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Year 2 S&P > Nutrition > Flashcards

Nutrition Flashcards

1
Q

What are the classifications of CKD, and how is each stage managed?

A

Stage 1 - Normal function: CKD risk factors such as hypertension, diabetes, and obesity

Stage 2 - Mild decrease in GFR: reduce CKD risk factors by managing diabetes, weight and hypertension

Stage 3 - Moderate decrease in GFR: Treat the complications of CKD by controlling ureamia and fluid restriction of needed. Also managing diabetes and hypertension.

Stage 4 - Severe decrease in GFR
Stage 5 - End stage : both (stage 4 and 5) treated by looking for kidney replacement as well as all the above; preventing malnutrition and electrolyte imbalances

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2
Q

What are the aims of nutritional intervention in the renal patient?

A
  1. Delay progression of CKD
  2. Minimise symptoms of ureamia (stage 4 and 5)
  3. Minimise effect of renal disease on blood biochemistry and fluid status
  4. Identify and treat malnutrition
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3
Q

What are uraemic symptoms?

A

Due to urea in the blood. Main uremic symptoms include:

  • Tiring easily, weakness
  • Anorexia and nausea
  • Muscle cramps
  • Bad taste in mouth
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4
Q

How is protein intake relevant to CKD patients?

A

In the past, low protein diets helped with uraemic symptoms. This is only a symptomatic treatment and does not affect disease itself much. A cochrane review showed that it did actually reduce progression in one year.

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5
Q

What is the recommended protein intake to reduce uraemic symptoms (aim 2)

A

0.75g/kg of ideal body weight (1.2 on PD; 1.4 on HD)

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6
Q

What are the main biochemical and fluid effects of CKD that can be controlled by nutrition (aim 3)?

A
  • hyperphosphataemia
  • hyperkalaemia
  • oedemea
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7
Q

How can nutrition delay the progression of CKD (aim 1)?

A

To delay renal function deterioration:

- Optimise glycemic control in diabetes (HbA1c

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8
Q

How can nutrition correct hyperphosphataemia?

A

Rarely done by reducing intake alone as phosphates are in many foods. Phosphate binders can be taken with food to reduce phosphate absorption.

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9
Q

What is the problem caused by hyperphosphataemia?

A

The high phosphate causes osteoporosis and calcium deposits and calcification. Calciphylaxis are chronic non-healing wounds.

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10
Q

What foods are high in phosphate?

A
  • Diary products
  • Seafood
  • Nuts
  • Chocolate
  • Hard cheese and processed cheeses
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11
Q

What are the non-renal causes of hyperkalaemia?

A

Diet, medications , constipation, blood transfusions, hyperglycaemia and acidosis can also cause it.

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12
Q

How can nutrition correct hyperkalaemia?

A

Avoiding foods with a high potassium content e.g fruits and spinach.
Change the way they are prepared - e.g potassium will wash away with water if vegetables are boiled.

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13
Q

How can nutrition correct oedema?

A

fluid restriction and reducing salt intake

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14
Q

What tips would you advise to reduce salt intake?

A
  • Do not add salt at the table
  • Reduce salt in cooking
  • Add herbs and spices
  • Reduced processed foods
  • Beware of salt substitutes such as LoSalt (not better)
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15
Q

What are the three sources of malnutrition in the renal patient?

A
  1. Disease related (uraemia, anorexia, acidosis)
  2. Treatment related (infections, dietary restriction, nutrient losses etc)
  3. Person related (depression, family support)
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16
Q

What are the BMI values for Obesity?

A

Non-asians:

  • Obese = 30-35 kg/m2
  • Severe Obesity = 35-40
  • Morbid Obesity = +40

Asians:

  • Obese = 25 - 30
  • Severe obesity = +30
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17
Q

What are the problems with BMI?

A
  • does not differentiate muscle and fat

- not account for distribution of body fat (low BMI but high waist circumference)

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18
Q

How do you measure waist circumference?

A

Measure at mid-point between the lowest rib and the iliac crest.

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19
Q

Why is waist circumference a better measure than BMI?

A

Abdominal obesity is a big risk. Excess visceral fat effects glucose metabolism and increases insulin release. Also has potential impact on liver metabolism.

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20
Q

What does excess visceral fat cause?

A
  • Deterioration of lipid profile
  • Impaired insulin sensitivity (have to produce a lot more insulin than others)
  • Increased susceptibility to thrombosis
  • Increased inflammation markers
  • Impaired endothelial function
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21
Q

How is obesity linked to energy inbalance?

A

Epidemiological studies shows that there is no relationship between energy intake and obesity.
However, there is a much stronger link between inactivity and obesity
However, these studies are very limited

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22
Q

What are the effects of obesity?

A
  • Ischaemic heart disease (along with hypertension, coronary thrombosis, congestive heart failure)
  • Type 2 Diabetes
  • Cancer (breast, endometrial, somach and colon)
  • Osteoarthritis
  • Mental health issues
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23
Q

What are the components of daily energy expenditure?

A
  • Resting metabolic rate (50-70%)
  • Thermogenesis (5-15%)
  • Physical activity (20-40%)
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24
Q

Why is obesity common?

A
  • cheap food

- thrifty genes

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25
Q

What is the role of the hypothalamus in control of weight?

A

The hypothalamus is the site of integration of metabolism. It receives input from both neural and hormonal sources

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26
Q

Give examples of orexigenic molecules

A
  • Nueropeptide Y
  • Agouti-related Peptide
  • Melanin-concentrating hormone
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27
Q

Give examples of anorexigenic molecules

A
  • Leptin
  • POMC
  • GLP-1
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28
Q

What genes expressed in skeletal muscle regulates body weight?

A
  • myostatin

- myogenin

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29
Q

What genes expressed in brown adipose tissue regulates body weight?

A

Uncoupling protein 1

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30
Q

What genes expressed in white adipose tissue regulates body weight?

A

Leptin, Lipoprotein Lipase

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31
Q

What genes expressed in the gut regulates body weight?

A

Glucagon-like peptide 1

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32
Q

Why are obesity rates increasing?

A
  • Energy intake is greater than energy expentesditure
  • Exercise decreasing
  • Food has changed over the years
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33
Q

How has the food we consume changed over the years, contributing to obesity

A
  • more processed meals
  • cheaper
  • increased snacking (energy between meals)
  • increase in energy density of food
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34
Q

What are the NICE recommendations for weight loss?

A
  • Diet
  • Exercise
  • Behavioural Therapy
  • Drug therapy e.g Orlistat
  • Suregry (if BMI>40)
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35
Q

What are the benefits of losing 10% of excess weight?

A
  • 50% decrease in fasting blood sugar
  • Lipid profile improves (10% decrease in total cholesterol, 15% decrease in LDL, 30% decrease in total triglycerides, 8% increase in HDL)
  • Average improvements of BP by 10/20mmHg
  • Overal 20-25% reduction in mortality
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36
Q

What are the aims of nutritional management for both T1 and T2 DM?

A
  • Good glycaemic control
  • Minimise risk of long-term microvascular and macrovascular complications
  • CVD risk reduction: weight, BP and lipid management
  • Enjoyment of food and good quality of life
  • Facilitation of health behaviour changes and self-management
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37
Q

What are the general treatment domains for T1 DM?

A

Insulin + Diet + Exercise

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38
Q

What are the general treatment domains for T2 DM?

A

Diet + Exercise +/- medication +/- insulin

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39
Q

What are the two main nutritional aims in the treatment of T1DM?

A
  1. Assessing carbohydrate intake and matching to insulin dose (Carbohydrate counting)
  2. Encourage good nutrition + weight management to reduce risk of CVD
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40
Q

What are the different types of insulin regiments?

A
  1. (most common) is the Basal/bolus - one long acting (Glargine or Determir) + rapid-acting with food
  2. Twice daily mixed insulin is normally used more in T2DM. Taken twice a day, once at breakfast and once at dinner. It relies of consistent eating time
  3. Insulin pump - continuous infusion of rapid-acting insulin with bolus for meals and snacks.
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41
Q

What are the pros and cons of using an insulin pump?

A
  • This is the most flexible, and physiologically gives greater control and accuracy.
  • However requires CHO counting. –> which has shown to reduce incidence of DKA/hypoglycaemia
  • Reduced risk of tissue complications and blood glucose swings
  • Expensive
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42
Q

Why is glucose monitoring important in T1DM?

A

This is very important in identifying patterns. Allows tests response to foods and medications. Enables adjustment of medication and calculation of insulin choices. Usually test pre and/or post meals. Most is still done through finger prick.

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43
Q

What are the pros and cons of continuous glucose measurements?

A
  • alerts if glucose levels becomes too high or too low
  • has a lag times of 15 minutes between blood and interstitial glucose levels
  • it can suspend insulin delivery if there is no response to a low-glucose warning
  • very expensive (only offered to patients with recc. or nocturnal hypos)
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44
Q

What foods don’t need to be counted for their carbohydrates?

A
  • Meat, fish, chicken, eggs and nuts (still has some)
  • Cheese (not much lactose)
  • Most vegetables (except starchy vegetables)
  • Diet drinks, sugar free drinks, most artificial sweeteners
  • Alcohol (but some alcohol drinks contain unfermented sugars)
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45
Q

What are the benefits of carbohydrate counting?

A
  • Improved glycaemic control
  • Better food freedom (can eat anything if counted)
  • Improved quality of life
  • fewer hyper/hypos
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46
Q

Give examples of structured educational programmes for diabetes control

A

DAFNE is a popular programme (Dose Adjustment for Normal Eating), ICICLE (Imperial College Insulin Carbohydrate Lifestyle Education) is another one.

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47
Q

What exercise is recommended for DM?

A
  • Aim to be active daily with >150 minutes of activity in a weak of moderate intensity activity
  • Undertake physical activity to improve strength on at least two days a week
  • Minimise sedentary periods
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48
Q

What are the nutritional aims in the treatment of T2DM?

A
  • Healthy Diet (to reduce CVD risk)
  • Weight reduction
  • Glycemic control
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49
Q

What are the healthy eating recommendations in T2DM?

A
  • Eat three meals a day (avoid skipping)
  • Include startchy carbohydrate foods (low GI)
  • Low fat diet, particularly decreased saturated fats
  • Eat more more fruits and vegetables (>5 a day) and more beans and lentuls
  • Aim for at least two portions of oily fish a week (containing omega-3)
  • Limit sugar intake and salt intake to (
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50
Q

What are the glycemic control recommendations in T2DM?

A
  • regular, moderate physical activity
  • low GI diets
  • restrict and monitor total energy intake, especially tital carbohydrate
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51
Q

What diabetes medication cause a gain in weight?

A
  • Insulin
  • Sulphonylureas
  • Thiazolidinediones
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52
Q

What is the best way to reduce the risk in developing Type 2 DM?

A

Weight loss (or maintain ideal BMI)

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53
Q

What is the first line of treatment for T2DM?

A

Lifestyle intervention.

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54
Q

What is the purpose of weight loss in T2DM patients?

A
  • reduces risk of CVD

- improves glycemic control

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55
Q

How can we reduce the risk of obesity in T2DM?

A
  • Preventative weight loss
  • Low calorie diet + exercise
  • Pharmaceuticals such as Orlistat
  • Surgery (gastric by-pass)
  • Combination of the above
56
Q

How do albumin levels change in malnourishment?

A

Falls

57
Q

How can you differentiate a fall in albumin that is due to malnourishment, from sepsis?

A

Sepsis usually ACUTELY affects plasma albumin

58
Q

What often causes unintentional weight loss

A

Cancer, Low grade infection, paraneoplastic syndrome, hyperthyroidism, uncontrolled T2

59
Q

Explain energy use after starvation

A

During starvation you use up glucose THEN glycogen in liver. Glycogen runs out after 24h. Then we start using triglycerides (fat). When this runs out we start using protein.

60
Q

What are the non-modifiable risk factors for CHD?

A
  • Gender
  • Age (>65)
  • Significnt Family History
  • Low socio-economic status
  • Ethnicity (South Asian)
  • Comorbidities (Diabetes and Renal Disease)
61
Q

What are the modifiable risk factors for CHD?

A
  • Diet
  • Exercise
  • Body Weight
  • Lipid
  • Smoking
  • Alcohol
  • Blood Pressure
62
Q

What counts as a significant family history for CHD?

A

Significant family history is if father/brother had CHD at

63
Q

How is fat intake recommended to be changed to reduce CVD?

A
  • switch from from animal fats –> plant fats to reduce saturated fat intake and replace with more unsaturated (mono/polyunsaturared).
  • avoid transfats
64
Q

What fats increase HDL and lower LDL?

A
  • mianly monounsaturated gives a large increase in HDL and lower LDL
  • polyunsaturated fatty acids also increase HDL but cause a large decrease in LD
65
Q

What is the recommendation regarding fruit and vegetable intake to reduce CVD?

A
  • Recommendation of 5 portions of fruit and veg a day.

- Reach increase of one portion of fruit/veg per day causes a significant reduction in risk of CHD a reduction in BP

66
Q

What is the recommendation regarding carbohydrate intake to reduce CVD? and why?

A
  • Recommended adult fibre intake is 18g/day
  • Complex carbohydrates include wholegrain brain, yams, sweet potato, porridge oats, barley, rice, pasta etc.
  • Low glycaemic index (GI) so slowly absorbed
  • Also contain both soluble and insoluble fibre - soluble fibre shown to lower blood lipid levels, whilst insoluble fibre aids bowel function and prevents constipation.
67
Q

What is the recommendation regarding salt intake to reduce CVD? and why?

A
  • Recommendation is
68
Q

What is the recommendation regarding alcohol intake to reduce CVD? and why?

A
  • Alcohol shown to increase BP
  • Recommendation of max 14units a week and 2-3 units a day
  • Avoid binge drinking
69
Q

What food substances reduce cholesterol absorption?

A

plant sterols and soya

70
Q

What are the aspects of the mediterranean diet

A
  • HIGH (8-10) intake of fruit and vegetable
  • High intake from pulses, beans and legumes
  • High intake of whole grain bread
  • Small portions of pasta and bread
  • High in fat but low in saturated fat
  • High intake of oily fish
  • Alcohol intake with meals
71
Q

Why do saturated fats increase LDLs?

A

High saturated fats leads to the down-regulation of ACAT, allowing cholesterol to form pools in the cells, signalling LDL receptor down regulation. LDL then circulates for longer periods.

72
Q

Why do unsaturated fats decrease LDLs?

A

They upregulate ACAT, which upregulaes the LDL receptor, making it more efficient in clearance.

73
Q

What fatty acid is particularly unsaturated at N-6?

A

linoleic acid

74
Q

What is the criteria for being labelled malnourished?

A
  • BMI less than 18.5 OR
  • Unintentional weight loss greater than 10% in the last 3 6 months OR
  • BMI 5% within last 3-6 months
75
Q

What is the impact of malnutrition?

A
  • Low weight and low energy
  • Falls and fractures
  • Muscle wasting and weight loss
  • Reduced mobility and reduced independence
  • Increased hospital admissions
  • Increased infections and increased confusion
  • Low mood
76
Q

Who is at an increased risk of malnutrition?

A
  • People with increased requirements e.g pyrexia, post-operative, cachexia
  • People over the age of 65
  • If they are bedbound/pressure sores/physical diabilities
  • If they are following a modified diets
  • heavy alcohol consumption
  • poor social situation
77
Q

What is nutritional screening?

A

Nutritional screening is the use of scores or flow charts to work out how malnourished a patient is.

78
Q

How is nutritional screening done?

A
  • calculate BMI
  • ask right questions
  • physical examination
    this information may be used to create a score, or by using flow charts.
79
Q

What categories of questions would you ask to conduct a nutritional screen?

A 
Ask about:
• Weight changes
- Change in clothes sizes/ring on finger
- Do dentures fit
• General diet
- Do they follow a special diet
- Do they follow any dietary restrictions
- Nutritional supplements
• Functionality
- Can they cook
- Can they exercise
•  GI symptoms
- pain
- diarrhoea, constipation
80
Q

What are the physical signs of malnutrition?

A
  • Mental health changes
  • Hair changes
  • Anaemia
  • Ascites (haemodialysis and HF patients only)
  • Diarrhoea
  • Pressure sores
  • Sunken eyes
  • Sore red eyes and lids
  • Poorly fitting dentures
  • Swollen/bleeding gums
  • Loss of subcutaneous fat
  • Muscle wasting
  • Oedema (using fingertip test)
81
Q

What treatment would you offer to a malnourished patient?

A 
Nutritional support.
Refer to a dietician for advice
- vitamin support
- high energy foods and drinks
- give patient a treatment plan
- social package of care
82
Q

What is refeeding syndrome?

What are the classical features of the syndrome?

A

A syndrome of metabolic disturbances that occurs when nutritional support is reinstated in severely malnourished/starved patients. The classic features include:

  • hypokalaemia
  • hypophophataemia
  • hypomagnesaemia
  • thaimine deficiency
  • salt and water retention
83
Q

What is the aetiology of refeeding syndrome?

A

After reintroducing food (especially carbohydrates), insulin is released, causing an uptake of glucose, potassium, phosphate and magnesium as well as utilization of thiamine.

84
Q

What are the consequences of refeeding syndrome?

A

cardiac arrhythmias (K, Mg, PO4), cardiac failure (PO4), cardiac arrest (K), respiratory distress (K, Mg), confusions, convulsions, and coma.

85
Q

What patients are at high risk of refeeding syndrome?

A
  • low BMI
  • unintentional weight loss
  • no nutritional intake for >5 days
  • low levels of K, Mg, PO4 prior to feeding
86
Q

How does body composition change with age?

A

(1) Fat mass tends to increase up to 75 years, then decreases
(2) Fat-free mass (FFM) decreases after age 40; rate of loss increases after 60yrs. FFM = bone and lean mass.
(3) Reduction in one’s body water.

87
Q

What affects your disability threshold?

A
  • baseline peak muscle mass
  • activity levels
  • overall health
  • the environment
88
Q

Why is muscle wasting more likely in the elderly population?

A
  • age-related changes
  • periods of starvation
  • periods of disease states
89
Q

Describe the change in body composition and energy utilisation during starvation

A
  • loss of both lean and fat mass
  • reduction in metabolic rate
  • increased energy from fat stores
  • protecting protein stores (although some still broken down)
90
Q

What three main evidence supports healthy eating?

A
  1. 7 Countries Study: VMRS:
    - Varying quantity of fats lowers cholesterol
    - Risk of CVD directly related to serum cholesterol
    - Mediterranean and Asian patterns compatible with low CHD
    - Sat fat increases population burden of CHD
  2. New England Journal of Medicine shows link between cancer and BMI
  3. DASH shows a diet rich in fruit, vegetables and while grains and limited in sugrary foods and red meats shown to have a significant effect on lowering systolic and diastolic blood pressire
91
Q

How would you treat malnutrition in CKD patients (aim 4)?

A
  • Adequate protein intake on dialysis (1.2g/kg)
  • 35 kcal for dialysis patients
  • give vitamins
  • enteral/parenteral nutrition
92
Q

What are the two types of lactic acidosis?

A
  • lactic acidosis type A: acute hypoxia

- lactic acidosis type B: rare and due to abnormal carbohydrate metabolism

93
Q

What are the main factors distinguishing child and adult nutrition?

A
  • higher nutritional requirement
  • immaturity (gastrointestinal, renal and immune)
  • dependence on others
94
Q

Why do infants have a higher nutritional requirement?

A
  1. Basal metabolic rate
  2. Activity
  3. Growth
  4. Temperature control
95
Q

How is the gastrointestinal tract immature in the infant?

A
  • GIT is leaky and immune response is immature
  • Breastfeeding bridges the immunological gap by coating the infant mucosa with secretory IgA (thought of as a layer of antiseptic paint)
96
Q

How is the renal system immature in the infant?

A
  • Poor ability to excrete a large solute load until 3 months of age
  • Important to carefully monitor solute consumption as vulnerable to excess plasma concentrates of these solutes
  • higher percentage of body water compared to adults, and are at a higher risk of dehyration
97
Q

What are the implications of an immature immune system in infants?

A

During gestation they receive IgG through placental transfer. Breast feeding provide further passive immunity.
The infant GIT is exposed to foreign proteins, opening opportunity to develop atopy.

98
Q

What are the advantages of breast feeding?

A

○ Lower risk of infection
○ Lower risk maternal breast cancer due to breasts tissue re-modelling.
○ Little evidence that there are lower risk of Diabetes, IBD and Obesity. However the evidence is weak.
○ Weak evidence on reduced risk of allergy. A lot of retrospective data. PROBIT study found no difference at 6 years old.
○ Neurodevelopmental advantage? A large meta-analysis showed a 3 point advantage. This is however controversial as it didn’t take into account maternal IQ or socioeconomic status. PROBIT did find that intervention group did very slight increase on better indeces.
○ Nutritionally complete
○ Correct temperature
○ Appropriate solute load. No risk of inaccurate reconstitution. Relatively low protein and sodium.
○ High bioavailability. High/better iron, folate (different from folic acid), fat (which is then 95% absorbed as it contains bile salt stimulated lipase).
○ Good digestibility
○ Promotes appropriate gut flora. May be a reason for reduced infection rate. Work also looking into the link to allergy.

99
Q

What are the disadvantages of breast feeding?

A

○ Transfer of HIV, CMV, Hepatitis. HOWEVER For sick infants, banked milk is safe as it is pasterised.
○ Transfer of chemical pollutants such as PCPs and Dioxins. However, recent results suggests no effect on neurodevelopment.

100
Q

What specialised formulas are you able to purchase?

A
  • Anti-reflux
  • High energy/nutrient dense for babies that can’t take volume
  • Inborn errors of metabolism such as phenylketonuria
  • Soya-based
  • Hypoallergenic where protein has been hydrolysed
  • For malabsorption syndromes
101
Q

What does the WHO recommend for weaning?

A

exclusive breast feeding for up to 6 months then solid foods afterwards

102
Q

What does early weaning lead to?

A
  • increased risk of allergy
  • increased risk of obesity
  • renal compromise
  • increased risk of infection
103
Q

What confers an increase risk of malnutrition?

A
  • increased requirements (e.g pyrexia, post-op, cachexia)
  • age >65y
  • bedbound/pressure sores/phyical disability
  • poorly controlled DM
  • hypo/hyperglycaemia
  • poor GI function
  • heavy alcohol consumption
  • poor social situation
104
Q

Describe the change in body composition and energy utilisation during cachexia

A
  • greater decrease in FFM and fat mass
  • increased energy requirement (due to tissue damage)
  • acute immune response leads to muscle loss
105
Q

What is sarcopenia?

A

An age-related loss of muscle mass and quality

106
Q

What factors influence sarcopenia?

A
  • decreased growth hormone secretion
  • decreased androgen
  • inactivity
107
Q

What are the consequences of lean body mass loss?

A 
10%
- reduced immunity
- more infections
20%
- poor wound healing
30%
- too weak to sit
- pressure sores
- pneumonia
40%
- death (by pneumonia)
108
Q

What are the clinical implications of age-related central fat accumulation?

A
  • increase risk of CVD
  • diabetes
  • stroke
  • hypertension
  • dysplipidaemia
109
Q

What are the clinical implications of age-related lean mass reduction?

A
  • altered motility

- increased dependence

110
Q

What are the clinical implications of age-related decrease in bone mass?

A

Increased risk of fractures

111
Q

Why does malnutrition tend to occur in the elderly?

A

As we age the body’s energy requirement reduces BUT protein, vitamin and mineral requirements remain unchanged.
Elderly require a higher density diet to fulfil requirements

112
Q

What are the risk factors of malnutrition in the elderly?

A

a) Medical: decreased appetite and thrist (ageing), decreased sensitivity of taste and smell (ageing), poor dentition and oral health, dysphagia, immobility
b) Psychological: depression, dementia and confusion
c) Social: isolation, poverty, diability

113
Q

What are the reasons a cancer patient may be malnourished?

A

1) Iatrogenic (surgery, radiotherapy, chemotherapy) causing pain, fatigue, dyspnoea, altered taste, nausea+vomiting
2) Inadequate symptom control (no appetite, early satiety, pain, taste changes, nausea
3) Different tumour sites may result in pain, altered GI function/motility, obstruction, malabsorption
4) An increased metabolic rate (cancer cachexia)

114
Q

What is cancer cachexia?

A

Multifactorial syndrome, which leads to on-going loss of skeletal muscle mass with or without the loss of fat mass, that cannot be fully reversed by conventional nutritional support and leads to progressive function impairment.

115
Q

What is the etiology of cancer cachexia

A
  • presence of a tumour or its metabilties leads to an inflammatory response
  • increased CRP levels
  • IL-1, IL-6 and Il-10 and TNF-a
  • as tumours grow more and more anaerobic metabolism occurs, the energy required for this can be derived from protein metabolism.
116
Q

What is the difference between substrate utilisation in starvation and substrate use in cancer cachexia?

A

Starvation:
Glucose decreases, Fat increases, protein utilisation also increases

Cancer:
all utilisation increases

117
Q

How is cancer cachexia diagnosed?

A

The clinical assessment of cachexia is done by looking for:
• Reduced food intake
• Catabolic drivers
• Assessment of muscle mass (or muscle strength)
• Functional assessment (through QLQ-C30 questions)
• Psychosocial assessment
Cachexia can be masked by oedema or obesity

118
Q

What are the implications for the new categorisation of cachexia?

A

More recently, cachexia has been broken down into three stages. Nutritional intervention in refractory cachexia isn’t effective. At that stage its more about reducing anxiety and improving QOL.

Pre-cachexia should be ‘treated’ with nutrition and physical activity. Lots of evidence shows that targeting people early on is much more beneficial. At refractory cachexia, only pharmaceuticals are useful.

119
Q

What are the goals of nutritional support in cancer cachexia?

A

Goals of nutritional support in cancer:
• Prevent cancer or treatment related malnutrition
• Increase treatment efficacy
• Maintain strength
• Maintain QoL
• Promote physical activity/minimise inactivity

120
Q

Compare the nutritional aspects of breast and lung cancer

A

BREAST:

  • often well (and over) nourished
  • treatable (long term is remission or a cure)
  • aggressive nutrition is rarely needed

LUNGL

  • often malnourished
  • focus more on QoL and symptom control
  • Require nutritional support and a care plan
  • Frequent cachexia
121
Q

What tumours have a high malnutrition risk?

A

Head and Neck, Oesophago-Gastric and Pancreatic

122
Q

What tumours have a medium malnutrition risk?

A

Prostate, Colorectal and Lung

123
Q

What tumours have a low malnutrition risk?

A

Breast, Sarcomas and NHL

124
Q

Why does anaerobic respiration only last for 30-40s?

A

First 20 seconds is due to conversion of ADP to ATP by phosphocreatine
Glycogen glycolysis produces lactic acid, after about 20 seconds of maximal exercise inhibits enzymes of the pathway.

125
Q

What is the most effective way to rapid increase creatine stores?

A

20g of creatine supplements for 5 days

126
Q

What are the risks of creatine supplementation?

A
  • increased body mass
  • increases the incidences of muscle cramps
  • fibre swelling reduces blood flow
127
Q

What is the prefered substrate for high and low intensity exercise?

A

CHO is the preferred substrate for high intensity exercise

fat is the preferred substrate for low levels of exercise

128
Q

How big are our glycogen and glucose stores?

A

315g

129
Q

What is ‘hitting the wall’

A

After 100 minutes of endurance exercise, the glycogen and glucose stores have been depleted.

130
Q

What CHOs are oxidised at higher rates?

A
  • Glucose, sucrose, maltose, maltodextrins and amylopectins

- Fructose, galactose and malyose have been shown to be oxidises at 25-50% lower rates

131
Q

What is the maximal effective dose of protein for stimulating post-exercise MPS?

A

20g

132
Q

What lifestyle modification has been shown to have the most significant effect on reducing systolic blood pressure?

A

Maintaining the DASH diet. Notable mentions:

  • low Na+ intake
  • regular aerobic activity
  • moderate alcohol consumption
133
Q

What is the cut-off point below which diabetes mellitus patients should be maintained?

A

48mmol/mol

134
Q

What is the most common cause of CKD?

A

Type 2 diabetes. Notable mention includes:

  • hypertension (arguably also the answer)-
  • acute kidney injury
135
Q

What is the best way to reduce the risk of developing type II diabetes?

A

Maintaining an ideal BMI. Notable mentions:

- Exercising for 20 mins a day

136
Q

What two main questions would you ask when beginning a nutritional assessment?

A
  • Have you lost weight?

- Was this intentional/through reduced intake?

137
Q

What are the advantages of eating oily fish?

A
  • plaque stability
  • reduced triglycerides
  • improved endothelial function
  • inhibit platelets
  • anti-arryhthmic
  • decrease clotting

Year 2 S&P (4 decks)

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