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GI > GI - small intestine and some metabolism > Flashcards

GI - small intestine and some metabolism Flashcards

1
Q

how are glucose and galactose absorbed in the small intestine?

A

Via SGLT1 transporter, using active transport (need sodium ions)

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2
Q

How is fructose absorbed in the small intestine?

A

Via the GLUT5 transporter, passively

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3
Q

How do absorbed sugars leave enterocytes of the small intestine?

A

Via GLUT2 transporter, passively

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4
Q

What cells secrete CCK?

A

I cells

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5
Q

What is the difference between endopeptidases and exopeptidases?

A

ends can cut within the protein chain, but exos cut within the chain

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6
Q

how are proteins absorbed in the small intestine?

A

active transport, H+ linked; and also some by endocytosis

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7
Q

how are single amino acids absorbed in the small intestine?

A

Via active transport, Na+ linked

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8
Q

what does pancreatic lipase do?

A

it cuts triglycerides into a monoglyceride plus 2 FFAs (free fatty acids)

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9
Q

what proportion of bile salts are lost in the faeces?

A

5%

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10
Q

what regulates Na+ absorption and K+ secretion?

A

aldosterone

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11
Q

what do the intestinal crypts secrete?

A

bicarbonate rich fluid

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12
Q

how are pancreatic proenzymes activated?

A

enterokinases on the epithelial cells activate trypsinogen to trypsin, trypsin in turn activates the others (e.g. procarboxypeptidases to carboxypeptidases)

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13
Q

what will cause the sphincter of Oddi to relax?

A

cholecystokinin

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14
Q

where does vasoactive intestinal peptide come from, and what does it make happen?

A

from all of the GI tract (from nerve terminals); it stimulates smooth muscle and secretory cells

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15
Q

what does CCK promote?

A

pancreatic acinar secretions and gall bladder emptying

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16
Q

which enzyme controls CCK secretion?

A

trypsin. if food is present, trypsin is ‘occupied’ - so CCK is released.

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17
Q

where does secretin come from, and what does it do?

A

From the S cells in the duodenum; it stimulates bicarbonate secretion of pancreas, and stimulates bile secretion

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18
Q

where does gastrin come from, and what does it do?

A

G cells in the gastric glands of the stomach; it targets the ECL cells (enterochromaffin like cells) and the parietal cells; this kicks off histamine and H+ secretion (basically gets gastric action going)

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19
Q

what is cholecystitis?

A

where bile is being reabsorbed, leads to jaundice and can lead to liver disease or failure

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20
Q

what is combined with bilirubin in the liver?

A

glucoronic acid, to make bilirubin gluconoride. this passes into the intestine.

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21
Q

what happens when bilirubin is hydrogenated by bacteria in the intestine?

A

it is converted to urobilinogen. this can be excreted in the faeces, or travels in the blood to the kidneys

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22
Q

what happens to urobilinogen in the kidneys?

A

it is excreted in the urine, or it is combined with oxygen to make urobilin and then excreted

23
Q

what and where are stellate cells?

A

near the sinusoids of the liver, between the hepatocytes and the sinusoidal endothelium
they store lipids and vitamin A
they regulate sinusoid contraction
they synthesise collagen

24
Q

where and what are kuppfer cells?

A

in the sinusoids of the liver

they release macrophages to get rid of bacteria and old RBCs

25
Q

how are bile salts recycled?

A
  1. bacteria in the terminal ileum and the colon deconjugate to make bile acids. bile acids can be reabsorbed passively. When bile acids get back to the liver they are reconjugated
  2. bile salts can be actively reabsorbed via Na+ cotransport.
26
Q

how are 600mg of bile acids lost per day?

A

they are passed out in the faeces. but 95% get recycled.

27
Q

what does the liver / gall bladder excrete?

A

The liver makes bile acids and conjugates them into bile salts which are excreted into the small intestine.

28
Q

how are bile acids conjugated?

A

with glycine or taurine

29
Q

why do CF patients have thick, sticky pancreatic secretions?

A

the chloride channel which works with the HCO3- secreting channel is mutated. Cl- ions can’t be moved out of cell so the transporter which exchanges a Cl- in for a HCO3- out can’t work as well.

30
Q

describe the rotations of the embryonic gut tube

A

week 6: 90deg anti clockwise rotation of the cranial and caudal limbs of the elongated midgut, around the central axis of the vitalline duct.
week 7-8: 90deg rotation of stomach longitudinally. this places the stomach to the left and the liver on the right. also the vagus nerve now along the anterior and posterior faces of stomach. and the dorsal mesentery is now moved into place to become the greater omentum, and the ventral mesentery where it will become the lesser omentum!
week 10: a further 180deg anti-clockwise rotation of the cranial and caudal limbs, around the vitelline duct axis. these already rotated 90 deg in week 6. this places the jejunum on the left now.

31
Q

when does the gut tube herniate into the umbilical cord, and when does it go back in?

A

in at week 6, and back at week 10

32
Q

what is an omphacele?

A

where the midgut is outside the abdominal cavity but covered with skin. The midgut has failed to go back in during week 10. don’t confuse with gastroschisis from abnormal embryonic folding, where there’s no skin covering the guts!

33
Q

what can be a cause of volvulus of midgut?

A

reversed rotation of midgut, duodenum remains intraperitoneal.

34
Q

what is the embryonic derivation of the myenteric and submucosal plexuses in the GI tract?

A

migrated neural crest cells from the ectoderm

35
Q

where and what are pit cells?

A

they are in the liver lobules and they release NK lymphocytes

36
Q

what does cholestyramine do?

A

it helps lower cholesterol by preventing bile acid reabsorption. Dietary fibre does this too.

37
Q

how are primary metabolites made?

A

oxidation, hydroxylation, hydrolysis and reduction. these are more reactive. CALLED PHASE 1 REACTIONS.

38
Q

How are secondary metabolites made?

A

Conjugation. These are inactive and easy to excrete. Done in PHASE 2 REACTIONS.

39
Q

Phase 1 metabolism by cytochrome P450 (CYP) - what else is used up?

A

Oxygen to water and NADPH+ to NADP+

40
Q

What might induce phase 1 metabolism

A

alcohol or drugs. or sprouts.

41
Q

When haem is turned into biliverdin and bilirubin, what else is used up?

A

NADPH2s

42
Q

What do bacteria do to bilirubin in the gut?

A

Make urobilinogen.

43
Q

What is stercobilin?

A

The compound excreted in faeces, made from urobilinogen (which comes from bilirubin)

44
Q

How does the liver get rib of bilirubin?

A

sticks it onto albumin, then adds glucoronic acid (conjugation), then excretes it.

45
Q

what might happen if you had too much haem to process?

A

pre-hepatic jaundice. the liver is overloaded.

46
Q

hepatitis and cirrhosis of the liver cause what type of jaundice?

A

intrahepatic jaundice.

47
Q

what illness can result from pancreatic blockage (e.g. tumour)

A

extrahepatic jaundice. the bilirubin is conjugated but it gets backed up.

48
Q

what do you need to do transamination in the tissues?

A

alpha ketoglutarate and pyrodixal phosphate (B6)

49
Q

what do you need to do deamination in the liver?

A

glutamate dehydrogenase

50
Q

what compound will transamination make?

A

glutamate, and adding another amine group to make glutamine

51
Q

why do you need to do transamination in the tissues?

A

because the ammonia is toxic.

52
Q

what does high levels of glutamate initiate?

A

synthesis of more enzyme to keep the urea cycle going

53
Q

what makes lactate into glucose

A

the CORI cycle

54
Q

why is vitamin B1 (thiamine) so important?

A

it’s used to make a cofactor which is needed for pyruvate dehydrogenase function. this is needed for the link reaction (pyruvate to acetyl CoA)

GI (5 decks)

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