Biochemical Aspects of GI Disease and Nutrition Flashcards
What does the following terms mean?
Dietary reference value
Recommended daily intake
Recommended daily amount
Estimated average requirement
Reference nutrient intake
Lower reference nutrient intake
What should you ask during a clinical assessment for GI diseae and Nutrition?
What is normal for patient – Weight (loss or gain; intentional unintentional)
• Family weight
– Food intake
– Chewing/swallowing
– GI symptoms
• Nausea, vomiting, altered bowel habit
– Drugs/alcoho
How do you measure the following functional assessments?
- Muscles mass
- Hepatic Secretory Proteins
- Immune Response in malnourished patients
Muscle mass - Grip strength/isometric knee extension/response to electrical stimulation
Hepatic secretory proteins - albumin (<35g/L), transferrin (<1.5 g/L)
Immune response in malnourished patients – Cell mediated immunity
Malnutrition
Up to 40% can be malnourished in hospital
what complication can happen due to the following:
Impaired immune response
Decreased respiratory muscle strength
Impaired wound healing
Inactivity
Decreased skeletal muscle strength
Impaired thermoregulation
Malabsorption’ – Wide group of conditions associated with disordered biochemistry – No specific clinical presentation • May be a group of signs or symptoms
Impaired immune response - Infection
Decreased respiratory muscle strength - Increased incidence of chest infection
Impaired wound healing - Prolonged recovery
Inactivity - Thromboembolism, pressure sores
Decreased skeletal muscle strength - Fatigue, inactivity, falls
Impaired thermoregulation - Hypothermia
What are the causes for the following presentation?
Pale bulky (offensive) stools - fat malabsorption or digestion
Abdominal distention, borborygmi (gurgling in stomach), watery diarrhoea and xs flatus
Vague malaise, tiredness and weightloss
Anaemia
Easy bruising or bleeding
Failure to thrive (infants)
What are different sources of energy?
What prediction equations are there to calculate GI disease?
Carbohydrates • Fats • Protein • Vitamins • Minerals • Fibre
Energy Requirements – Calorimetry • Estimation from body weight – 25-35 kcal/kg/24h • Prediction equations – Schofield equation – Harris-Benedict equation – Ireton-Jones formula
What is the difference between intrinsic and extrinsic sugar?
What are starches made up of?
What are digestive ezymes that break up carbohydrate?
How are carbohydates absorbed?
Where is amylase produced and what does it help digest?
Sugars – Intrinsic • Naturally e.g. as part of the cellular structure
– Extrinsic • Non natural e.g. refined sugar
Starches • α glucan polysaccharides • Amylose – Straight chain glucose polymer with molecular mass 100 000 Da
• Amylopectin – Branched chain glucose polymer with molecular mass >1 000 000 Da
- Digestive Enzymes - Salivary amylase, pancreatic amylase, and brush border enzymes (dextrinase, glucoamylase, lactase, maltase, and sucrase)
Absorption – Secondary active transport (cotransport) with Na+ – Facilitated diffusion of some monosaccharides • Enter the capillary beds in the villi • Transported to the liver via the hepatic portal vein
• Digestion – Amylase • Salivary and pancreatic • Digestion of α-1,4 bonds in starch • Produces – Maltose – Maltotriose – Short branched oligosaccarhides – α-limit dextrins
What are the actions of the following enzymes and what are the actions and products?
Maltase
Sucrase
Isomaltase
Sucrase -isomaltase
Lactase
What percentage of carbs are not absorbed?
Carbohydrates in the bowel is metabolised by bacteria to produce what?
Who commonly has primary lactase deficiency? What are causes of secondary lactase deficiency?
What can you use to investigate carbohydrate absorption
Up to 20% of dietary starch is not absorbed
- Carbohydrate in the bowel metabolised by bacteria to produce short chain fatty acids (energy source for colonocytes) + methane + hydrogen
- Primary lactase deficiency – Europeans 5 – 15% have deficiency – Africans/Asians >70% deficiency
- Secondary Lactase deficiency – Inflammatory bowel disease – Chronic alcoholism – Coeliac disease – Tropical Sprue
- Lactose tolerance test – Serial glucose measurements after 50 g lactose
Hydrogen breath tests help to diagnose either intolerance to sugars or small intestinal bacterial overgrowth (SIBO). The test measures how the amount of hydrogen present in your breath changes after you consume a sugar solution.
What oes the following tests indicate?
Glucose hydrogen breath test
Lactose hydrogen breath test
Fructose hydrogen breath test
Sorbitol hydrogen breath test
Lactulose hydroen breath test
– Glucose hydrogen breath test
• bacterial overgrowth in the (upper) small intestine
– Lactose hydrogen breath test
• problem digesting lactose products
– Fructose hydrogen breath test
- Problem digesting fructose e.g. honey, vegetables, fruits and grains. – Sorbitol hydrogen breath test
- Sorbitol is a sugar alcohol (polyol) used to investigate rapid intestinal transit.
– Lactulose hydrogen breath test
• Lactulose - galactose and fructose. Transported intact to the colon measure of orocecal transit time (OCTT).
What are the different types of fats?
How is fat absorbed and digested?
Types of fats: Triacylglycerol – Triglyceride • Phospholipids • Sterols
Fat – Emulsified by bile phospholipid – Stabilised and emulsified by bile salts – Lipase digestion to monoacylglycerol and free fatty acids with pancreatic lipase – Solubilised in micelles
Absorption of glycerol and short chain fatty acids – Absorbed into the capillary blood in villi – Transported via the hepatic portal vein
Absorption of monoglycerides and fatty acids – Cluster with bile salts and lecithin to form micelles – Released by micelles to diffuse into epithelial cells – Combine with proteins to form chylomicrons – Enter lacteals and are transported to systemic circulation
What are the essentials fatty acids such as linoleic acid and alpha linoleic acid precursors of?
– Arachadonic acid • C20:4, ω-6
– Eicosapentaenoic acid • C20:5, ω-3
– Docosahexaenoic acid • C22:6, ω-3
What is fat absorption dependent on?
– Bile production • Dependent on liver secretion – Bile salts – Phospholipid – Cholesterol • Patent ducts
– Pancreatic enzymes • Functioning pancreas
Investigation of Fat absorption
• 14C-Triolein breath test – If 14C-labelled triolein absorbed, 14C02 will appear in breath – But lung/liver disease may give false results
Faecal fat excretion no longer used.
How is protein broken down?
How protein metabolism mesured?
- Nitrogen balance – Patients on ITU or long term nutrition • Nitrogen excretion = urinary nitrogen + faecal nitrogen
- Variability of faecal output • Urinary nitrogen = urinary urea nitrogen + non urea nitrogen – Non urea nitrogen is usually ~ 20% of urinary urea nitrogen – Faecal nitrogen is ‘constant’ ~ 1-2 g/24 hour
- Urinary urea nitrogen can be used as an assessment tool (but) – Becomes less useful with increasing severity of illness
– Inaccurate where there is urine infection (urea-splitting organisms)
Where does majority of absorption hapeb?
jenum
What are different ways of supplementing nutrition?
What screening tool can be used for nutrition?
wha
Food supplements • Enteral (using the gut) • Parenteral (intravenous)
Simplest form – appropriate diet – Appropriate staff
- Estimating requirements
- Food enrichment – Fortified puddings – Fortified supplements (juice type) – Modular supplements (protein, carbohydrate) – Nutritionally complete supplements (milky type)
Why is enteral feeding used?
What conditions would you give enteral feeding?
E.g Disturbed swallowing and MND
What are sources of delivery of enteral feeding?
- Nutrients delivered to the gut – Stimulate gut hormones – Help maintain gut integrity – Nutrients absorbed into portal circulation – More physiological than TPN
- Different routes of delivery
Into the stomach
– nasogastric or orogastric tube
– gastrostomy – oesphagostomy
• Beyond the stomach
– nasoduodenal tube
– jejunostomy
Refeeding syndrome
- consisting of metabolic disturbances that occur as a result of reinstitution of nutrition to patients who are starved, severely malnourished or metabolically stressed due to severe illness.
- When too much food and/or liquid nutrition supplement is consumed during the initial four to seven days of refeeding, this triggers synthesis of glycogen, fat and protein in cells, to the detriment of serum concentrations of potassium, magnesium, and phosphorus.
- Cardiac, pulmonary and neurological symptoms can be signs of refeeding syndrome.
- The low serum minerals, if severe enough, can be fatal
Essentially quickly refeeding = more insulin = potassium,, magnesium and phosphorous go inside cells too quickly
Thiamine gets used up quickly too causing deficiency
who are at risk of refeeding syndrome?
What are the signs?
- Patients with anorexia nervosa
- Patients with chronic alcoholism
- Oncology patients
- Postoperative patients
- Elderly patients (comorbidities, decreased physiological reserve)
- Patients with uncontrolled diabetes mellitus (electrolyte depletion, diuresis)
- Patients with chronic malnutrition: – -Marasmus – -Prolonged fasting or low energy diet – -Morbid obesity with profound weight loss – - High stress patient unfed for >7 days – -Malabsorptive syndrome (such as inflammatory bowel disease, chronic pancreatitis, cystic fibrosis, short bowel syndrome)
- Long term users of antacids (magnesium and aluminium salts bind phosphate) • Long term users of diuretics (loss of electrolytes)
How do you feed those who are at risk of refeeding syndrome?
What are medically induced malnutrition?
Gastric Sleeve
Roux en Y Gastric Bypass
