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104: Theme 1 > Nutrition > Flashcards

Nutrition Flashcards

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
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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.
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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
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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
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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
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6
Q

What are non-essential amino acids?

  • list them
A

The body can produce these

  • Alanine
  • Aspartate
  • Cysteine
  • Glutamate
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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
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8
Q

What is the product of Lipid digestion?

A
  • pancreatic lipase converts TG to
    • monoacylglycerol
    • fatty acids
    • glycerol
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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)
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10
Q

What are the disaccharides and what are there monosaccharides?

A
  • Maltose
    • 2x Glucose
  • Sucrose
    • glucose, fructose
  • Lactose
    • glucose, galactose
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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

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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
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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
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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
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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
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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
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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
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18
Q

What are the mechanisms behind malnutrition?

A
  • Inadequate intake
  • Impaired nutrient digestion/ processing
  • Excess losses
  • Altered requirements
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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
  • Peptic Ulcer
    • caused by H. pylori, irritation, poor blood supply, high acid and pepsin content
  • can also be from the intestines, pancreas or liver
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20
Q

Give examples of Excess Loss that would cause malnutrition

A
  • vomiting
  • NG tube drainage
  • Diarrhoea
  • Surgical drains
  • Fistulae
  • Stomas
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21
Q

Give examples of altered/ increased metabolic demand that would cause malnutrition

A
  • inflammation
  • cancer
  • burns/ wounds
  • brain injury
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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
  • 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
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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
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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”

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25
Q

What measurements/ anthropometry are taken when monitoring malnutrition?

A
  • 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
Q

Explain the MUST screening tool for malnutrition

A
  • 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
Q

What is the action plan when the risk of malnutrition is established?

A
  • 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
Q

What are the routes of feeding?

A
  • 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
Q

What is refeeding syndrome?

A

Severe electrolyte and fluid shifts associated with metabolic abnormalities in malnourished patients undergoing refeeding

  • this can be orally, generally or parenterally
30
Q

What is the physiological cause of re-feeding syndrome?

A
  • 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
Q

How is refeeding syndrome treated/ avoided?

A
  • 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
Q

What micronutrient deficiency are there in the UK population?

A
  • 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
Q

What micronutrient deficiencies are associated with

  • Alcohol liver disease
  • IBS
  • Obesity
A
  • 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
Q

How is vitamin C absorbed?

A
  • 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
Q

What is Biotin, what are it’s sources and what could its deficiency result in?

A
  • Vitamin H or B7
  • Water soluble
  • Found in
    • liver
    • egg yolk
    • soybeans
    • milk and meat
  • Deficiency causes
    • dermatitis
    • anorexia
    • alopecia
    • myalgia
    • paraesthesia
36
Q

Hows is Biotin absorbed and acquired?

A
  • Acquired through
    • the diet
    • and bacterially
  • absorbed via carried mediated Na dependent process
    • SMVT- sodium-dependent multivitamin transporter
37
Q

What is Cobalamin and how is it obtained?

A
  • 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
Q

What is Folic Acid and how is it acquired?

A
  • 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
Q

What causes Folic acid malabsorption and what malaise would it cause?

A

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
Q

What is Niacin, how is it acquired?

A
  • Vitamin B3/ Nicotinic acid
    • water-soluble
    • used in NAD
  • Acquired directly from diet and endogenously
    • Tryptophane converted to Niacin through the kynurenine pathway
41
Q

What is Niacin deficiency associated with?

A
  • Pellagra
  • Dermatitis
  • Diarrhoea
  • Dementia
42
Q

What is Riboflavin, how is it acquired?

A
  • 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
Q

What is Riboflavin deficiency associated with?

A
  • may be associated IBS
  • chronic alcoholism
44
Q

What is thiamin, how is it acquired and what is its deficiency associated with?

A
  • 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
Q

What is Vitamin A, and how is it absorbed?

A
  • 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
Q

What is vitamin D, what is the impact of its deficiency?

A
  • 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
Q

What is vitamin E and what is its action?

A
  • 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
Q

What is vitamin K? Explain its importance in our diet

A
  • 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
Q

How is calcium absorbed?

A
  • 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
Q

How is Iron absorbed?

A
  • 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
Q

What are the six mechanisms of Malabsorption?

A
  • 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
Q

What diseases cause Mal-digestion malabsorption?

A
  • Chronic pancreatitis
  • Cystic fibrosis
  • Pancreatic carcinoma
53
Q

What diseases cause malabsorption due to an inadequate absorptive surface?

A
  • Intestinal resection
  • Gastro colic fistula
  • Jejuno-ileal bypass
54
Q

What diseases cause malabsorption due to Bile salt deficiency?

A
  • Cirrhosis
  • Cholestastasis
  • Bacterial overgrowth
  • Impaired ileal reabsorption
  • Bile salt binders
55
Q

What diseases cause malabsorption due to lymphatic obstruction?

A
  • Lymphoma
  • Whipple’s disease
  • Intestinal lymphangiectasia
56
Q

What disease cause malabsorption due to Vascular disease?

A
  • Constructive pericarditis
  • Right-sided heart failure
  • Mesenteric arterial
  • Venous insufficiency
57
Q

What diseases cause malabsorption due to Mucosal disease?

A
  • Infection: giardia, Whipple’s disease, tropical sprue)
  • Inflammatory diseases
  • Radiating enteritis
  • Eosinophilic enteritis
  • Ulcerative jejunitis
58
Q

How does critical illness effect the human growth hormone?

A
  • 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
Q

What are clinical manifestations of growth hormone dysregulation?

A
  • Hyperglycaemia
  • Hyperlipidaemia
  • Hyperbolic rate
  • Muscle rate
  • Poor myotrophic response to exercise
60
Q

Why is it important to consider the nutritional needs of acutely and chronically ill patients?

A
  • 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

104: Theme 1 (4 decks)

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