export_gi 3 Flashcards

1
Q

where does digestion occur?

A

upper part of SI

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2
Q

intraluminal phase

A

secrete enzymes

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3
Q

epithelial phase

A
  • brush border hydrolases

- enterocytes

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4
Q

nutrients absorbed in proximal SI

A

calcium, fat, AAs, sugar

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5
Q

nutrients absorbed in middle SI

A

sugars, AAs

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6
Q

nutrients absorbed in distal SI

A

bile salts, vit B12

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7
Q

3 types of carbs

A

mono-, di-, polysaccharides

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8
Q

what types of carbs are absorbed?

A
  • mono

- di/poly need to be digested

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9
Q

enzymes that break down carbs

A

salivary amylase (mouth), HCl (stomach), pancreatic amylase (SI)

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10
Q

brush border enzymes for carbs

A

maltase, isomaltase, sucrase, lactase

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11
Q

lactose intolerance

A
  • no lactase
  • inc luminal osmolarity–>
  • net water gain in lumen–>
  • luminal distension–> peristalsis
  • diarrhea
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12
Q

how is glucose absorbed into epithelial cells?

A
  • secondary active: Na-glucose cotransporter (SGLT) - apical
  • facilitated: glucose transporter (GLUT) - basolateral
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13
Q

transport from interstitial fluid to blood

A

capillary pores

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14
Q

protein digestion products

A

AAs, dipeptides, tripeptides

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15
Q

what enzymes digest protein?

A
  • pepsin, HCl (stomach)
  • trypsin, chymotrypsin, carboxypeptidase (pancreatic)

-enterokinase, aminopeptidase (brush border)

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16
Q

what activates pepsinogen

A

HCl –> pepsin

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17
Q

what cells secrete pepsinogen?

A

chief cells

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18
Q

what cells sectere HCl?

A

parietal cells

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19
Q

cascade of enzyme activation of enterokinase…

A

trypsinogen –> trypsin –> activates other zymogens

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20
Q

endopeptidase vs exopeptidase

A

endo- cleaves anywhere in protein

exo- only cleaves terminal amino acid

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21
Q

how do AAs cross apical membrane?

A
  • secondary active, coupled to Na+

- multiple types for diff AAs

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22
Q

how do AAs cross basolater membrane?

A

facilitated diffusion

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23
Q

how are small peptides transported?

A

secondary active coupled to H+ into cytosol

-broken down to AAs inside

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24
Q

where is all protein digestion done?

A

upper SI

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25
Q

how are full proteins absorbed?

A

transcytosis- e ndo then exocytosis

26
Q

what enzyme digests lipids?

A

lipases

27
Q

emulsification

A

break down of fat into droplets
-mechanical disturuption

-bile salts and phospholipids

28
Q

what are triglycerides broken into?

A

monoglyceride + 2 FAs

29
Q

bile salt fxns

A

emulsify fat

30
Q

where and what are bile salts made (from)?

A

liver, cholesterol

31
Q

colipase

A
  • amphipathic

- binds water-soluble lipase to fat droplets

32
Q

what happens once triglys are broken down?

A
  • some absorbed

- micelles

33
Q

micelles

A

contain small amounts of fat-soluble vitamins and cholesterol

34
Q

how are monoglys and FAs absorbed?

A

simple diffusion

35
Q

chylomicrons

A
  • tryglys, phospholipids, cholesterol, fat-sol vitamins
  • secreted by exocytosis into interstitial fluid

-enter lymph system and empty in veins in thoracic duct

36
Q

what happens to FAs and monoglys in epithelial cells?

A

enter smooth ER and form triglys –> packaged to chylomicrons in golgi

37
Q

olestra and orlistat

A

can’t be digested by lipases, lipase inhibitor

38
Q

fat-soluble vitamins

A
  • A,D,E,K
  • absorbed with lipids

-dissolved in droplets, micelles, chylomicrons

39
Q

water-soluble vits

A

require diffusion or special transport proteins

-exception: vit B12

40
Q

vit B12

A
  • absorbed when bound to intrinsic factor

- complex binds to receptors on lumin surface or ilium

41
Q

what secretes intrinsic factor?

A

parietal cells in stomach

42
Q

why do we need vit B12?

A

-RBC production

43
Q

causes of low B12?

A

diet, loss of parietal cells, ileum injury

44
Q

where is most water absorbed?

A

80% SI

45
Q

what drives fluid absorption?

A

osmotic gradient?

46
Q

where/how is sodium transported?

A

active in jejumum, ileum, and colon

-generates osmolarity gradient

47
Q

how are Cl- and HCO3- absorbed?

A

passively following Na+

48
Q

how is iron controlled?

A
  • cellular storage and carrier proteins
  • control absorption not excretion

active transport into intestine epithelial cells

49
Q

intracellular storage molecule for iron

A

ferritin (get into cell via DMT1)

50
Q

what happens to free iron?

A

in bloodstream in transferrin complex (transport protein linked to ferritin in cells)

51
Q

what happens to iron-ferritin in epithelial cells?

A

released back to lumen, excreted

52
Q

during normal iron stores…

A
  • inc ferritin synth

- dec absorption

53
Q

during low iron stored

A
  • dec ferritin synth

- inc absorption

54
Q

hemochromatosis

A

too much iron absorption –> toxic effects

55
Q

causes of pancreatitis

A
  • alcohol, drugs, gallstones, genetic mutations
  • blocked duct
  • acinar cell injury
  • defective intracellular transport
56
Q

symptoms of pancreatitis?

A

abdominal pain, nausea, vomiting

57
Q

effects of chronic pancreatitis

A
  • acinar cell loss

- pancreatic fibrosis

58
Q

causes of liver disease

A

drugs, toxins, viral, alcohol, metabolic

59
Q

hepatic failure

A
  • 80-90% liver function lost

- hepatic destruction

60
Q

symptoms of liver failure

A
  • jaundice
  • hypoalbuminemia (dec synth of liver cells)

-hyperammonemia (inability to clear toxin ammonia products)

61
Q

acute liver failure

A
  • hepatic necrosis

- induced by dugs/toxins

62
Q

cirrhosis

A
  • liver cell necrosis, inflammation
  • hypatocyte dysfunction

-due to alcohol, hepatits