Nutrition Flashcards
What is the chemical name for Omega 6?
- what is the final product?
- Linoleic Acid
- found in vegetable and safflower oils
- converts to Arachidonic Acid
- found in Meat, poultry and eggs
What is the chemical name for Omega 3
- what are its final products when digested?
- A-Linolenic Acid
- found in leafy veg, canola, walnut and soybean oils
- converts to Eicosapeanoic Acid then Docosahexaenoic acid
- these are found in fish oils, there is a poor conversion of these therefore it is needed in the diet.
What is the function of dietary fat?
- makes food taste better
- carries important fat-soluble vitamins
- vit A: night vision, and BW
- vit D: hormone, bone health, immune system
- vit E: antioxidant
- vit K: blood clotting factors
- component of the cell membrane
- a precursor of steroid hormones and vitamin D
What are essential amino acids?
- list them
Amino acids we need to get from our diet
- Histidine
- Isoleucine
- Leucine
- Methionine
- Phenylalanine
- Threonine
- Tryptophan
- Valine
- Lysine
What are conditionally non-essential amino acids?
- list them
The body can produce these with essential a.a acting as precursors
- Arginine
- produced from glutamate and glutamine in the intestines
- Asparagine
- Glutamine
- Glycine
- Proline
- produced from glutamate and glutamine
- Serine
- Tyrosine
- requires Phenylalanine: can have Phenylketonuria- genetic mutation makes you unable to carry out the conversion
What are non-essential amino acids?
- list them
The body can produce these
- Alanine
- Aspartate
- Cysteine
- Glutamate
What enzymes are involved in Fat digestion?
- In the Stomach: gastric lipase
- produced from gastric cells in the fundic mucosa
- The Liver and gallbladder: bile acids
- cholic and chenodeoxycholic acid: form micelles, increasing the surface area
- The Small Intestine: pancreatic lipase, pro colipase
- pro-lipase converted to colipase by trypsin: colipase makes pancreatic lipase more effective
What is the product of Lipid digestion?
- pancreatic lipase converts TG to
- monoacylglycerol
- fatty acids
- glycerol
What enzymes are involved in Protein digestion?
- In the Stomach: Pepsin
- chief cells in the stomach produce pepsinogen
- converted to pepsin in the presences of HCl ( released from parietal cells)
- Pancrease secretions into the small intestine:
- produces trypsinogen
- converted to trypsin using enteropeptidase
- trypsin goes on to convert proenzyme endopeptidases into their active form
- chymotrypsin
- elastase
- carboxypeptidases
- Exopeptidases are secreted at the brush border of the SI: (there are many of them)
- produces trypsinogen
What are the disaccharides and what are there monosaccharides?
- Maltose
- 2x Glucose
- Sucrose
- glucose, fructose
- Lactose
- glucose, galactose
What enzymes are involved in the final digestion of disaccharides digestion?
- where are they found?
- Sucrase-isomaltase
- Lactase
- Maltase-glucoamylase
> found on enterocytes, the digestions occur on the brush-border of the small intestine
How and where is COH absorbed?
- occurs on the brush border of the small intestine
- Glucose + galactose: via Na+ symport into the intestinal villi
- Fructose: via GLUT 5 transporter into the intestinal villi
- Both transported out of the villi into the lumen via GLUT 2 transporter
How is fat absorbed in the small intestine?
- fatty acids enter the intestinal villi
- endoplasmic reticulum and golgi body form them into chylomicrons: allows it to be water-soluble
- chylomicrons leave villi and enter lymph in the lacteal, takes chylomicrons to the blood system
How are proteins absorbed in the small intestine?
- amino acids enter enterocytes by various transporters and leave the intestine into the blood via facilitated diffusion
- di and tripeptides enter the enterocytes via Human peptide transporter 1 (PEPT1): then converted into amino acids and follow the same absorption process
- the amino acids are transported to the liver through the hepatic portal system
What happens to non-starch polysaccharides?
(Fibre)
- not digested or absorbed
- Soluble fibres (pectin/gum) are fermented by bacteria in the colon leads to the production of
- CO2, H2, CH4
- Short fatty acids
- Acetate: enters peripheral circulation
- Propionate: taken up by the liver
- Butyrate: used as energy substrate by colonic cells (enhances microbial growth)
- Insoluble fibres make up the cellulose in the diet
What are the two severe forms of protein-calorie malnutrition (PCM)?
- Marasmus
- seen in early infancy
- no oedema or skin changes
- Kwashiorkor
- 2+ years
- growth retardation
- skin changes
- abnormal hair
- hepatomegaly
- apathy
Which diseases is malnutrition most likely to occur in?
- GI/ Liver disease
- GI malignancy
- Oesophageal
- Gastric
- Pancreatic
- Colorectal
- surgery patients are also at risk
What are the mechanisms behind malnutrition?
- Inadequate intake
- Impaired nutrient digestion/ processing
- Excess losses
- Altered requirements
Give examples of impaired nutrient digestion and processing
- Gastritis
- can lead to gastric atrophy
- Pernicious Anaemia: intrinsic factors isn’t secreted –> B12 not absorbed
- gastric barrier
- can lead to gastric atrophy
- Peptic Ulcer
- caused by H. pylori, irritation, poor blood supply, high acid and pepsin content
- can also be from the intestines, pancreas or liver
Give examples of Excess Loss that would cause malnutrition
- vomiting
- NG tube drainage
- Diarrhoea
- Surgical drains
- Fistulae
- Stomas
Give examples of altered/ increased metabolic demand that would cause malnutrition
- inflammation
- cancer
- burns/ wounds
- brain injury
What are the two types of fasting?
and what are the differences?
- Uncomplicated fasting
- uses ketogenesis using fatty stores, reduces gluconeogenesis
- less protein used, less protein mass used
- uses ketogenesis using fatty stores, reduces gluconeogenesis
- Stress fasting
- a smaller proportion of energy from fat stores and ketogenesis
- more amnio acids lost is stress starvation
- a bit lower nitrogen balance
- significant increase in salt and water retention- more likely to have oedema
- a smaller proportion of energy from fat stores and ketogenesis
What is the impact of uncomplicated starvation in healthy people?
- Decreased skeletal and muscle mass in the first day
- muscle function reduces by day 5
- 18% loss of muscle mass leads to physiological disturbance
- cardiac output reduces by 45%
- respiratory/ diaphragmatic muscular mass and contractility reduces
- Gut and immune function reduce
- ~40% weight loss is fatal
What things need to be monitored when trying to prevent malnutrition?
- low weight
- weight loss
- poor intake or predicted to become poor (surgery)
- poor absorptive capacity
- High nutrient losses
- increased nutritional needs - burns, sepsis
“End-of-the-bed-o-gram”
What measurements/ anthropometry are taken when monitoring malnutrition?
- BMI
- can estimate using mid-upper arm circumference (MUAC)
- < 23.5 cm, likely to be < 20kg/m3
- >32.0 cm, likely to be >30kg/m3
- can estimate using mid-upper arm circumference (MUAC)
- Estimating height from ulna length (patients that cannot stand)
Explain the MUST screening tool for malnutrition
- Add the following scores from each category
- BMI score: 0-2 score
- Weight loss score (unplanned weight loss in the last 3-6 months): 0-2 score
- Acute diseases effect score: if present score 2
- Overall risk
- 0 = low risk
- 1 = medium risk
- 2+ = high risk
What is the action plan when the risk of malnutrition is established?
- 0- Low risk
- repeat screening
- weekly if in the hospital
- monthly in care homes
- annually in the community
- repeat screening
- 1- Medium risk
- diet diary for 3 days
- if the diet is ok repeat the screening
- if it isn’t alright follow local guidelines/ increase intake
- 2+ - High risk
- refer to a dietitian, nutritional support team/ implement local policy
- set goals to improve, monitor and review
What are the routes of feeding?
- Oral
- safest, cheapest, most acceptable
- contraindications: unsafe to swallow, damaged/ non-functioning gut
- Enteral: using the gut
- Percutaneous/ Nasal
- Gastric/ Jejunal
- Endoscopic/ interventional radiology access
- Parenteral: bypassing the gut
- total parenteral nutrition: fluid with nutrients
What is refeeding syndrome?
Severe electrolyte and fluid shifts associated with metabolic abnormalities in malnourished patients undergoing refeeding
- this can be orally, generally or parenterally
What is the physiological cause of re-feeding syndrome?
- during starvation, trans-membrane pumps aren’t active to conserve energy
- Na and water drift intracellularly
- K and Phos drift intracellularly and are excreted to keep plasma levels stable
- as soon as energy is restored through feeding they are switched on causing
- a sudden drop in plasma K ad Phos –> arrhythmias
- a sudden surge in plasma nad water –> overload
How is refeeding syndrome treated/ avoided?
- be aware of the risk and check electrolytes before feeding
- begin electrolyte replacement before feeding
- refeed slowly and gradually
- continue to monitor and replace as needed
What micronutrient deficiency are there in the UK population?
- iron-deficiency anaemia in adult women and older girls
- periods and strict diets)
- low vitamin D- increased risk of
- rickets in young people
- osteomalacia in adulthood
- functional riboflavin (B2) deficiency
- older children
- adults
What micronutrient deficiencies are associated with
- Alcohol liver disease
- IBS
- Obesity
- Alcohol liver disease
- thiamine (B1)
- vitamin D
- IBS
- iron
- B12, B6, B1
- vitamin D
- vitamin K
- folic acid
- Selenium, zinc
- Obesity
- vit D
- copper
- Zinc
How is vitamin C absorbed?
- transport occurs at the brush border in the small intestine
- occurs through a carrier-mediated Na dependant mechanism
- SVCT1, SVCT2 (vitamin C transporter-1/2)
water soluble
What is Biotin, what are it’s sources and what could its deficiency result in?
- Vitamin H or B7
- Water soluble
- Found in
- liver
- egg yolk
- soybeans
- milk and meat
- Deficiency causes
- dermatitis
- anorexia
- alopecia
- myalgia
- paraesthesia
Hows is Biotin absorbed and acquired?
- Acquired through
- the diet
- and bacterially
- absorbed via carried mediated Na dependent process
- SMVT- sodium-dependent multivitamin transporter
What is Cobalamin and how is it obtained?
- vitamin B12: important for the formation of red blood cells
- Water-soluble
- obtained from animal products and from the colon microbiome
- dietary B12 binds to protein heptocorrin
- released from this complex in the Si in trypsin
- then binds to the gastric intrinsic factor
What is Folic Acid and how is it acquired?
- vitamin M or B9
- acquired from the diet from poly and mono-glutamate
- also synthesised in the colons microbiome
- water soluble
- folate hydrolase releases folate from its conjugated polyglutamate form in the upper SI
- folate has three carriers
- FOLT: folate reduced carrier
- PCFT/HCP1: proton-coupled folate transporter
- FOLR1: GPI-anchored folate receptor
What causes Folic acid malabsorption and what malaise would it cause?
Causes of Malabsorption
- Tropical sprue
- Gluten induced enteropathy
- Bowel resections or diseases i.e crohns
- alcohol
- Phenytoin: epilepsy drug
- Cytotoxic drugs
Causes macrocytic anaemia
What is Niacin, how is it acquired?
- Vitamin B3/ Nicotinic acid
- water-soluble
- used in NAD
- Acquired directly from diet and endogenously
- Tryptophane converted to Niacin through the kynurenine pathway
What is Niacin deficiency associated with?
- Pellagra
- Dermatitis
- Diarrhoea
- Dementia
What is Riboflavin, how is it acquired?
- Vitamin B2
- water-soluble
- used to form FMN –> FAD
- Acquired from diet
- diary products
- eggs
- meats
- leafy greens
- absorbed via RFVT 3 into the intestine
- RFVT1/2 from the intestine into the blood
- RFVT1 from blood to tissue
What is Riboflavin deficiency associated with?
- may be associated IBS
- chronic alcoholism
What is thiamin, how is it acquired and what is its deficiency associated with?
- vitamin B1
- water-soluble
- acquired from whole grains, nuts, dried legumes
- absorbed via THTR1 and THTR2 transporters
- expressed throughout the GI tract
- deficiency can be genetic in rare cases
- usually related to poor dietary intake
- excessive alcohol use
- causes Wernicke-Korsakoff syndrome
What is Vitamin A, and how is it absorbed?
- Retinol
- lipid-soluble
- From the diet absorbed as either Retinylester or Cartenoids (pro-vitamin A)
- Retinyl ester: Liver, egg, butter, milk, fortified cereal
- Carotenoids: Carrots spinach, collards, pumpkins, squash
- conversion to vitamin A takes place in enterocytes
What is vitamin D, what is the impact of its deficiency?
- Lipid-soluble
- Presents in two forms vitamin D2- ergocalciferol and vitamin D3- cholecalciferol
- D3 is from UV rays
- D2 is dietary which is then converted to D3 in the digestive system
- Deficiency: effects Ca++ and Pi homeostasis
What is vitamin E and what is its action?
- Found as Tocopherol or tocotrienols
- alpha, beta, delta, gamma
- the alpha-tocopherol is predominant in foods apart from in soy where it is the gamma version
- lipid-soluble
- membrane-bound
- powerful antioxidant: protects from ROS
What is vitamin K? Explain its importance in our diet
- fat soluble
- presents as vit K1 (more active) and vit K2 (usually storage form, less active)
- used to form clotting factors
- newborns are at risk of haemorrhagic disease due to limited vit. k placenta permeability and breast milk. therefore they receive an injection
How is calcium absorbed?
- Site of absorption
- Dairy products: primarily in the duodenum, jejunum
- Plant products: fermentation of plant products in the colon
- Mechanism of absorption
- 20-30% absorbed in an acid medium
- it was a vitamin D-dependent calcium transport system when intake is low and the requirement is high
- happens in the duodenum
- passively intake in the jejunum when intake is high
- 20-30% absorbed in an acid medium
How is Iron absorbed?
- Site of absorption
- the end of the proximal small intestine for both harm and non-haem sources
- Mechanism of absorption
- Haem absorbed as an intact porphyrin complex
- Non-haem ironized from ferric to ferrous form: 35% of this absorbed when stores are low
What are the six mechanisms of Malabsorption?
- Mal-digestion
- poor secretion of digestive enzymes
- Inadequate absorptive surface
- SI damage, infection, or removal
- Bile Salt Deficiency
- effects lipid digestion and fat-soluble vitamins
- Lymphatic obstruction
- impact on lipid absorption
- Vascular disease
- due to hypovolaemia
- Mucosal disease
What diseases cause Mal-digestion malabsorption?
- Chronic pancreatitis
- Cystic fibrosis
- Pancreatic carcinoma
What diseases cause malabsorption due to an inadequate absorptive surface?
- Intestinal resection
- Gastro colic fistula
- Jejuno-ileal bypass
What diseases cause malabsorption due to Bile salt deficiency?
- Cirrhosis
- Cholestastasis
- Bacterial overgrowth
- Impaired ileal reabsorption
- Bile salt binders
What diseases cause malabsorption due to lymphatic obstruction?
- Lymphoma
- Whipple’s disease
- Intestinal lymphangiectasia
What disease cause malabsorption due to Vascular disease?
- Constructive pericarditis
- Right-sided heart failure
- Mesenteric arterial
- Venous insufficiency
What diseases cause malabsorption due to Mucosal disease?
- Infection: giardia, Whipple’s disease, tropical sprue)
- Inflammatory diseases
- Radiating enteritis
- Eosinophilic enteritis
- Ulcerative jejunitis
How does critical illness effect the human growth hormone?
- cytokines released in illness, causing decreased GH sensitivity
- decreased synthesis of GH-binding protein
- decreased expression of GH-receptors
- causes decreased hepatic sensitivity to GH:
- IGF-1, IGFBP-1 and ALS synthesis decreased
- decreased skeletal muscle hypertrophy/ protein catabolism isn’t inhibited
- Overall increases the synthesis of GH due to negative feedback system
- GH-activated tyrosine kinases inhibit Insulin activated PI3-kinase
- the action of Insulin is inhibited
What are clinical manifestations of growth hormone dysregulation?
- Hyperglycaemia
- Hyperlipidaemia
- Hyperbolic rate
- Muscle rate
- Poor myotrophic response to exercise
Why is it important to consider the nutritional needs of acutely and chronically ill patients?
- may have a higher catabolic state: make patients weaker may hamper their recovery
- may have a reduced appetite due to the illness ( or age)
- their treatment may require ‘nil by mouth’, must consider this in older frailer patients, and younger patients
