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GI System Final I > Digestion and Absorption process of GI > Flashcards

Digestion and Absorption process of GI Flashcards

1
Q

Where does digestion start and end

A

begins in the stomach and ends in small intestine

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2
Q

Where does absorption take place

A

small intestine

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3
Q

2 main paths of absorption

A

cellular and paracellular

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4
Q

Cellular absorption

A

lumen –> apical membrane –> intestinal epithelial cell –> basolateral membrane –> bloof

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5
Q

Where are the transporters for cellular absorption

A

in membrane

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6
Q

Paracellular absorption

A

intestinal epithelial cell –> lateral intercellular space –> intestinal epithelial cell

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7
Q

2 types of digestive activity

A

cavital (luminal) digestion and membrane (contact) digestion

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8
Q

Cavital digestion

A

digestion from action of enzymes of salivary glands, stomach and pancreas

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9
Q

Membrane digestion

A

hydrolysis by enzymes of epithelial cells

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10
Q

Folds of Kerckring

A

longitudinal folds of small intestine

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11
Q

Function of villi and microvilli in small intestine

A

increase surface area

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12
Q

Where are the villi the longest and where are they the shortest

A

longest in duodenum and shorter in terminal ileum

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13
Q

Site of activity of digestive enzymes

A

microvillar surface

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14
Q

Barrier that allows some passage of nutrients, water, electrolytes

A

microvillar surface

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15
Q

Enterocytes

A

epithelial cells of intestine

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16
Q

Function of enterocytes

A

digestion, absorption, and secretion

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17
Q

Goblet cells

A

mucus-secreting cells

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18
Q

Function of goblet cells

A

physical, chemical and immunological protection

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19
Q

Paneth cells function

A

mucosal defense against infection and bacteria

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20
Q

What controls the flux of solutes and fluid between lumen and blood

A

enterocyte membrane

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21
Q

4 ways enterocytes move solutes and fluid

A

pinocytosis, passive diffusion, facilitated diffusion, and active trasport

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22
Q

Where does pinocytosis occur and whats its function

A

base of microvilli and used for uptake of protein

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23
Q

What movement takes place during absoprtion

A

transmural

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24
Q

Monosaccharides are absorbed by

A

enterocytes

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25
Q

Three end products of carbohydrate digestion

A

glucose, galactose, and fructose

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26
Q

What does lactose break into

A

glucose and galactose

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27
Q

What does sucrose break into

A

glucose and fructose

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28
Q

What breaks down starch

A

alpha amylase

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29
Q

What can starch break into

A

maltose, dextrins, maltotriose

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30
Q

Transport mechanisms for absorption of carbs

A

co-transport and facilitated diffusion

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31
Q

GLUT 2

A

gets glucose, galactose and fructose from intracellular into blood

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32
Q

SGLT1

A

takes glucose and galactose out of the lumen into intracellular

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33
Q

GLUT5

A

takes fructose from lumen to intracellular

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34
Q

What kind of transport is SGLT 1

A

secondary active transport

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35
Q

Where is the Na/K ATPase located on the cells for carb absorption

A

basolateral side

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36
Q

Lactose intolerance

A

failure to digest carb

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37
Q

Why does lactose intolerance occur

A

brush-border lactase is lacking

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38
Q

Result of lactose intolerance

A

osmotic diarrhea– undigested lactose remains in lumen and holds water

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39
Q

What happens to unabsorbed and undigested lactose

A

ferments into methane and hydrogen gas causing excess gas

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40
Q

How are proteins digested to absorbable forms

A

proteases in stomach and small intestine

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41
Q

Stomach protease

A

pepsinogen –> pepsin

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42
Q

Small intestine proteases

A

trypsinogen –> trypsin, chymotrypsinogen –> chymotrypsin, proelastase –> elastase, proccarboxypeptidase (A or B) –> carboxypeptidase (A or B)

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43
Q

Endopeptidases

A

pepsin, trypsin, chymotrypsin, elastase

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44
Q

Exopeptidases

A

carboxypeptidase A and B

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45
Q

What does protein breakdown into in the stomach

A

amino acids and oligopeptides

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46
Q

What does protein breakdown into in the small intestine

A

amino acids –> dipeptides and tripeptides, oligopeptides –> amino acids –> dipeptides and tripeptides

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47
Q

Function of trypsin

A

catalyzes hydrolysis of trypsinogen (autocatalysis)

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48
Q

Transport mechanisms for absorption of proteins

A

co-transport and facilitated diffusion

49
Q

Luminal cotransporters for amino acids

A

Na+/amino acid cotransporter – one for each kind of amino acid - neutral, acidic, basic, and imino

50
Q

How do dipeptides and tripeptides cross the luminal surface

A

H+/ Dipeptide or Tripeptide cotransporter

51
Q

Basolateral (Blood) side of protein absorption

A

facilitated diffusion- one kind for each amino acid - neutral, acidic, basic, and imino

52
Q

Disorders of protein assimilation

A

occur when there is a deficiency of pancreatic enzymes or transporter problem

53
Q

Chronic pancreatitis and cystic fibrosis

A

deficiency of pancreatic enzymes

54
Q

Congenital trypsin absence

A

absence of trypsin makes it seem like all pancreatic enzymes are gone

55
Q

Cystinuria

A

genetic disorder where amino acids are secreted in the feces

56
Q

Process of cystinuria

A

defect in or absence of Na+/amino acid co-transporter

57
Q

Hartnup disease

A

can’t absorb neutral amino acids (tryptophan)

58
Q

Genetics of Hartnup disease

A

recessive genetic disorder

59
Q

Symptoms of Hartnup disease

A

diarrhea, red scaly skin, photosensitivity, short stature

60
Q

Urine samples of Hartnup disease

A

abnormally high excretion of neutral amino acids (trypotophan) and their by products (serotonin)

61
Q

Cystic fibrosis transmembrane conductance regulator (CTFR)

A

chloride ion channel

62
Q

Mutation in CTFR

A

associated with deficiency of pancreatic enzymes

63
Q

What organ is the first to fail in cystic fibrosis

64
Q

How are lipids digested to absorbable forms

A

lipases in stomach and small intestine

65
Q

Triglyceride breakdown into

A

via lingual, gastric, and pancreatic lipases into monoglyceride and 2 fatty acids

66
Q

Cholesterol ester breakdown into

A

via cholesterol ester hydrolase into cholesterol and fatty acid

67
Q

Phospholipid breakdown into

A

via phospholipase A2 into lysolechitin and fatty acid

68
Q

Why lipid breakdown is complicated

A

lipids need to be solubilized in micelle and transported to apical membrane for absorption

69
Q

Lingual and gastric lipases…

A

initiate lipid digestion in stomach

70
Q

Where are lipid droplets emulsified

A

in stomach by dietary proteins – with NO bile acids

71
Q

What enzyme in the stomach helps lipid digestion and how

A

CCK because it slows gastric emptying allowing more time for breakdown

72
Q

Where does most lipid digestion occur

A

small intestine

73
Q

Function of bile salts

A

emulsify fat

74
Q

Pancreatic enzyme and lipid digestion

A

enzymes secreted into small intestine to complete digesiton

75
Q

Pancreatic lipase

A

inactivated by bile salts

76
Q

Colipase

A

secreted an inactive for and activated by trypsin and binds to pancreatic lipase to displace the bile salt

77
Q

Cholesterol ester hydrolase

A

catalyze cholesterol production and hydrolyze triglycerides into glycerol

78
Q

Phospholipase A2

A

proenzyme is activated by trypsin

79
Q

Optimal pH for pancreatic lipase

80
Q

Products of lipid digestion

81
Q

Micelle structure (5)

A

bile salt, hydrophilic side, hydrophilic side, nonpolar lipid and phospholipid

82
Q

5 steps of processing a lipid

A
  1. solubilization by micelles, 2.diffusion of micellar content across apical membrane, 3.reesterification, 4.chylomicron formation, 5.exocytosis of chylomicron
    * *includes Apo B ** on chylomicron
83
Q

No ApoB on chylomicron can lead to

A

abetalippoproteinemia and you can’t absorb dietary lipids

84
Q

Abnormality of lipid assimilation

A

steatorrhea

85
Q

Pancreatic insufficiency

A

failure to secrete adequate pancreatic enzymes

86
Q

Function of pancreatic enzymes

A

regulate acidity of duodenum

87
Q

Zollinger-Ellison syndrom

A

gastric secreting tumor causing H+ increase and overload of acid in duodenum

88
Q

Pancreatitis

A

impaired HCO3 secretion and impaired enzyme secretion

89
Q

Deficiency of bile salt

A

interferes with formation of micelles

90
Q

Causes of bile salt deficiency

A

ileal resection and small intestinal bacterial overgrowth (SIBO)

91
Q

Ileal resection and bile salt deficiency

A

interrupts enterohepatic circulation of bile salts and bile salt pool is reduced

92
Q

Small intestinal bacterial overgrowth (SIBO)

A

bacteria deconjugate bile salts causing failure of micelle formation and fat malabsorption

93
Q

Two main causes of small intestinal bacterial overgrowth

A

decrease in gastric acid secretion and small intestin dysmotility

94
Q

Clinical presentation of SIBO

A

chronic diarrhea, weight loss, and malabsorption

95
Q

Tropical sprue

A

reduction in number of intestinal epithelial cells which reduces microvillar surface area

96
Q

Why is lipid absorption impaired in tropical sprue

A

because surface area for absorption is decreased

97
Q

S/S of tropical sprue

A

steatorrhea, deficient in folate and B12, diarrhea

98
Q

Treatment for tropical spure

A

tetracycline and folate

99
Q

Non-tropical sprue (celiac sprue)

A

autoimmune disorder where antibodies develop against gluten

100
Q

S/S of non-tropical sprue

A

malabsorption and deficiency in vitamin B12, folate, iron, calcium, vitamin D, and vitamin A

101
Q

Prevalence of Non-tropical sprue

A

caucasian and european ancestry and woman

102
Q

GI symptoms of celiac spure

A

abdominal pain, constipation, diarrhea, steatorrhea

103
Q

Non Gi symptoms of celiac sprue (due to nutrient deficiency)

A

tingling in hands, itchy skin, easy bruising

104
Q

Fat soluble vitamins

A

A, D, E, K

105
Q

Mechanism of fat soluble absorption

A

same as lipids

106
Q

Water soluble vitamins

A

B1,2,3,12, C, biotin, folic acid, nicotinic acid, and pantothenic acid

107
Q

How are water soluble vitamins absorbed

A

Na+ dependent cotransport in small intestine

108
Q

Vitamin B12 importance

A

complexes with other proteins– R protins, intrinsic factor, and transcoalbumin II

109
Q

2 disruptions in absorption of vitamin B12

A

gastrectomy and gastric bypass

110
Q

Gastrectomy

A

loss of parietal cells and intrinsic factor source

111
Q

Gastric bypass

A

exclusion of stomach, duodenum, and proximal jejunum alters absorption of vitamin B12

112
Q

Pernicious anemia

A

stomach doesn’t produce enough intrinsic factor and decrease in B12

113
Q

Common causes of pernicious anemia

A

atrophic gastritis and autoimmune condition

114
Q

Atrophic gastritis

A

chronic inflammation of stomach mucosa causing loss of parietal cells

115
Q

Abnormalities of absorption of vitamin D

A

Rickets, osteomalacia due to inadequate Ca2+ absorption b/c deficient vitamin D

116
Q

2 sources of D3 in vitamin D formation

A

Sunlight and Diet

117
Q

Vitamin D effects of body (3)

A

increase in gut Ca2+ absorption, increase bone calcification and increase bone resorption

118
Q

Enzyme that makes vitamin D usable to body

A

1 alpha hydroxylase

119
Q

Usable form of vitamin D

A

1,25 Dihydroxy D3

GI System Final I (7 decks)

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