Lecture #21 - Carbs Flashcards

1
Q

Salivary glands/saliva

  1. What pH?
  2. Contains what two things and what does that start?
  3. How does mucous help? What is mucous?
A

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2
Q

Stomach:

  1. S____ and m____ of food with what? And slowly releases what into the intestine?
  2. Secretes three things and what’s the function of these things?
A

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3
Q

Stomach diagram:

  1. Mucous is produced but just enough - why?
  2. How can you get ulcers in stomach and what two things can increase the risk of increasing H+ secretion?
  3. Parietal cells secrete what? What does this do? (it does 2 things)
  4. Acid and what else is released in a controlled manner into the stomach?
A

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4
Q

Pancreas:

  1. What’s the pH?
  2. Secretes what?

Liver:

  1. Synthesis of what? (stored in what? and important for what?)

Small intestine:

  1. Final phase of what?
A

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5
Q

Digestion - what are the two main phases?

A

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6
Q

Hydrolysis of bonds connecting monomer units in food macromolecules:

  1. What are the bonds called between starch molecules or between disaccharides?
  2. What bonds do you hydrolyse in protein digestion?
  3. What about triacylglycerol?
A

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7
Q

Carbohydrates

  1. How much percentage of our energy intake?
  2. There are four types of carbs - name them and their constituents/examples
A

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8
Q

Cellobiose and lactose - what are they and which one can’t we digest?

A

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9
Q

Please go read P478 - 479 in your textbook; it’s for info on starch and its two types and how its broken down etc

a-1,4-glycosidic on horizontal and a-1,6-glycodisidic on branching

A

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10
Q

Fructose - why does it have adverse effects on health? What disease is associated with increase in fructose

Sucrose - disaccharide of what?

A

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11
Q

Go read the table of enzymes involved in carb digestion and memories it

A

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12
Q

Starch - two types but another is like one of the types - where do the three come from?

What enzyme hydrolyses the a-1,4 glycosidic bonds in the three types of starch? What do you end up with once you repeatedly attack it with amylase?

Then at the brush border, what happens? What else can you say about the brush border?

A

Last Q - the fact that enzymatic reactions take place before absorption (at the brush border)

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13
Q

Lactose deficiency

  1. What is lacking? What two reasons for why it could be lacking?
  2. What does eating lactose cause? Why?
  3. So what can lactose intolerant people eat instead?
A
  1. Genetic or the cells on villi damaged by e.g. virus so not producing the enzymes like lactase
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14
Q

Glucose transport

  1. Sugars are what and so can’t simply diffuse across membranes. They require specific what?
  2. What are the two types of transport what has these “pores”?
A

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15
Q

What are the type transporters what glucose uses to get into the intestinal epithelial cell and then out of it? What are their classifications

  1. Getting into the intestinal epithelium cell:
    - What is the transporter and by what mechanism does it work?
    - How does it prevent the concentration gradient of the sodium from disappearing?
    - Is this an active process?
  2. How does glucose get out of the cell and into the blood? Does it require energy?
  3. So overall, is the absorption of glucose an energy-requiring process?
A

SGLT 1, a secondary active

GLUT 2, a facilitative transporter

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16
Q

Sodium-potassium pump - how does it work? What comes in when its phosphorylated and what is phosphorylated and where does the phosphate group come from?

A

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17
Q

Sodium-potassium pump - how does it work? What comes in when its phosphorylated and what is phosphorylated and where does the phosphate group come from?

A

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18
Q

By which transporter does fructose come into the intestinal cell?

What are both fructose and glucose transported into liver cells by?

A

Something different and it’s got diff metabolism

GLUT 2

19
Q

Coeliac disease

  1. Disease of what organ?
  2. Body reacts against what? (gluten)
  3. Antibodies react with what? Where is it present?
  4. What happens to the villi and what does that mead?
  5. What symptoms?
A

Coeliac disease is a common disease of the digestive system involving inflammation of the small intestine. It is an autoimmune disease in which the body is stimulated to mount an immune response against its own tissue proteins. The inflammation is due to an autoimmune reaction against a wheat protein (gluten) which produces antibodies that react with an enzyme (transglutaminase) present in the small intestine. The inflammation leads to a flattening of the villi lining and disrupts the function of the intestinal mucosa leading to malabsorption of nutrients. Symptoms are highly varied between individuals and can include diarrhoea, constipation, nausea, flatulence, persistent abdominal pain, fatigue, anaemia and weight loss. The disease is also associated with a higher incidence of osteoporosis and intestinal cancers. Diagnosis is by intestinal biopsy and a blood test to detect antibodies to gluten and transglutaminase. The only treatment is a lifelong gluten-free diet.