3.1 Malnutrition

Abdominal Cavity

Abdominal cavity lined with peritoneum --> a serous (fluid secreting) membrane

  • made up of parietal (outer wall) and visceral (coating organs)
  • reduces friction and allows organs to move freely

Superficial lymphatic vessels drain with the subcutaneous veins.Deep lymph vessels drain with the deep veins into external iliac, common iliac and lumbar lymph nodes.

Peritoneal cavity has 2 sacs àgreater and lesser - Only communication is epiploic foramen between the 2

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Embryonic Development

  • Week 3 Gastrulation: Formation of 3 germ layers (Ectoderm, Mesoderm and ENDODERM)
    • GI tract is main organ formed from endoderm
  • Week 4: Embryonic folding: Converting a flat germ disc into a 3D structure
    • Disk on the roof of yolk sac forms a tube
  • The GI tract is the main organ system derived from the endodermal germ layer.
  •  Initially it has a flat disc-like shape forming the roof of the yolk sac and closely opposed to the ectoderm. 
  • Its formation is dependent on embryonic folding.
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Gut Tube Formation

  • Middle fusion transforms flat endoderm into a gut tube
  • Rapid growth of somite’s results in lateralfolding. 
  • Midgut remains attached to yolk sac by vitelline duct, which eventually becomes obliterated, allowing it to obtain its free position in the abdomen
  • Passive event to form primitive gut tube
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Mesenteries and Abdominal Cavity

  • Gut tube attached to posterior abdominal wall by mesentery
  • Dorsal mesentery associated with all parts
  • Foregut has Ventral mesentery associated with it attaching it to anterior ab wall
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Week 6

  • Still has gut tube
  • Has more shape
  • Liver has grown in the ventral mesentery splitting it into lesser omentum and falciform ligament (connects liver to anterior abdominal wall)
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Stomach: Rotation and Growth

  •  Stomach starts to rotate 90Oclockwise around longitudinal axis
  • Now posterior (behind stomach) and anterior (in front of stomach) vagus trunks
  • Then has growth in the walls at a different rate
    • Greater and lesser curves
  • Rotates along anteroposterior axis
  • Pylorus gets pulled up 
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Stomach and Mesenteries

Formation of omental bursa (lesser sac)

·      Liver grows rapidly at beginning of development

·      Stomach twists and space behind stomach omental bursa forms

·      Pyloric pulls up causing duodenum to have C shape

·      Dorsal mesentery runs along greater curvature

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Midgut Formation

  • ·      Suspended from the dorsal abdominal wall
  • Communicates with yolk sac by vitelline duct
  • Rapid elongation of primary intestinal loop during development
  • In the adult it begins immediately distal to the entrance of the bile duct into the duodenum until the proximal 2/3 of the transverse colon.
  • SMA blood supply.
  • During development gut loop gets pushed out at about 6 weeks as the liver has grown so much, at week 12 starts to go back in 
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Rotation of Midgut

  • 270˚ counter clockwise rotation (axis – SMA, the artery that supplies it)
  • 90 degrees when first comes out then 180 when goes back in
  • Then gets fixed into position with mesentery 
  • Elongation of small intestines loop = jejunum & ileum coiled loops
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Liver and Gallbladder Development

  • Outgrowth at the distal end of the foregut (endoderm of foregut) as the liver bud
  • Celiac trunk blood supply
  • Connection between liver and foregut is bile duct, eventual growth off bile duct which is gall bladder
  • At 12 weeks liver starts producing bile
  • Bile duct will eventually run posterior to duodenum
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Pancreas Development

  • Dorsal pancreatic bud and ventral pancreatic bud
  • As stomach and duodenum rotated ventral bud rotates dorsally to dorsal bud
  • Buds eventually fuse
  • Dorsal bud forms most of it on top, ventral below
  • Have own ducts
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Carbohydrates

  • should by 50% of total dietry energy

Function

  • Energy Source (via glycolysis and TCA cycle)
  • Fuel for Central Nervous System (brain requires 120g/day)
  • Control of blood glucose and insulin metabolism
  • Effects on satiety/gastric emptying àpromote satiety
  • Cholesterol and triglyceride metabolism (increases conc in blood)
  • Fermentation (Production of short-chain fatty acids) & Control of colonic epithelial cell function
  • Bowel laxation/motor activity
  • Effects on large bowel microflora
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Dietary Fibre

  • In vegetable components (plant cell walls – NSP = Non-starch Polysaccharides; Non-digestible CHO)
  • Not digested in small intestine and end up in colon
  • Needs to have a health benefit which is a reduced glycaemic response, reduces cholesterol, helps with constipation
  • Soluble (pectin, b-glucan)/ insoluble (cellulose)
  • Associated with starch in foods
  • Role --> Bulking effect (can hold more water), speeds up colonic transit time (goes through colon faster)
  • Fermentation provides short chain FA (e.g. butyrate, acetate, propionate)
    • Major energy fuel for epithelial cells of the colon
    • Can go to liver through hepatic vein
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Anaemia Preventing Vitamins

  • Thymidylate synthesis- rapid cell division
  • If insufficient high turnover cells will suffer e.g. rbc
  • B12
    • In animal products, yeast (+ intrinsic factor)
    • Deficiency àmegaloblastic anaemia, neuropathy (impaired sense of myelin)
    • Cofactor in DNA synthesis
  • Folate
    • In green vegetable
    • Deficiency - anaemia, increased risk of neural tube defect
    • Pregnant women advised to take
  • Methionine synthetase (a B12 dependent enzyme which catalyses a reaction that yields free folate in tissues via methylation of homocysteine to methionine) provides the link between the physiological functions of B12 and folate
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Vitamin D

  • also a hormone
  • SOURCES
    • D3(Cholecalciferol) - Fish oils, egg yolk, butter (margarine)
    • 7-Dehydrocholesterol - Animal fats, plant sterols  (skin - UV light)
  • METABOLISM
    • D3undergoes liver + kidney hydroxylation’s:
    • 25 hydroxycholecalciferol (25(OH)D3) or Calcidiol
    • 1,25 dihydroxycholecalciferol (1,25 diOH D3) or Calcitriol (the physiologically active form of Vitamin D)
  • ACTIONS of VITAMIN DDEFICIENCY - Rickets (Children), Osteomalacia (Adults), TOXICITY (>250mg/day)  
    • Intestinal absorption of Ca + Phosphorus (Ca binding protein - CALBINDIN)
    • Renal reabsorption of Ca & PO4        Normal bone formation
    • Low levels of plasm Ca stimulates STH and Vit D synthesis
    • Activated Vit D increases intestinal Ca absorption and regulates Ca excretion from kidney and bone
    • When plasma Ca is high calcitonin is secreted from thyroid gland and promotes Ca excretion in kidneys and prevents bone from releasing Ca
    • Neuromuscular & immune functions, apoptosis & inflammation (VDRs form dimers with RXR and regulate gene expression)
  • weakness, nausea, loss of appetite, headache, abdominal pains, cramp and diarrhoea, hypercalcaemia and calcification of soft tissues
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Calcium

  • need approx - 1.2kg 
  • needed for bones (99%), cell signalling and muscle function
  • can get from milk and dairy products, added to flour and hard water
  • absorbed in intestines by Ca binding protein (calbindin), regulated by vit D, can be affected by food (habitatual food intake, mea ingestion and phytates)
  • Low levels of plasma Ca stimulates PTH and Vitamin D synthesis.  Activated vitamin D increases intestinal Ca absorption and regulates Ca excretion from the kidney and bone.
  • Calcitonin is secreted from the thyroid gland when plasma Ca is high and promotes Ca excretion in kidney and prevents bone from releasing Ca. 
  • Bone mineralisation affected by other hormones (e.g. oestrogens), exercise, smoking
  • Peak bone mass occurs at 30 Higher mass àlonger period of time before mass and mineral content decline to risk of fracture
  • affected by genetics, endocrine, smoking, nutrients, mechanical
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Iron

  • needed for Hb, electron transport (ferrous 2+ and ferric 3+), chromatome P450
  • stored in reticulo-endothelial system (speen and liver) and bone marrow
  • reflected by plasma ferritin (major strorage protein)
  • transferrin transferes Fe to bone marrow

Absorbtion

  • only in ferrous, enhanced by reducing agents
  • enhanced by dietary (vit c, fructose, alcohol, meat), physiological (Fe deficiency and anemia, fasting and pregnancy)
  • inhibited by dietary (tannins, polyphenols, phosphates, other minerals), physiological (Fe overoad, achlorhydria Cu deficiency)
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Formation of Bile

  • 1-2L of bile produced daily
  • bile salts for emulsification od fat are synthesised from cholesterol in liver
  • required for uptake of fat and hence fat soluble vitamins
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Enterohepatic Recycling of Bile

  • bile synthesised in liver released into GI tract by gall bladder, emulsified by fat and helped it to be stored and goes back to liver by portal circulation
  • some bile not taken up so body takes up more cholesterol to help make bile
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Platelet Aggregation

  • Decreased thrombosis-inhibition of platelet aggregation, decreased blockage of artery
  • Thromboxane will cause platelet aggregation
  • Prostacyclin inhibits platelet aggregation
  • EPA competes with arachidonic acid for COX- reduction in COX metabolites
  • Produces TXA3 which isn’t as good at aggregating platelets

  • Types of oily fish - Mackerel, herring, pilchards, salmon, sardines, trout, Kippers

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Dietary Risk Factors for Obesity

Fat

  • Unbalanced proportion of saturated fats and reduced n-3 fatty acids
  • Many ‘fast foods’ and convenience products contain high levels of fat
  • Leads to passive overconsumption of energy
  • Some evidence that individuals with reduced ability to oxidise fat are at risk of weight gain

Sugar

  • Rapid increase in blood glucose
  • ‘Hidden’ energy consumption
  • ”Free sugars” (sugar-sweetened drinks, cereals, chocolate, sweets, fruit juice & table sugar).

Alcohol

  • Decreases fat oxidation & increases fat storage
  • 7 kcal/g

High fat/energy dense foods lead to passive overconsumption

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Definitions of Undernutrition

Undernutrition can be:

       Generalised – deficiency of calories (negative energy balance) 

       Specific – deficiency of an essential nutrient 

       Primary – related to the diet 

       Secondary – related to an illness or condition

Causes

  1. Reduced delivery of nutrients to the gastrointestinal system.

      Decreased food availability

      Mechanical (e.g. can’t swallow, like if you have cancer)

      Functional (neurological)

  1. Increased demand for nutrients.

      Physiologicalàpregnancy

      Pathophysiologicalàunderlying disease increases demands

  1. Inability for gastrointestinal system to absorb nutrients.

      Intrinsic problem, Post-surgery

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Response to Calorie Undernutrition

  • Lack of carbs the insulin response is reduced, less insulin
  • Has implications as anabolic, as normally suppress protein cabalism, so muscle broken down to amino acids and goes to liver for gluconeogenesis
  • Triglycerides break down and FA and glycerol released as reduced insulin suppression of lipolysis
    • Glycerol gluconeogenesis
  • FA used instead of glucose as energy source, as cells become resistant to glucose so it can be used for CNS. FA goes to ketone bodies used for the brain and for energy
  • Will keep going on for however long there are fat stores, when gone there is protein tissue breakdown
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PEM - Protein Energy Malnutrition

·      Protein-Energy-Malnutrition affects 400+ million people worldwide. 

·      Form depends on protein-carbohydrate balance:

·      Dry PEM =Marasmus (no oedema, general)

o  Severe calorie and protein deficiency                        

·      http://www.euskaljakintza.com/wp-content/uploads/2009/03/kwashiorkor.jpgWet PEM = Kwashiorkor(oedema, specific)

o  Severe protein deficiency (Ghanaian 1st – 2nd child) – linked to low plasma albumin concentrations (hypoalbuminemia)

Might not have another deficiency but mainly protein

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Effects of General Malnutrition

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Refeeding Syndrome

  • ·      Can’t give lots of food straight away
  • ·      Insulin stimulates the pumps for circulating electrolytes so there is more in the cell
  • ·      There are now deficits in the circulating electrolytes which 
  • ·      Rhabdomyolysis is when the skeletal muscle has been broken down
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Enteral Nutrition Support

  • Provided when patients are expected to (or have) not received adequate nutrition for 7 days
  • Small bowel feeding administered with pump over 8-20 hours
  • Formulas come in a variety of energy densities (0.8 to 2.0 kcal/ml)
    • Most patients with standard fluid requirements will tolerate 1 to 1.2 kcal/ml
  •  How to feed 14.2x weight (kg) +593
    • Can add x PAL (physical activity level) (1.25
    • Can add x Stress factor (1.15)
    • Or reffeding syndrome (o.25 x REE)
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Coeliac Disease

       Gluten Enteropathy – Flattening of Small Intestinal Mucosa as immunological response to wheat protein.

       Consequences

      Malabsorption - Wasting in adults, Failure to thrive in children.

      Steatorrhoea.

      Abdominal discomfort.

       Treatment

      Achieve normal weight gain / growth rate. 

      Acutely – correct dehydration, Ca2+/ vitamin deficiencies. 

      Chronic – gluten-free diet (any food containing Wheat, Barley, Rye, & Oats). Need to be aware of hidden ingredients – e.g. sauces.

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Crohn's disease

       Chronic inflammation of GIT – most commonly in the ileum or colon.

       Consequences

      Obstruction leading to fistulae 

      GIT haemorrhage leading to anaemia 

      Malabsorption, diarrhoea, pain, weight loss.

- Ulceration mouth to anus

       Treatment

      Elemental diets, corticosteroids 

      Calorie / protein / vitamin / Ca2+/ fluid supplementation 

      Biopsy and surgical resection / stoma?

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Head and Neck Oncology

       5-10% of malignant tumours.

       Consequences

      Reduced saliva production. 

      Reduced mastication and swallowing. 

      May need anti-emetic. 

      May need more calories and fluid.

       Treatment

      Liquidize, eat little and often. 

      Keep daily record of weight and consumption. 

      Increase protein

      Gradually change diet to avoid refeeding syndrome. 

      Avoid diet / low fat foods. 

Percutaneous EndoscopicGastrostomy tube

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Type 1 Diabetes Mellitus

       Caused by insulin deficiency and characterised by polyuria and weight loss.

       Consequences

      Need to balance food intake, insulin and physical activity level. 

      Educate to identify mood changes, awareness of hypoglycaemia resembling alcohol intoxication.

       Treatment

      Regular meal and insulin pattern. 

      Limit fat to 35% of energy requirements (high fat increases insulin resistance / impairs glucose tolerance). 

      Increase soluble fibre and complex carbohydrates (decreases sudden glucose loading).

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Hyperlipidaemia

       Excess lipids in blood.

       Consequences

      TC:HDL ratio of 5+ = increased risk of CHD.

       Treatment

      Realistic weight loss target by realistic lifestyle change. 

      Decrease saturated fats, salt, smoking and excess alcohol.

       Increase monounsaturated fats, Non-Starch Polysaccharides, exercise, (oily fish and garlic as anti-thrombogenic?).

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