Digestion and absorption and Mobilisation Flashcards

1
Q

Where does most of the digestion occur?

A

In the small intestine

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2
Q

What is the difference between amylose and amylopectin?

A

Amylose= Unbranched glucose subunits
Amylopectin= branched

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3
Q

What is the main enzyme in carbohydrate digestion and where is it found?
What bond does it break?

A

alpha-amylase
Saliva and pancreatic secretions
Breaks alpha 1,4 glycosidic links. This means that 1,6 linkages are not broken so it yields branched dextrins from amylopectin.

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4
Q

What does isomaltase do?

A

It is a brush border enzyme in the small intestine that works on the alpha 1,6 linkages in the dextrins to degrade amylopectin to maltose and glucose

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5
Q

What are different types of transporter in the brush border for monosaccharide absorption?

A

SGLT1- glucose and galactose
GLUT1- glucose
GLUT2- glucose, galactose and fructose
GLUT5- fructose

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6
Q

What are the 2 main enzymes involved in the digestion of proteins?

A

Endopeptidases- break bonds in the centre of chains
Exopeptidases- Break bonds near the ends of chains

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7
Q

Where does digestion of proteins take place?

A

In the stomach (pepsin which is an endopeptidase) and the small intestine (enzymes from the pancreas and brush border)

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8
Q

How are amino acids absorbed?

A

Can occur passively or via facilitated diffusion and active transport mechanisms via Na+ dependent co-transporters

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9
Q

How can small peptides be abdorbed?

A

Small peptides can be transported into the enterocytes by active transport with H+ ions which are then hydrolysed by intrinsic tripeptides and dipeptidases and then amino acids are then absorbed into the blood

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10
Q

Where is calcium absorbed and how?

A

Absorbed along the whole length of the small intestine by both passive and active transport.
Calcium binds to a binder protein in the brush border which facilitates diffusion into the enterocyte.
Calcium can then bind to a protein in the cell called calbindin which maintains the concentration gradient and allows high amounts of calcium to be taken up into the cell as insoluble Ca2+ salts are formed in the cell.
Calcium is then pumped across the basolateral membrane by Ca2+ ATPase pump

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11
Q

How does most iron absorption occur?

A

Through a haem membrane carrier. Fe2+ diffuses into the enterocyte with a haem molecule and then separates inside the enterocyte through an enzyme controlled reaction.
Transport into the blood is then facilitated by ferroportin on the basolateral membrane
(Absorption is mostly in the form of Fe2+ not Fe3+)

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12
Q

What form does iron move around the blood in?

A

Fe2+ is oxidised to Fe3+ and is then transported in the blood bound to transferrin

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13
Q

Where is vitamin B12 absorbed?

A

In the terminal ileum

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14
Q

What must happen to avoid B12 being destroyed in the stomach?

A

It must bind to haptocorrin (R-protein) in saliva to protect it in the stomach

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15
Q

Where is major lipase, cholesterol esterase and phospholipase secreted?
Are they water soluble? What is the significance of this?

A

In pancreatic juice from the pancreas.
Yes they are water soluble which means that they only work on the surface of fat droplet so if it is large they can’t access fats in the middle of the fat droplets.

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16
Q

What process occurs to overcome the problem of large lipid droplets?

A

Emulsification- bile salts coat lipid droplets and stop them stick together (coalescing). This keeps fat droplets small and therefore provide a larger surface area for enzymes such as lipase to work.

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17
Q

How are most fatty acids absorbed into the blood?

A

Most fatty acids are insoluble so are taken up in the form of micelles

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18
Q

What happens to micelles in the enterocytes?

A

They are repackaged as triglycerides and then combined with proteins in the Golgi to form ‘chylomicrons’. They are then transported to lacteals

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19
Q

What is the unstirred layer? How does this aid fat absorption?

A

This is a layer of fluid in contact with the epithelial surface that does not mix with the rest of the chyme (gastric juices and partly digested food).
Micelles have to diffuse through this layer. The unstirred layer is more acid closer to the epithelium which promotes a reduction in the ionisation (less charged) of fatty acids making them more easy to absorb across the lipid membrane (as they are uncharged)

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20
Q

Where are bile salts reabsorbed? How?

A

In the ileum
Ionised bile acids are absorbed by active transport
Unionised acids are fat soluble and therefore can be absorbed passively.

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21
Q

Why can’t fatty acids be used in gluconeogensis?

A

This is because acetyl coA cannot be converted back into pyruvate as it is a one way reaction. Beta oxidation produces acetyl coA.

You can’t go round the cycle either like you can with amino acids as you aren’t putting excess carbon atoms into the cycle like you are amino acids.

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22
Q

Why are ketones produced?

A

Ketones are produced when acetyl coA conc is less in need in the Krebs cycle so acetyl coA is essentially in excess.

Ketones are water soluble so they can then be used as a fuel source is the brain (they can cross the blood brain barrier) which means other energy sources (e.g. glucose) are no longer required which preserves them.

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23
Q

what is acyl coA?

A

This is essentially any fatty acid molecule with a co enzyme A attached

24
Q

What is beta oxidation?

A

This is the production of acetyl coA from fatty acids. One 16C fatty acid can produce 8 acetyl coA compared to glucose producing just 2 acetyl coA (one from each pyruvate) which shows how energy dense a fatty acid molecule is.

25
Q

How is lactate produced in the body?

A

Glucose is converted into glycogen where it is stored. When enough glycogen has been stored, some of the remaining glucose is converted into lactate. Lactate can then be converted back into glucose to increase blood glucose when it gets low.

Lactate is also produced in anaerobic respiration as a result of glucose being broken down in anaerobic conditions.

26
Q

How are amino acids used in gluconeogenesis>

A

Amino acids can join the TCA cycle in various forms or can be converted into pyruvate. They can then follow a series of reactions to reform glucose.

27
Q

What is the order that molecules are used?

A

Glucose (first 6 hours)
Glycogen (1 day)
Amino acids (3 days)
Fatty acids after that

28
Q

What happens to excess ketones?

A

They are excreted in urine

29
Q

Where are lipids stored?

A

In adipose tissue

30
Q

Where are lipids broken down?

A

In the liver. Beta oxidation occurs in the mitochondria

31
Q

What is meant by ‘starvation in a sea of plenty’?

A

This refers to people with type 1 diabetes who can’t produce insulin. They eat meals high in glucose which goes into their blood but as insulin is not produced, they don’t absorb it which means there body is in a state of starvation as they are using other sources such as fats and amino acids instead. This continues even when they continue to each meals high in glucose (unless insulin is present).

32
Q

How are fatty acids regulated?

A

There is no hormone to regulate fatty acids. Instead, ATP conc becomes high so movement down the ETC slows so less NADH is taken up so TCA cycle slows resulting in an increase in acetyl coA which in excess is converted into ketones.

33
Q

What happens to the amount of insulin and glucagon in the blood during fasting?

A

Concentration of insulin decreases in order to prevent glucose uptake into cells.
Concentration of glucagon increases so glycogen stores are converted into glucose to maintain stable glucose levels.

34
Q

Can glycerol be converted into glucose?

A

Yes- in the liver

35
Q

What do chief cells in the stomach release? Why?

A

They release pepsinogen.
Pepsinogen is converted into pepsin when mixed with HCl which breaks down proteins into amino acids. The role of pepsinogen is to prevent pepsin from always being active and then breaking down the protective proteins in the lining of the stomach.

36
Q

What is the gastrocolic reflex?

A

This is a reflex that occurs when you eat a meal that causes food already in the digestive tract to be pushed through. This what makes room for food when you eat and causes you to do to the toilet soon after a meal.

37
Q

What hormone does food in the stomach cause the release of?

Where is it released from?

A

Gastrin

G-cells in the stomach

38
Q

What does gastrin cause?

A

Gastrin causes stimulation increase in histamine which results in secretion of HCl, Chief cells which produce Pepsinogen and increases stomach motility (movement of food into the duodenum)

39
Q

Where is Secretin produced?

What is the role of secretin?

A

In S cells in the mucosa of the duodenum

Secretin is released when food (specifically HCl and the acidity) moves into the duodenum. It then goes into the blood stream and goes to the pancreas to cause the release of a bicarbonate mix which neutralizes the acidic chyme.
Secretin also goes back into the stomach to inhibit stomach motility so stomach moves less slowly through the stomach (inhibits gastrin)

40
Q

What is the role of Cholecystokinin?

A

This enzyme is released from the I cells in the duodenum when food (specifically fat) moves in from the stomach to the duodenum. It is released into the blood stream and travels to the pancreas where it stimulates the release of pancreatic enzymes such as lipase. Also goes to the gallbladder to cause it to contract which releases bile salts.
It also inhibits gastrin and stomach motility.

41
Q

Where is the vomiting reflex controlled?

A

In the vomiting center

42
Q

What is Brunners Gland?

A

This is a gland in the submucosa of the duodenum which essentially secretes secretin to neutralize the acidic chyme and inhibit gastrin release in the stomach to slow movement through there.

43
Q

What are the 3 main phases of digestion? Briefly describe each?

A

Cephalic phase- approach of food and food in the mouth. Signals sent to salivary glands, stomach, pancreas and liver to prepare GI tract for digestive and absorptive functions.

Gastric Phase- presence of food in the stomach. This increases blood flow to the stomach, secretion of gastric juices and motility. Also prepares GI tract for movement into small intestines by increasing motility of chyme already there and stimulates secretion from pancreas and gall bladder.

Intestinal phase- presence of food in small intestines. Inhibits gastrin secretion and stomach motility so can focus on digestion of chyme already in small intestine. Stimulates secretion from pancreas (relaxation of Sphincter of Oddi so digestive juices can flow in) and contraction of gall bladder to release bile salts.

44
Q

What are the 3 pairs of salivary glands and what is there role?

A

Parotid glands- produce serous salvia (watery secretions high in enzymes such as alpha-amylase.). Very little mucus.
Submandibular glands- mixed secretion that is both serous and mucus.
Sublingual glands- Mucus saliva. Contains no enzymes and large amounts of mucus.

45
Q

What is the role of alpha-amylase?

A

Breaks down alpha 1,4 glycosidic bonds to form maltose and glucose.

46
Q

What is the role of thiocyanate and sialoperoxidase?

A

Catalyse the breakdown of hydrogen peroxide. This inhibits bacteria.

47
Q

What is the role of Haptocorrin?

A

Binds to Vitamin B12 so that it can move through the acidic environment of the stomach without being degraded. It is then absorbed in the small intestine.

48
Q

What parts of the GI tract is served by the Sacral division of the parasympathetic system?

A

Distal ends of GI tract so rectum and ends of the colon.
The rest is served by the vagus nerve.

49
Q

What part of the GI tract is innervated by the Cervical ganglion (sympathetic stimulation)?

A

Oesophagus
Stomach
Small Intestine

Rest is innervated by the Superior and Inferior Mesenteric ganglions.

50
Q

Does the parasympathetic nervous system have an excitatory or inhibitory effect on the GI tract?

A

Excitatory (opposite to cardiovascular system)

51
Q

What is the main function of the myenteric plexus?

What is the condition called where it fails to develop this plexus in new-borns?

A

Motility of food through the gut by peristaltic movements of the bowels

Hirschsprung disease- severe constipation, faeces get stuck in the colon

52
Q

What is the main function of the submucosal plexus?

A

GI secretion and blood flow

53
Q

Where is Somatostatin produced?

What is the main stimulus for release?

What is the main action?

A

D-cells in the stomach, pancreas and small intestine

Presence of acid in the GI tract

Inhibits Gastrin release and on ECL cells (release histamine)

54
Q

Where is Histamine produced?

What causes its releases?

What is it’s action?

A

ECL cells in gastric mucosa of stomach

Gastrin and vagus nerve

Increases H+ conc due to HCl.

55
Q

What is the significance of the chemoreceptor trigger zone lying outside the blood brain barrier?

A

Can respond to toxic substances in the blood and therefore trigger vomiting. If it was in the brain then this wouldn’t be possible as the toxic substances can’t get here.

56
Q

How is a toxic substance conveyed from the ECL cells to the brain and to which centre?

A

ECL secretes serotonin in response to toxins in the stomach which is then conveyed by the vagus nerve (CN 10) to the CTZ which then triggers the vomiting centre

57
Q

How is a toxic substance conveyed from the vestibular apparatus to the brain and via what structure?

A

The vestibular nerve conveys information by the vestibulocochlear nerve (CN 8) to the chemoreceptor trigger zone (CTZ) and then on to the vomiting centre