Undernutrition Flashcards
(36 cards)
What is undernutrition?
Less than adequate energy and/ or protein intake
- Insufficient nutrient intake
- Disordered nutrient uptake/ use
What may cause insufficient nutrient intake?
- Food insecurity/ famine
- Voluntary fasting/ starving
- Anorexia nervosa
- Depression
- Illness
- Medication
Common in elderly and children
What may cause disordered nutrient uptake/ use?
- Digestion, absorption and transport difficulties e.g Coeliac Disease
- Wasting disorders
- Increased metabolic demands
What is a chronic energy deficiency?
- Over a long period
- Low but stable body weight –> in a steady state
- In energy balance but at a low cost
- Several energy saving homeostatic responses to adapt to changes to allow energy balance to be maintained
What is acute energy deficiences?
- Sudden decline body weight –> >10% loss of body weight over 3-6 months
- Often existing disease –> adaptations to conserve energy may not happen
- Energy deficiency + infection/ injury = faster loss of body weight –> due to catabolic response to injury
What happens to energy expenditure during acute critical illness?
Increased BMR
Occurs in patients with
- fractures (depends on number of fractures –> multiple = higher increase), post-operative, cancer, liver disease, sepsis and fever.
The greatest loss is in burns patients - doubling of BMR with 40% burns.
(Some energy savings from being bed bound)
What are the mediators of the acute catabolic response to injury?
Hormones
- Raised Catecholamines and Cortisol
- Promote increase in metabolic rate, nitrogen loss and glucose production
- Early reduction in insulin are later increased as insulin resistance develops
Pro-inflammatory cytokines
- TNFa, IL-I, IL-6
- Stimulate acute phase protein synthesis in liver
- e.g Mobilise clotting factors
What is the body composition changes occur in chronic energy deficiency?
- Reduction of weight, height, BMI, fat mass and fat free mass –> produces considerable energy saving, as less weight means the body is able to adapt to lower energy intake as the demand is lower.
- Viscera: Skeletal muscle ratio is increased –> Skeletal muscle is lost –> has effect on BMR as visceral fat is more metabolically active in resting situations, have a relative impact on energy expenditure
- Usually shorter, indicating chronic nature –> stunted growth especially if occurs from childhood, can continue on to adulthood
- Poor insulation against the cold –> decreased fat mass means there is less fat to insulate. Have a greater vasoconstriction response, susceptible to hypothermia.
What are the energy adaptions from CED to RMR?
Reduced RMR in CED due to
- reductions in body weight (FFM) –> less metabolism occurring in organs and tissues
- possible enhanced metabolic efficiency –> oxygen consumed can produce more ATP?
Keys et al 1950
- 36 individuals, partaking in a political stance against WW2 –> semi-starvation trial
- 24 week starvation period, then re-nourished after
- Idea to understand the impact of WW2 on famine
Results
- BMR decreased by 25% per kg of fat free mass
- Most rapid decline was in the first 2 weeks
What are the energy adaptions from CED to physical activity?
- Likely a decrease in voluntary PA –> behavioural change, do more sedentary activities
- Can be seasonal variation in those people who need to work hard - agricultural labour –> in some areas in certain seasons food is more abundant that in others
- No real evidence of mechanical efficiency –> amount of work per amount of mass
- Ergonomic efficiency –> adjust way of carrying heaving loads
- Reductions in recovery after exercise –> less fit/ have less exercise capacity
Physical, ergonomic and and behavioural
What is the energy adaption from CED to thermogenesis?
Thermic effect of food (TEF)/ diet induced thermogenesis
- Very little data in the area
- Possibility that this is reduced in CED
Response to cold
- Heat loss from less insulation
- Greater vasoconstriction and earlier onset of not shivering thermogenesis to compensate for lack of adipose tissue
- If temp continues to drop there is hypothermia risk
What are the overall energy adaptations to CED?
Negative energy balance
- Increased metabolic efficiency? –> Decreased BMR and thermogenesis –> Lower energy expenditure
- Decreased energy stores –> Lower body size –> Decreased BMR and thermogenesis –> lower cost of activity –> lower energy expenditure
- Decreased physical activity –> lower energy expenditure
Discuss weight changes with negative energy balance
Rapid initial loss
- Water loss associated with depletion of liver and muscle glycogen reserves
Much slower loss
- Energy balance regained at lower body weight
Why?
As less food is eaten there is a decreased energy cost of
- Digestion
- Absorption
- Synthesis of triglyceride reserves and glycogen reserves
- Decreased protein turnover –> protein synthesis more likely to be inhibited/ reduced
As body weight decrease
- BMR decreases
- Decreased cost of physical activity
What regulatory mechanisms behind the energy adaptations to CED?
Adaptations are aimed at maintaining function/ survival
Nervous system
- Reduction of sympathetic nervous system activity with underfeeding –> lower levels of adrenaline, noradrenaline
- Discovered in animal models and short term human studies
Endocrine
- Thyroxine (T3) reduced in starvation –> thyroid hormones are the main hormones in regulating metabolic rate. Less T3 to stimulate metabolism
- Other potential mediators include leptin, insulin, insulin-like growth factor, progesterone
What are the consequences of CED?
Decreased muscle strength and endurance:
- Associated with lower muscle mass
- Also strength is reduced per unit of muscle
- Suggests functional changes in skeletal muscle
- Decline in fast type 2 fibres/ conversion to slow type 1
- Reduction in substrate storage
Reduced immunity:
- Delayed wound healing post op
- Prolonged hospitalisation
- Mortality increases sharply with BMI <16
- Chest infection –> less muscle mass to do the contractile function of breathing
Altered autonomic nervous function:
- Sympathetic nervous system activity decreases
- Parasympathetic nervous system activity increases
- Receptors for neurotransmitters alter in number –> potential cognitive impairment
- Drugs that work on receptor site may need a dose alteration
Psychological:
- Depression
- Anxiety
- Reduced will to recover
- Potential eating disorder risk
What are the consequences of severe malnutrition?
- Lethargy and irritability
- Decreased appetite
- Impaired thyroid function
- Impaired cortisol and growth hormones responses
- Respiratory tract infections
- Altered immune function
- Impaired cardiac function?
- Impaired hepatic synthetic function and hepatobiliary function –> hepatobiliary system refers to liver, gall bladder and bile ducts and how they work together
- Impaired macronutrient absorption
- Intestinal infections
- Changes to microbiota
- Loss of skin integrity
- Reduced b-cell function
- Impaired pancreatic exocrine function
How is undernutrition assessed?
History –> try to identify reason
AED –> % weight loss - vs onset
Body composition
- height for age
- weight for height
- skinfold thickness
- mid-upper arm circumference –> FFM amount
Muscle function
- hand-grip strength
Blood tests
- Hormones –> T3, insulin, GH, PTH
- Serum albumin –> indicator of inflammation but not for nutrition status
What happens to metabolism in starvation?
Glucose is preserved for the tissues that depends on it:
- Brain
- Erythrocytes
- Renal medulla
Long-term use of amino acids for fuel is minimised:
- Preserve muscle function
Energy from other sources:
- FFA and glycerol from TAG fat stores (adipose tissue) –> fat oxidisation by B oxidation –> glycerol used to synthesis glucose in gluconeogenesis
- Generation of glucose in gluconeogenesis from non-CHO sources –> glycerol from lipolysis, lactate from anaerobic respiration, carbon skeletons from some amino acids
What happens to the metabolic rate during fasting?
First week
Before starvation kicks in there is a transient increases in BMR over 2-3 days –> because of increase in gluconeogenesis and mobilisation of energy stores
Then BMR decreases to lower level from loss of body mass and decreased cellular energy consumption –> decrease in protein synthesis
Short term fasting (3-4days)
- Glycogen stores depleted within first 24 hours
- Plasma glucose decreases (low physiological range)
- Low insulin
- Increased glucagon
- SKM amino acids mobilised by proteolysis –> usually transaminated into glutamine and alanine and the exported from muscle to liver for gluconeogenesis
- Lipolysis occurs in adipose tissue where SKM will use FFA for fuel and glycerol will be used for gluconeogenesis
- Body weight decreases rapidly –> up to 5kg in few days (healthy adult)
Overall, no circulating glucose and depleted glycogen stores means the body relies on fat mobilisation. Lipolysis of TG from AT into FFA and glycerol for liver and muscle utilisation.
Lactate, glycerol and amino acids being used for gluconeogenesis which provides most of the glucose for the RBC, brain and kidney.
What happens during starvation?
After 1 week
- Further decreases in glucose and insulin
- Gradual sparing of protein as nitrogen in urine as form of ammonia
- Muscle amino acid release slows as the body is trying to preserve the body and muscle mass
- Increase in lipolysis –> FFA and glycerol
- Glycerol used in gluconeogenesis
- FFA oxidation in liver –> acetyl CoA –> ketone bodies which can be used by the brain as an energy source (ketogenesis)
- Where glucose is used outside the brain, RBC and kidney, pyruvate and lactate are recycled by gluconeogenesis –> lactate removed from RBC
- Glutamine that has been released is taken up by kidney
What happens to ketone body levels during starvation?
Overnight fast
- 0.2mmol/L
2-3 weeks starvation
- 7-9mmol/L (steady state)
What is the function of ketone bodies during starvation?
Supply 2/3 of brain fuel requirements
Reduce the need for protein catabolism
What are the key process that occur in 2-3 weeks of starvation?
Gluconeogeneis
Ketogenesis
Lipolysis
B-fatty acid oxidation
Lactate and pyruvate recycling from RBC
Kidney increase contribution to gluconeogenesis
Summarise what occurs in starvation
<24 hours
- Muscle and liver glycogen used up
- Increased ketogenesis from adipose tissue triacylglycerol
- Increased catabolism of muscle protein for gluconeogenesis
After 2-3 weeks
- Plasma ketone bodies high enough to significant utilisation by CNS
- Less need for protein catabolism for gluconeogenesis - muscle spared
When adipose tissue reserves are exhausted
- much increase catabolism of muscle and other tissue protein as metabolic fuel
Death results from loss of essential tissue protein - organ dysfunction
