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NUTR2101 > Week per week study questions > Flashcards

Week per week study questions Flashcards

1
Q

what are the ADGs? purpose ?

A

ADGs- Australian dietary guidelines. Their purpose is as a nutrition education tool that translates scientific evidence on the role of food nutrient composition into consumer friendly information. Targeted at the healthy general population aimed at preventing chronic disease and deficiency.

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2
Q

Five ADGs

A
  1. to maintain healthy weight: Be physically active + choose amounts of food and drink to meet your energy needs
  2. support and promote breastfeeding
  3. limit saturated fat, sugar, added salt and alcohol
  4. care for your food and store it safely
  5. enjoy wide variety of foods from 5 food groups everyday. + drink plenty of water.
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3
Q

What is the AGHE?

• How does it translate to a daily meal plan?

A

Australian guide to healthy eating.
gives proportions of the different food groups you should be consuming everyday.
- visual representation of recommended portion sizes of different food groups. Whole foods- not macronutrients.
- giving you a representation of what your plate should look like: proportions in reference to each other.

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4
Q

• What are the NRV’s (complete descriptions of

the 6 references in terms of what they aim to achieve, how they are determined)

A

Nutrition reference values- a set of targets for macro and micronutrients, age and sex specific. Aimed at preventing deficiencies and toxicity in the general healthy pop.

  1. EAR: estimated average requirement - (determined by biomarker- sign of deficiency- 50% showed deficiency 50% didn’t.
  2. RDI: Recommended dietary intake (97-98% showed no deficiency)
  3. AI: adequate Intake (used when EAR cannot be determined)- average daily nutrient level based on observation or experimentally based approximations or estimates of nutrient uptake of a group of apparently healthy people.
  4. UL: upper limit (10% showed toxicity) - upper limit like to pose no adverse health effect on most individuals in the general population.
  5. SDT: suggested dietary targets - Daily intake of certain nutrients that may help prevent chronic disease.
  6. EEL: estimated energy requirements. - average dietary energy intake that is predicted to maintain energy balance in a healthy adult of defined age, gender, weight, height and physical activity level consistent with a healthy person.
  7. AMDR- acceptable macronutrient distribution range (= maximise general health outcomes) (+14)
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5
Q

• What must be stated on the nutrition information panel?

A

The ingredients- from most to least

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6
Q

• What are the definitions of (and the differences between) digestion and absorption?

A

digestion- breaking down foods into molecules that can be absorbed (by enterocytes + delivered into blood)
absorption- uptake of monomers and micronutrients from the lumen of the GIT through the absorptive cells into the blood and lymph for transport through the blood.

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7
Q

• Trace a cheese and salad sandwich through the digestive processes, naming the various structures and secretions involved in the digestion and absorption of food constituents in the sandwich

A

Month (mechanical and chemical digestion)
| Saliva (lysosomes, mucus, salivary amylase, lingual amylase)
|
oesophagus
(lower oesophageal sphincter)
Stomach
(secretions: HCL, gastric lipase, gastrin, mucus)
(pyloric sphincter)
SI
(secretions: gastrin, CCK, secretin, gastric inhibitory peptide)
(iliocecal sphincter)
LI
rectum
Anus

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8
Q

• Describe the different forms of absorption

A
  1. passive
  2. facilitated: carrier protein
  3. Active: requires ATP
  4. endocytosis : cell wall engulfs substance.
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9
Q

• What is the entero-hepatic recirculation?

A

recycling of bile in the liver-

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10
Q

• How are nutrients being transported in the body once

absorbed?

A

In blood- CVS- (via capillaries - water soluble) to liver then to other organs and tissues and lymph- lymphatic system (via lacteals) fat soluble and larger particles- enter CVD at thoracic duct)

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11
Q

• What occurs to indigested food compounds before they leave the body?

A

get fermented by the gut bacteria in the colon

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12
Q

• What are prebiotics and probiotics ? What is their respective function?

A

Prebiotic- non-digestible carbs that feed bacteria and promote their growth.
probiotics- live bacteria, identical to what is found in gut. populate gut adequately.

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13
Q

Define metabolism, catabolism, anabolism, energy

metabolism, substrates, intermediates, products

A

Metabolism: biochemical reactions that occur in the body (biochemical reactions from substrate to products)
product: compound resulting from pathway
intermediates: compounds formed and used throughout pathway
substrate: start of pathway compounds.
anabolism: (use energy) pathways that build molecules (small-> big)
catabolism: (release energy) pathway that break down molecules (big –> small)
energy metabolism: reactions that result in the production of energy- breaking down macronutrients to produce energy.

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14
Q

• What are the Cori cycle and the citric acid cycle?

A

cori cycle: converts lactic acid back to glucose in liver.

citric acid cycle:

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15
Q

• What is the role of niacin and riboflavin in energy

metabolism

A

Niacin (vit B3) : NAD

Riboflavin: FAD

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16
Q

• What does oxidation and reduction mean?

A

Oxidation: loss of electrons
Reduction: gain of electrons
OILRIG

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17
Q

• What is the role of niacin and riboflavin in energy

metabolism

A

Niacin (vit B3) : NAD (niacin functions are co- enzyme)
Riboflavin: FAD
assist dehydrogenase enzyme in transferring the hydrogen all along ETC

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18
Q

• How are glucose, triglycerides, amino acids and
ethanol converted to ATP? Explain the pathway for
each macronutrient in dot points, naming the key steps
with substrate and product

A

Glucose:
aerobic (glycolisis- pyruvate Acetyl CoA- citric acid cycle- ETC) (32 ATP)
anaerobic (glycolysis- pyruvate- lactic acid) (2 ATP)
Fats:
lipolysis– Beta oxidation– acetyl CoA– CAC- ETC
1 16C carbon= 106 ATP
protein:
??
amino acids:
alcohol: 1. MEOS 2. catalase 3. alcohol dehydrogenase

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19
Q

• Define ketogenesis, ketosis, ketoacidosis, ketolysis

A

Ketogenesis: formation of ketone bodies

ketosis: raised levels of ketone bodies in the body tissues which is typically when the body doesnt have enough glucose to burn.
ketoacidosis: pancreas is damaged, no insulin produced- rely only on fatty acids- metabolic state- v high concentrations of ketone bodies - lowers body pH.
ketolysis: reutilisation of ketone bodies.

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20
Q

• Where are ketone bodies (KB) formed?

A

in the liver by breakdown of excess fatty acids

fuel for heart, brain and muscle.

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21
Q

• How are KB formed?

A

from the breakdown of fatty acids- occurs in metabolic environment where fat is primary source of E.

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22
Q

• Where are KB used?

A

extra hepatic tissue only- brain, muscles and heart.

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23
Q

• In what conditions are KB formed?

A

metabolic environment where fat is the primary source of E

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24
Q

• Describe the pathway of gluconeogenesis. Can typical
fatty acids be used as substrate for gluconeogenesis?
Why? Why not?

A

gluconeogenesis- forming new glucose from glycogenic amino acids carbon skeleton (oxaloacetate).
no they can’t- transformed- Not the same carbons-
( from lactic acid (cori cycle) and amino acids)
neo- new
genesis- generating
gluco- glucose
glycogenolysis- glycogen— glucose
gly- glycogen
lysis- break down.

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25
Q

• How is ATP produced during fasting (from a few hours to a few days of fast)

A
  1. hepatic glycogen breakdown
  2. muscle glycogen
  3. protein breakdown
  4. fat breakdown
  5. ketogenesis: ketone bodies.
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26
Q

• What takes place during prolonged fasting to spare

lean body mass? Explain your answer comprehensively

A

ketogenesis: ketone body production (fat stores from adipose tissue)

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27
Q

• What are the 6 factors, and their role, regulating energy metabolism?

A
  1. liver
  2. substrates
  3. ATP concentrations- “status’
  4. functioning enzymes
  5. Hormones
  6. presence of vitamins and minerals.
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28
Q

protects the stomach lining

A

Mucus

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29
Q

promotes HCL secretion

A

Gastrin (hormone) (G - cells)

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30
Q

emulsifies fat

A

Bile

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31
Q

neutralises gastric juice activity

A

Bicarbonate

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32
Q

Surpresses HCL (parietal cells) secretion

A

GIP/ somatostatin

33
Q

forms bolus

A

saliva

34
Q

activates pepsinogen

A

HCL ( from parietal cells)
- kills bacteria
denatures proteins
aids in mineral absorption

35
Q

signals pancreatic juices secretion

A

CCK

36
Q

hydrolyses starch

A

amylase

37
Q

Binding of fatty acids to glycerol

A

Esterification

38
Q

Oxidation of fatty acids to acetyl-CoA

A

beta oxidation

39
Q

Hydrolysis of glycogen to glucose

A

glycogenolysis

40
Q

Production of glucose from the amino acids’ carbon skeletons

A

gluconeogenesis

41
Q

Oxidation of glucose to pyruvate

A

glycolysis

42
Q

Formation of ketone bodies

A

Ketogenesis

43
Q

Hydrolysis of triglycerides into fatty acids and glycerol

A

lipolysis

44
Q

Formation of gene products

A

translation -protein synthesis

45
Q

How do you explain to your friend the concept of
“carbohydrate quality” using the glycemic index and
glycemic load?

A
  • carbohydrate containing food can be rated for their quality based on their GI
    Gi ranks carbohydrate containing foods based on their effects on blood sugar levels about two hours post digestion (compares food servings that have gram per gram the same amount of carbs) - rated against glucose GI 100.
    Glycemic load: amount of carbohydrate in the food serving consumed * GI divided by 100 - more accurate reflection of blood glucose
46
Q

• What is the AI for fibre in Australia? What endpoints was used to determine adequate intake?

A

AI (adequate intake- based on median endpoints)
women- 19-70- 25g/ day
men- 30g / day
changes in stool weight with various forms of fibre.
No UL
endpoints: adequate gastrointestinal function and adequate laxation.
people with healthy bowl movements- get the healthy population. with fibre. Who’s healthy.

47
Q

• Blood glucose homeostasis is tightly regulated. Explain the mechanisms that regulate high and low blood sugar levels, including the relevant hormones and their effect.

A

High- insulin produced by pancreas - glucose uptake into cells (GLUT4) (insulin dependent) liver- glucose independent.
low- glucagon, crotisol, epinephrine - breakdown of glycogen to glucose= raise in blood sugar levels

48
Q

• What are 3 monosaccharides and 3 disaccharides in the diet?

A

monosaccharides:
glucose, fructose, galactose
disaccharides:
maltose (glucose + glucose alpha 1,4 glycosidic bond), lactose (galactose + glucose beta 1,4 glycosidic bond) , sucrose( Glucose + fructose - alpha 1,2 glycocemic bond)

49
Q

ARE ARTIFICAL SWEETENERS SAFE?

A

pros: dont contribute to blood sugar levels
cons: disrupt gut microbiota- decrease levels of good microbiota= bad metabolic outcomes.
phycological- eating less sugar therefore can eat more food.

50
Q

• What defines digestible and indigestible carbohydrates?

A

Digestible: Starch: Amylose and amylopectin
indigestible: Fibre: fraction of the edible part of the plant that is resistant to digestion and absorption in human intestine usually with complete or partial fermentation in the large intestine.
= depends on the types of bonds in the carbohydrate.
starch = alpha bonds
fibre= beta bonds everywhere in indigestible.

51
Q

polysaccharide:

A

a carbohydrate whose molecules consist of a number of sugar molecules bound together.

52
Q

• Why would fructose be considered a “good” sugar for

diabetics?

A

insulin independent- The insulin resistance is thus not a problem (type 2: lifestyle) Type 1 autoimmune: pancreatic beta cells are damaged- therefore no insulin produced.

53
Q

• What are the consequences of consuming a lot of fructose?

A

Fatty liver disease- is transformed much faster to glyceraldehyde–> higher amounts of pyruvate-> high fatty acid synthesis?
Cell uptake is not insulin dependent (GLUT4)

54
Q

• How do amylose, amylopectin and glycogen differ from each other? Comment on structures, bonds, and enzymes used to break the structure down.

A

Amylose: continuous linear chain of glucose molecules linked by alpha 1-4 glycosidic bonds.
Amylopectin: (higher GI) branched chain of glucose molecules linked by alpha 1-4 glycosidic bonds and alpha 1- 6 glycosidic bonds== more quickly digested as there is more SA for enzyme activity.
glycogen: Many more branched points in glycogen then in amylopectin. same bonds- enzymes can hydrolyse glucose molecules quickly for quick release of glucose into the blood.
Enzymes: Amylase breaks alpha 1-4 bonds
amydextrinase breaks the alpha 1-6 bonds (branching bonds)

55
Q

• Which from amylose and amylopectin has a lower GI?

A

Amylose has a lower GI- it is harder to breakdown, less quickly digestible.

56
Q

Explain four benefits of meeting the fibre requirements daily, by providing mechanisms of action for the benefits.

A
  1. promote bowel health
  2. reduce obesity
  3. assisting in blood glucose
  4. reducing plasma cholesterol
  5. substrate for gut bacteria
57
Q

• Describe the 3 pathways of alcohol metabolism from substrate to end products, mentioning enzymes and intermediates.

A

alcohol–> acetaldehyde -(ALDH2)–>acetate —> acetyl CoA

  1. Alcohol dehydrogenase (enzyme) ADH
  2. MEOS (used to drinking regulariry) microsomal ethanol oxisisive system (CYP2E1)
  3. Catalase (enzyme)
58
Q

Two types of starch?

A

Amylopectin and amylose

59
Q

• How much alcohol is in a standard drink?

A

10g of alcohol. (based on assumption that the liver metabolises 10g of alcohol / hour)

60
Q

• What is the rationale to qualify this quantity a standard alcoholic drink in Australia?

A

10g / 100ml

61
Q

glycogen storage disease

A

liver cannot convert glycogen to glucose or glucose to glycogen.
- enzyme defects
= poor physical growth, Low blood sugar levels, liver enlargement.
must consume frequent meals and cornstarch between meals. higher fat intake

62
Q

Carbs digestion

A

mouth- salivary amylase
SI: pancreatic amylase- continues intestinal alpha dextrinase. Brush boarders: specific enzymes
Maltose_ maltase

63
Q

Saccaride absorption

fate?

A

active and passive
facilitated: fructose
fate?
liver converts fructose and galactose to intermediates of glycolysis.
storage of glucose
excess glucose–> FA via acetyl CoA being diverted to lipogenesis.

64
Q

Insulin resistance

A

The receptors aren’t responding- the glucose stays in the blood stream. blood glucose rises= more insulin is produced by the pancreas

65
Q

Glycemic index

A 
measure of your bodies responce to blood sugar responce. 
slow to raise- low GI 
fast to raise- High GI 
depends on ratio between amylase and amylopectin 
processed?
fat added?
acidity- lowers GI 
ripeness of a fruit
66
Q

Soluble fibre

A

forms jelly like structure in presence of water
type of dietary fibre
pectin, gums, inulin, resistant starch

67
Q

insoluble fibre

A

doesn’t change in the presence of water

cellulose, ligin

68
Q

physiological functions of fibre

A
  1. promoting bowel health- increasing feacal bulk- strech the wall of GIT- triggers gut wall to start peristalsis
  2. reducing obesity and weight gain- assisting in appetite control- prevents overeating slows down gastric emptying
  3. assisting in blood glucose- the enzymes find it harder to access the glucose, therefore absorb it slower
  4. reducing plasma cholesterol- promotes binding and excretion of cholesterol.
  5. substrate for gut bacteria- promotes growth and diversity production of SCFA which have numerous health benefits
69
Q

physiological functions of fibre

A
  1. promoting bowel health- increasing feacal bulk- strech the wall of GIT- triggers gut wall to start peristalsis
  2. reducing obesity and weight gain- assisting in appetite control- prevents overeating slows down gastric emptying
  3. assisting in blood glucose- the enzymes find it harder to access the glucose, therefore absorb it slower
  4. reducing plasma cholesterol- promotes binding and excretion of cholesterol.
  5. substrate for gut bacteria- promotes growth and diversity production of SCFA which have numerous health benefits
70
Q

Diverticular disease

A
  • not enough good peristalsis from insufficient bulk accompanying low fibre diet. in colon= strong P required to propel smaller Mass= creation of diverticulae (pockets) in soft tissue walls of colon.

Diverticulosis- presence of diverticulae
diverticulitis- inflammation of ‘’

71
Q

Alcohol absorption

A

rapid= simple diffusion
80% SI 20% stom
cannot be stored therefore has priority.

72
Q

Alcohol E value

A

7kcal or 29KJ/g

73
Q

alcohol percentage

A

the percentage that is pure alcohol

74
Q

ALDH2

A

produces flush- certain populations
not enough will cause immune reaction
not enough will cause Acetaldehyde build up= hangover

75
Q

alcohol dehydrogenase

A

main metabolic pathway for alcohol

gastric cells 20 % and hepatocytes 80% (liver)

76
Q

Meos

A

moderate to excessive intake (activated when ADH system can’t keep up)
occurs in hepatocytes (liver)
mediated by P4502E1
Assists in building a tolerance to alcohol over time

77
Q

Catalase pathway

A

in hepatocytes or other cells (liver)
oxidation occurs in the peroxisome via peroxisomal catalase
uses hydrogen peroxide to form acetaldehyde and water

78
Q

The rate at which the liver break down alcohol

A

5-10g per hour (very fluctural) Cannot be sped up

NUTR2101 (7 decks)

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