lung cancer pts malnourished?

A

Iatrogenic causes of decreased intake; inadequate symptom control (no appetite, early satiety, pain, taste changes); tumour site (functional and physiological causes of malnutrition = GI function/motility, obstruction, malabsorption); increased metabolic rate; cancer cachexia

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32
Q

What are the iatrogenic causes of malnutrition?

A

Decreased intake, increased energy expenditure/losses; surgery: pain, SOB, fatigue; radiotherapy: odynophagia, mucositis, SOB, fatigue, dysgeusia, xerostomia, pain; chemotherapy: fatigue, N/V, mucositis, anorexia, infection, malabsorption, bowel changes, dysgeusia

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33
Q

What is cancer cachexia?

A

Multifactorial syndrome, which leads to on-going loss of skeletal mass with or without the loss of fat mass, that cannot be fully reversed by conventional nutrition support and leads to progressive functional impairment -> -ve protein/energy balance, anorexia, reduced oral intake, abnormal metabolism

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34
Q

What are the differences in metabolism in cancer cachexia?

A

x

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35
Q

How do you clinically assess cancer cachexia?

A

x

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36
Q

What are the stages of cancer cachexia?

A

At precachexia use nutrition and physical activity; refractory cachexia use pharmaceutical

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37
Q

What are the roles of nutritional interventions?

A

Early intervention: oral nutritional support; benefits vs risks of preop support, predicted Tx outcomes or side effects, psychosocial and psychological status

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38
Q

What are the goals of nutritional support?

A

x

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39
Q

Which artificial nutritional supports exist?

A

Mod-severely malnourished if given 7-14d pre-op, prophylactic tube placement for certain anti-cancer therapies; anticipated inability to ingest/absorb nutrients for 7-14d in a malnourished patient during Tx

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40
Q

Why do breast cancer pts increase weight?

A

Average of 2kg between CTx cycles: hormonal influence, dysguesia, increased appetite 2ry to steroids, reduced physical activity -> BMI >40 2x risk of death; excess adiposity associated with 30% increased risk of mortality -> THUS: increase physical activity decreases risk 20%, avoid weight gain, abdominal girth <80cm, body fat <36%; BMI<25

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41
Q

What advice for diet in breast Ca pts?

A

x

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42
Q

Compare lung vs breast cancer pts in terms of nutrition

A

x

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43
Q

How is immunity affected by weight loss?

A

x

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44
Q

Why is weight lost?

A

x

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45
Q

What is the difference between nutritional goal and guideline?

A

Goal: sets target = fat intake should be 35% of total intake; guideline: tells you how to get there = low fat dairy products, avoid fried food

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46
Q

Who sets goals and guidelines for nutrition?

A

WHO, country specific agencies: Public health England, based on recommnedations: committee on medical aspects of food policy and scientific advisory committee on nutrition

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47
Q

Why are goals and guidelines needed for nutrition?

A

Amount of each nutrient needed = nutritional requirement which are different for each nutrient and between individuals and life stages

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48
Q

What is RDA?

A

Recommended daily amount; average amount of nutrient which should be provided per head in a group of people if the needs of practically all members of the groups are to be met, aim of preventing deficiency

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49
Q

What are UK dietary reference values?

A

UK COMA in 1991, take account distribution of requirements within a popn or group; uses: Lower reference nutrient intake, estimated average requirement, reference nutrient intake and safe intake -> statistical concepts relating to physiological requirements for health and well-being among popn groups; intended as a guide or reference for health professionals, food planners and the food industry, not unconditional recommendations

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50
Q

What are the objectives of UK DRVs?

A

Nutrient recommendations: amount judged appropriate to maintain health in most individuals in a given popn; obj: criteria of adequacy: prevention of deficiency, sufficient for storage, safe upper limits, optimal intakes (prevent chronic disease)

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51
Q

How do you determine nutritional requirement?

A

Metabolic demand + efficiency of utilisation = nutrient req.; methods: obs of intakes, balance studies, physiological est, clinical studies, functional tests

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52
Q

What is the reference nutrient intake?

A

Amount of nutrient that is enough to ensure that the needs of nearly all group being met, so many in the group will need less -> 97.5% of popn

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53
Q

What is the lower reference nutrient intake?

A

The minimum req; sufficient to meet req of 2.5% of popn

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54
Q

What is safe intake?

A

Level/range of intakes at which there is no risk of deficiency and below where there is risk of toxicity; there isn’t evidence of benefit above this level, BUT could have undesirable/toxic effects -> for some minerals and vitamins: pantothenic acid, biotin, vit E/K, manganese, molybdenum, chromium, luoride

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55
Q

What is the estimated average requirement?

A

Estimate of average requirement for energy or a nutrient ~50% of group of people will require less and 50% will require more; for group of people receiving adequate amounts, the range of intakes will vary around the EAR

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56
Q

What is the metabolic basis of energy needs?

A

Estimation of energy needs: energy stored (lipids) = energy intake (carbs, protein, fat and alcohol) - energy expenditure (BMR, physical activity, adaptive thermogenesis)

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57
Q

What is the best source of energy?

A

Carbs: 4 kcal/g; protein: 4; fat: 9; alcohol: 7; fibre ~0-2; water: 0

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58
Q

What is protein?

A

EAR = 0.6g/Kg BW/d, RNI = 0.75g/kg/d; extra for growth in infants and children and pregnant/breastfeeding women; allows for 70% of protein consumed is incorporated into body; 1g of protein = 17J/4kcal of energy; av. 16% dietary energy in UK

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59
Q

What are fats and carbs?

A

% of energy intake, fat = <35% EI (Sat =<11%); carbs = 50% EI (free sugars =<5% EI)

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60
Q

What is alcohol?

A

Guideline by Dep of health (UK); based on ethanol and health outcomes, but contributes to energy: 7kcal per g

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61
Q

What are the limitations of DRVs?

A

Don’t apply to individual specific popn not represented; DRV’s best evidence but not definitive; don’t apply to diseased; not everything is absorbed; variability in absorption; don’t change behaviour alone

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62
Q

Which substances have an intake below LRNI?

A

Iron: IDA and low iron stores in proportion of adult women and older girls; Vit D: low vit D status in adults and older children, implicating bone health, increasing risk of rickets and osteomalacia (23% of 19-64y)

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63
Q

Which groups of popn are at risk of low vit D so need supplements?

A

Pregnant/breast feeding; children <=5y; breast fed infants from 6m; formula fed infants (<500mls/d); individuals with high skin pigmentation; individuals who have little/no exposure during summer, or wear clothing which covers most of skin in summer; living in institutions; elderly

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64
Q

What are the 3 main categories that increase cardiovascular risk?

A

Those with CVD, those at high multifactorial risk; those with single raised risk factor (>= 6 elevated total chol:HDL ratio, stage 1 (>140/90-160/100)/2 (160/100) HTN and familial dyslipidaemia

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65
Q

What are the non-modifiable risk factors of CHD?

A

x

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66
Q

What are the modifiable risk factors of CHD?

A

Apple shape have a higher risk

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67
Q

What is the interheart study?

A

Nine potentially modifiable risk factors which account for over 90% of risk of an initial acute MI -> looked at relative contribution of the risk factors; diet has a big impact on lots of these factors, explaining 50% of CHD events

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68
Q

What are the JBS3 UK recommendations for prevention of CVD?

A

Differences from JBS2: no recommendation for total fat consumption or restriction for cholesterol intake, replace sat fat with poly unsat fat rather than monounsat fat, consider regular consumption of whole grains and nuts

69
Q

What is the mediterranean diet?

A

Composed of: abundant plant foods (fruit, veg, cereals, beans, nuts and seeds) with olive oil as main source of dietary lipids and low consumption of red meat and (to mod) of dairy products/wine. Recommend around 8-10 portions of fruit and veg, diet is quite high in fat which should come from olive oil, nuts and seeds, low in sat fats, high intake of oily fish

70
Q

What is the Lyon Diet heart Study?

A

Mediterranean-type diet -> total fat <30%, SFA <10% and cholesterol <300mg/d; more omega-3 fats, fruit and veg, less sat fat and partial replacement by rapeseed or olive oil, more emphasis on fresh foods -> mortality was reduced by 70% on the intervention diet and CVD deaths were reduced by 76%

71
Q

What is the PREDIMED study?

A

2 patient groups: 1 with olive oil (1L/week), 1 with 30g of nuts/week -> reduction in cardiovascular risk but NO change in weight so mortality is not attributed to weight

72
Q

What are the different dietary fats?

A

Sat FA: no double bonds, down reg LDL receptors and reduces LDL removal from circulation. Monounsat FA: one double bond. Polyunsat fat: 2 or more double bonds, divided into 2 groups - linoleic and alpha linoleic acid and both are essential; Omega 3/6 both sub types and demonstrated cardioprotective effects. Trans FA: double bond in trans rather than cis form. NB: Bad fats are solid at room temp

73
Q

What are the effects of Trans FA?

A

^LDL and decrease HDL, so increased CHD; 2% increase in total energy from TFA increases CHD by 23%; OVERALL: TFA has greater effect than sat FA on CHD

74
Q

How do dietary fats affect the lipid profile?

A

PUFA and MUFA reduce LDL when replacing CHO; all fats except trans increase HDL; MUFA increase HDL more than PUFA, but PUFA lower LDL more than MUFA

75
Q

What is coconut oil and how is it good for you?

A

HIGH in sat fats, so increase LDL, but increases HDL more

76
Q

How are nuts good for you?

A

x

77
Q

What are the NICE and JBS3 guidelines for oily fish?

A

‘Do not routinely recommend eating oily fish for the sole purpose of preventing another MI. If people choose to consume oily fish, healthcare professionals should be aware that there is no evidence of harm, and fish may form part of a Mediterranean-style diet’. (NICE, 2013) ‘There is good observational evidence that the n-3 fatty acids (derived from fish consumption) are cardioprotective with epidemiological studies showing that regular fish consumers are at lower risk of fatal CHD, including sudden death’ (JBS3, 2014)

78
Q

What is the recommendation of fruit and veg?

A

At least 5 portions/day, with 8-10 even better; 400g/wk = 5 portions; increased consumption of fruit and veg is related to reduced risk of CHD (7% reduction for 3 portions -> each increase of 1 portion of fruit and veg a day lowered risk of CHD by 4% and risk of stroke by 6%), can also help lower BP

79
Q

What is the recommended fibre intake?

A

18g/day adults but current UK intake ~12g/d -> include both soluble and insoluble fibre, with soluble helping to lower blood lipid levels (fruits, veg, oats and pulses) and insoluble helping to prevent constipation and improve bowel function (wholegrain cereals); complex carbs with low glycaemic index are beneficial

80
Q

Which foods have a low glycaemic index?

A

Food that doesn’t increase the glycemic index as fast so it isn’t too hard for the insulin response to deal with it

81
Q

How is fibre associated with CVD?

A

CVD risk reduced 9% with additional 7g of fibre/day (2-4 portions of fruit and veg, 1 portion of wholegrain food and 1 portion of lentils) -> total dietary fibre is inversely associated, insoluble fibre and fibre from cereal and veg were inversely associated with risk of CVD, those with higher fibre intake = healthier lifestyles

82
Q

What are the different definitions of sugars in dietary recommendations?

A

High intake of sugar has an adverse effect on lipid levels; average intake of sugar per day in UK is 90g

83
Q

What is the effect of salt in CVD?

A

High intake leads to increase in BP; Advise not to add salt to food in cooking or at table; sources of UK salt: 35% from cereal/cereal products, 26% from meat and meat products, 8% from milk and milk products

84
Q

How does HTN affect CHD risk?

A

Decreasing SBP 3-5mmHg reduces CHD risk by 10% and stroke by 15% (DASH trial - showed that lowering salt intake will lower BP and risk of HTN)

85
Q

Why does salt reduction work in CVD?

A

x

86
Q

What is the effect of alcohol on CVD?

A

Alcohol increases BP

87
Q

What are the effects of antioxidants on CVD?

A

Vit E: no effect on all cause mortality or CVD risk, high doses increase risk of mortality; Beta carotene: increase risk of death and CVD death

88
Q

How does benecol reduce LDL levels?

A

Competes with cholesterol so less dietary cholesterol is absorbed so reduction in LDL levels

89
Q

What is the optimal amount of plant sterols?

A

2g (425 tomatoes), but average daily plant intake of adults: 150-400mg/day

90
Q

What are soya proteins and how do they affect CVD risk?

A

Quite a lot of soya is needed in the diet to reduce cholesterol by a small amount

91
Q

Which dietary factors reduce LDL cholesterol levels and by how much?

A

x

92
Q

Which lifestyle modifications reduce SBP?

A

x

93
Q

What is the thrifty gene hypothesis?

A

Mankind evolved during 1000s of years of starvation, and only obese would survive famines, so genes for obesity have been selected -> now a harmful set of genes as we’re living too long

94
Q

How is feeding regulated?

A

Tightly reg in humans and body weight is stable (animals overfed the given free diet, they reduce back to set point, underfed with free diet increase back to set point).

95
Q

What is the role of the hypothalamus in weight reg?

A

Lateral hypothalamus and dorsomedial hypothalamus; ventromedial hypothalamus = satiety centre and lateral hypothalamus = feeding centre

96
Q

What is NPY?

A

36 a.a.; rich in tyrosine; stimulates feeding when injected intracerebroventricularly to rats

97
Q

What is GLP-1?

A

Satiety factor; animals stop eating and fall asleep

98
Q

What is leptin?

A

Synthesised in fat cells -> are endocrine cells and tells the brain if there are fat stores; tend to eat less if leptin is high

99
Q

What are the 2 types of diabetes?

A

T1DM seems to be environmental -> seasonal, after flu like virus, might knock out some islet cells; T2DM is genetic

100
Q

What is the genetics of diabetes?

A

Type 2 is 100% concordant -> suggesting there are genetic influences to diabetes, genetic predisposition to overeating or how they eat thus behaviour is genetic -> a few loci have been found for T1DM but none for T2DM

101
Q

Which substances are known to influence feeding?

A

Leptin, GLP-1, NPY, MCH and orexin

102
Q

How can we prevent diabetes?

A

Exercise reduces diabetes by 20%; 2x better than metformin

103
Q

What are the markers of nourishment?

A

Albumin is a plasma protein and levels fall in malnourished people and sepsis (acute effect); liver slows synth of albumin and starts making CRP instead, so albumin levels correlate inversely with CRP; body weight should be recorded whenever you see a patient, know dry weight (pts with renal failure get rapid increase weight so you can figure out how much to dialyse), malnourishment causes chronic reduction in weight; intentional vs unintentional (cancer, diabetes and thyroid) weight loss

104
Q

When does unintentional weight loss occur?

A

Due to low grade infection, undiagnosed malignancy, paraneoplastic syndrome (tumour makes substance that has various unpredictable effects, no idea what substance is)

105
Q

What happens during starvation?

A

Insulin levels fall in normal person and trigger release of energy; conversion of fats to ketones which are useful fuel; insulin levels fall, glucose, glycogen, TG, protein all used, glycogenolysis is turned on <24h, then insulin very low switches on ketogenesis; bicarb falls and gets ketocis, so not true ketoacidosis

106
Q

What is insulin?

A

Signal that you have been fed; switches on all pathways that use up glucose and store glycogen and fat, suppresses ketone production -> glycogen synthase and glycolysis in liver and muscle ON, and gluconeogenesis if OFF

107
Q

What is the pathology of type 1 DM?

A

IS destroys islets of langerhans in the pancreas; result of total deficiency of insulin; all cells of body therefore fail to take up glucose; plasma glucose therefore rises, leaks into urine and large volumes of urine result; complete insulin deficiency causes acidosis; when insulin levels = 0, liver behaves as if no fuel for brain to keep working and makes huge amount of ketones, turning the blood acidic with ketones in urine and brain can’t function in acid pH

108
Q

What is diabetic ketoacidosis?

A

Blood glucose high as can’t enter cells; blood full of ketones, severe dehydration and air hunger as they want to blow off the CO2

109
Q

What is T2DM?

A

Resistance to insulin action; 2ry rise in glucose; pancreas makes lots of insulin to try and counteract this, eventually pancreas exhausts itself and T2DM ensues

110
Q

What is the pathology of T2DM?

A

Sufficient insulin here to suppress ketogenesis

111
Q

What is obesity?

A

A disease: excessively high accumulation of body fat/adipose tissue in relation to lean body mass-> amount of adiposity includes concern for distribution of fat and size of adipose tissue deposits

112
Q

What is a problem with BMI?

A

High muscle mass = high BMI; doesn’t tae into account distribution of body fat; high waist circumference = high risk, so just measure waist circumference

113
Q

What is the epidemiology of BMI in uk?

A

Highest in age group 55-64; ethnic group - in caucasian and bangladeshi; regional variation: Scotland higher than south of England; higher in social class 5 (poorest); smokers: lower BMI but greater central obesity

114
Q

What are the effects of obesity?

A

Obesity is known to lead to both chronic and severe medical problems. Biggest killer – coronary heart disease Biggest impact on morbidity and quality of life – diabetes Ostearthritis – weight bearing joints Infertility: in women as PCOS and men are more likely to be impotent Cancers: breast, endometrial

115
Q

Which diseases are at increased risk with increased BMI?

A

T2DM, cholelithiasis, HTN, CHD

116
Q

What does the shape of your body have to do with the risk of CHD?

A

Android (apple) is worse than gynoid (pear) obesity; waist circumference is important to measure; it’s such a risk due to impact on liver metabolism, it has the ability to change lipid and insulin homeostasis.

117
Q

What are the waist circumference action levels?

A

x

118
Q

What is the energy balance that occurs in the body?

A

Weight stable = E in = E out + E stored; weight gained = E in exceeds E out; increased intake and decreased expenditure; energy intake increases and inactivity increases too, so hence increase in obesity

119
Q

What is the homeostasis and hedonism interaction for appetite?

A

Pleasure from food is very rewarding

120
Q

How has the diet changed over the least 50y?

A

Food has become cheap, energy taken between meals has increased, energy density of food increased and increased processing of food

121
Q

What is the effect of 10% weight loss on risk effects?

A

x

122
Q

What are the NICE recommendation for obesity?

A

Diet, exercise, behavioural therapy, drug Tx, surgery (BMI >40)

123
Q

How can you diagnose malnourishment?

A

BMI less than 18.5; unintentional weight loss greater than 10% innlast 3-6m; BMI <20 with unintentional weight loss >5% within last 3-6 months

124
Q

What are the causes of malnutrition?

A

Uraemia, nausea, vomiting, anorexia, taste changes, fatigue; poor appetite; early satiety; unpalatable restricted diet; frequent hospital admissions; infections; increased nutritional requirements; depression, anxiety; drug side effects

125
Q

Which patients are at increased risk of malnutrition?

A

Increased requirements (post-op, cachexia, infection, chronic illness); age >65; bedbound/pressure sores/physical disabilities; modified diet

126
Q

What is the impact of malnutrition?

A

Increases morbidity and mortality; delays wound healing; reduces immune function increasing risk of illness and infection; increased risk of pressure sores; reduces QOL; prolongs hospital stay; falls and fx; muscle wasting and weight loss; low weight/energy; low mood

127
Q

What is the malnutrition carousel?

A

Hospital admissions are at risk of malnutrition; longer stay, more complications; more support needed after hospital; 70% pts weigh less on hospital discharge; more GP visits; more prescriptions; more hospital admissions

128
Q

What is nutrition screening?

A

Used to assess pts nutritional status, using scores or flow chart to work out if pt is well nourished/mild to mod malnourished/severely malnourished; 0-2 = no action required, 3= start plan and rescreen weekly; 4+= start nutrition care plan and refer to dietician

129
Q

How do you ID malnutrition?

A

Hx, physical examination, encourage weights/screening in your pts

130
Q

What are the physical signs of malnutrition?

A

Mental health changes, hair chnages, anaemia, ascites, hungry, diarrhoea, dermatitis (legs), pressure sores, sunken eyes, sore red eyes and lids, poorly fitting dentures, swollen/bleeding gums, dry/cracked lips; loss of subcut fat, muscle weighting, oedema (fingertip test), ascites (renal/liver/heart failure)

131
Q

What questions would you ask when taking a malnutrition history?

A

Weight changes (intentional weight loss in last 3m, change in clothes size, ring size), diet (special diet, restrictions, nutritional supplements, appetites less than before), functionality (exercise tolerance/lethargy), GI sx (diarrhoea, constipation, frequency, abdo pains)

132
Q

What is refeeding syndrome?

A

Syndrome consisting of metabolic disturbances that occur as a result of reinstitution of nutrition to pts who are starved or severely malnourished

133
Q

How do electrolytes change in RFS and how does RFS come about?

A

Starvation -> glycogen stores utilised -> decreased insulin, increased glucagon secretion -> gluconeogenesis, protein catabolism and mobilisation of lipids -> protein, fat, mineral, electrolyte and vitamin depletion, Na/H2O intolerance -> refeeding: eating (CHO main energy) -> glucose enters blood by enteral, parenteral, oral, IV route -> pancreas secretes insulin in response to glucose -> Insulin promotes cell uptake of glucose, increased utilisation of thiamine -> increased cell uptake of K, Mg, P, causing low serum levels of K, Mg, P -> RFS

134
Q

What are the consequences of refeeding syndrome?

A

1) Phosphate: cardiac - altered myocardial function, arrhythmia, congestive cardiac failure; respiratory: acute ventilatory failure; neuromuscular: lethargy, confusion, weakness, paralysis. 2) Potassium: arrhythmia, cardiac arrest, resp distress, paralysis, weakness, rhabdomyolysis. 3) Magnesium: arrhythmia, tachycardia, resp distress, ataxia, confusion, muscle tremors, tetany

135
Q

Which patients are at risk of RFS?

A

ONE OR MORE: BMI <16; unintentional weight loss >15% over 3-6m; little or no nutritional intake for >10d; low levels of K, P and Mg, before feeding. TWO OR MORE: BMI <18.5, unintentional weight loss >10% in 3-6m, little or no nutritional intake for >5d, Hx of alcohol abuse or drugs

136
Q

What should you check for in RFS and how do you treat it?

A

Check U+E’s, bone profile, Mg daily; K, P and Mg closely; provide vit prep for 1st 10d, give less than 30 min before food, vit B co strong and thiamine OR pabrinex I/II (IV), multivit/trace element supplement (OD)

137
Q

What are the 3 main types of diabetes?

A

Type 1, 2 and gestational (glucose intolerance first discovered in pregnancy); other types: MODY, LADA, drug induced, 2ry to endocrinopathies

138
Q

What are the common characteristics of type 1 and 2 DM?

A

x

139
Q

What are the high risk groups for T2DM?

A

Complex interplay of genetic/env factors in T2DM -> people with diabetes in the family are 2-6x more likely to get diabetes; ethnicity: T2DM >6x more common in south Asian and 3x in African/Afro-Caribbean, also black and south asian develop diabetes ~10y earlier; obesity: accounts for 80-85% of overall risk of developing T2DM

140
Q

What are the aims of nutritional management of T1/2DM?

A

Good glycaemic control (HbA1c ≤ 48 mmol/mol and limit hypos). Minimise risk of long-term microvascular and macrovascular complications. CVD risk reduction: weight, blood pressure and lipid management. Enjoyment of food and good quality of life Facilitation of health behaviour changes and self management

141
Q

What are the aspects of nutritional management of T1DM?

A

Aim to coordinate lifestyle and insulin therapy with focus on flexibility, good glycaemic control and CVD risk reduction -> 2 main aspects: assessing carb intake and matching to insulin dose (count carbs and match to activity levels) and encourage good nutrition (healthy eating, weight management, CVD risk reduction)

142
Q

What are the insulin time action profiles of each of the insulin treatments and what are the insulin therapies?

A

Basal/bolus: long acting background insulin (glargine/determir) and rapid-acting insulin (novorapid/humalog/apidra) with food, 0.5-0.8 units of insulin per kg, half for food and half for basal rate, adjust insulin to match food timing and quantities, CHO counting; twice daily mixed: novomix/humalog, consistent meal pattern and carb intake; continuous subcut insulin infusion - insulin therapy: continous infusion of rapid-acting insulin with bolus for meals and snacks, CHO counting

143
Q

What are the benefits of insulin pump therapy?

A

Can be considered for adults and children >12y; attempts to meet target HbA1c results in disabling hypoglycaemia

144
Q

What is blood glucose monitoring?

A

ID patterns, tests response to foods and med, enables adjustment of meds and calculation of insulin doses, usually test pre/post meals

145
Q

Where do most carbs come from in diet?

A

x

146
Q

How do you count carbs?

A

There can be errors in estimating carb values; which can lead to an increase in blood glucose, so more insulin is needed

147
Q

Why do you count carbs in T1DM?

A

x

148
Q

Which foods aren’t counted in carb counting?

A

x

149
Q

What are the pros and cons of counting carbs in T1DM?

A

x

150
Q

What is DAFNE?

A

BERTIE is modified version -> less fixed, more flexible

151
Q

What is the nutritional management of T2DM?

A

Want carb-awareness

152
Q

How can you eat well with diabetes?

A
  1. Eat regular meals -> avoid skipping meals, space them evenly throughout the day, match carb intake to insulin action if needed, try to have breakfast (control appetite and BGL, prevent snacking and overeating; 2. Keep an eye on portion sizes 3.Carbs count 4. Cut the fat 5. Get your five a day 6. Cut back on salt 7. Eat more fish 8. Eat more beans 9. Limit added sugar 10. Keep hydrated Avoid ‘diabetic foods’ See a dietitian
153
Q

What is glycaemic index?

A

x

154
Q

What affects Glycaemic index?

A

x

155
Q

How is glycaemic index determined?

A

x

156
Q

Which foods have a high, medium and low glycaemic index on the scale?

A

x

157
Q

What are the benefits of physical activity?

A

x

158
Q

What are the targets for exercise that adults should aim for?

A

>=150min of moderate intensity activity per week, or 75 of vigorous intensity activity across the week or combination AND undertake physical activity to improve muscle strength >=2d/week, minimise extended sedentary periods

159
Q

What is moderate intensity activity?

A

Activity that raises your heart rate, makes you breathe faster and feel warmer. You should still be able to talk, but not able to sing the words to a song. Examples:Walking fast Water aerobics Riding a bike on level ground or with few hills Doubles tennis Pushing a lawn mower Hiking Skateboarding Rollerblading Volleyball Basketball

160
Q

What is a vigorous intensity activity?

A

Activity that makes you breathe hard and fast and accelerates your heart rate. If you’re working at this level, you won’t be able to say more than a few words without pausing for breath. Examples:Jogging or running Swimming fast Riding a bike fast or on hills Singles tennis Football, rugby or hockey Skipping rope Aerobics Gymnastics Martial arts

161
Q

How can you manage weight in T2DM?

A

Weight reduction for overweight/obese person with T2DM is effective in improving glycaemic control and CV risk factors, total energy intake < total energy expenditure -> reduced bodyweight , HBA1c and reduced CV risk factors maintained over 4 yrs is the look ahead study in US

162
Q

How do low carb diets work in T2DM?

A

Very low calorie diet -> 800 cal per day for 8 weeks (optifast meal replacements and non-starchy veg), diabetes remission was induced in 7/11 and retained normal blood glucose control after 3 m

163
Q

What is metabolic surgery for DM?

A

Achieves superior glycaemic control compared with various medical/lifestyle interventions. Best results with Gastric bypass. Best reduction in long term complications if within first 12 months of diabetes diagnosis. Long term nutritional monitoring and follow up required

164
Q

How can we prevent T2DM?

A

Weight loss is the most important predictor of risk reduction for Type 2 diabetes. Weight loss of at least 5 to 7 % is effective to reduce risk. No evidence for the most effective dietary approach for weight loss. Diet alone, increased physical activity alone or a combination of the two is equally effective in reducing risk.

165
Q

What are the recommendations for the prevention of T2DM in high risk groups?

A

x

166
Q

How is gestational diabetes managed?

A

x

167
Q

How is a diabetic pt dealt with in the hospital?

A

High incidence of malnutrition in hospital. Poor appetite and poor dietary intake common. Importance of meeting nutritional requirements (immune system, wound healing, feeling of well-being). Healthy eating principles may not be appropriate while in hospital. Foods that are higher in calories (including fats and sugars) may be required. Important to re-iterate healthy eating should be resumed on discharge. Education can be provided on discharge.

168
Q

What are the structured education programmes in diabetes?

A

x

Y2 S&P - Water & Electrolytes, Cardiovascular, Nutrition, Physiology of infection (4 decks)

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