Nutrition Flashcards
(60 cards)
1
Q
What is the chemical name for Omega 6?
- what is the final product?
A
- Linoleic Acid
- found in vegetable and safflower oils
- converts to Arachidonic Acid
- found in Meat, poultry and eggs
2
Q
What is the chemical name for Omega 3
- what are its final products when digested?
A
- 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.
3
Q
What is the function of dietary fat?
A
- 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
4
Q
What are essential amino acids?
- list them
A
Amino acids we need to get from our diet
- Histidine
- Isoleucine
- Leucine
- Methionine
- Phenylalanine
- Threonine
- Tryptophan
- Valine
- Lysine
5
Q
What are conditionally non-essential amino acids?
- list them
A
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
6
Q
What are non-essential amino acids?
- list them
A
The body can produce these
- Alanine
- Aspartate
- Cysteine
- Glutamate
7
Q
What enzymes are involved in Fat digestion?
A
- 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
8
Q
What is the product of Lipid digestion?
A
- pancreatic lipase converts TG to
- monoacylglycerol
- fatty acids
- glycerol
9
Q
What enzymes are involved in Protein digestion?
A
- 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
10
Q
What are the disaccharides and what are there monosaccharides?
A
- Maltose
- 2x Glucose
- Sucrose
- glucose, fructose
- Lactose
- glucose, galactose
11
Q
What enzymes are involved in the final digestion of disaccharides digestion?
- where are they found?
A
- Sucrase-isomaltase
- Lactase
- Maltase-glucoamylase
> found on enterocytes, the digestions occur on the brush-border of the small intestine
12
Q
How and where is COH absorbed?
A
- 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
13
Q
How is fat absorbed in the small intestine?
A
- 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
14
Q
How are proteins absorbed in the small intestine?
A
- 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
15
Q
What happens to non-starch polysaccharides?
(Fibre)
A
- 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
16
Q
What are the two severe forms of protein-calorie malnutrition (PCM)?
A
- Marasmus
- seen in early infancy
- no oedema or skin changes
- Kwashiorkor
- 2+ years
- growth retardation
- skin changes
- abnormal hair
- hepatomegaly
- apathy
17
Q
Which diseases is malnutrition most likely to occur in?
A
- GI/ Liver disease
- GI malignancy
- Oesophageal
- Gastric
- Pancreatic
- Colorectal
- surgery patients are also at risk
18
Q
What are the mechanisms behind malnutrition?
A
- Inadequate intake
- Impaired nutrient digestion/ processing
- Excess losses
- Altered requirements
19
Q
Give examples of impaired nutrient digestion and processing
A
- 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
20
Q
Give examples of Excess Loss that would cause malnutrition
A
- vomiting
- NG tube drainage
- Diarrhoea
- Surgical drains
- Fistulae
- Stomas
21
Q
Give examples of altered/ increased metabolic demand that would cause malnutrition
A
- inflammation
- cancer
- burns/ wounds
- brain injury
22
Q
What are the two types of fasting?
and what are the differences?
A
- 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
23
Q
What is the impact of uncomplicated starvation in healthy people?
A
- 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
24
Q
What things need to be monitored when trying to prevent malnutrition?
A
- 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”
25
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
* Estimating height from ulna length (patients that cannot stand)
26
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
27
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
* 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
28
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
29
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
30
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
31
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
32
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
33
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
34
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
35
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
36
Hows is Biotin absorbed and acquired?
* Acquired through
* the diet
* and bacterially
* absorbed via carried mediated Na dependent process
* SMVT- sodium-dependent multivitamin transporter
37
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
38
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
39
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
40
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
41
What is Niacin deficiency associated with?
- Pellagra
- Dermatitis
- Diarrhoea
- Dementia
42
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
43
What is Riboflavin deficiency associated with?
- may be associated IBS
- chronic alcoholism
44
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
45
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
46
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
47
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
48
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
49
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
50
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
51
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
52
What diseases cause Mal-digestion malabsorption?
- Chronic pancreatitis
- Cystic fibrosis
- Pancreatic carcinoma
53
What diseases cause malabsorption due to an inadequate absorptive surface?
- Intestinal resection
- Gastro colic fistula
- Jejuno-ileal bypass
54
What diseases cause malabsorption due to Bile salt deficiency?
- Cirrhosis
- Cholestastasis
- Bacterial overgrowth
- Impaired ileal reabsorption
- Bile salt binders
55
What diseases cause malabsorption due to lymphatic obstruction?
- Lymphoma
- Whipple's disease
- Intestinal lymphangiectasia
56
What disease cause malabsorption due to Vascular disease?
- Constructive pericarditis
- Right-sided heart failure
- Mesenteric arterial
- Venous insufficiency
57
What diseases cause malabsorption due to Mucosal disease?
- Infection: giardia, Whipple's disease, tropical sprue)
- Inflammatory diseases
- Radiating enteritis
- Eosinophilic enteritis
- Ulcerative jejunitis
58
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
59
What are clinical manifestations of growth hormone dysregulation?
- Hyperglycaemia
- Hyperlipidaemia
- Hyperbolic rate
- Muscle rate
- Poor myotrophic response to exercise
60
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
