Digestion of CHOs Flashcards

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1
Q

What are CHOs digested to

A

Simple sugars

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2
Q

Proteins are hydrolysed to

A

Di & tripeptides and free AAs

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3
Q

TAG metabolism

A
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4
Q

Primary function of salivary glands

A

Production of fluid & digestive enzymes for homogenisation, lubrication & digestion of CHO (amylase) and lipid (lingual lipases)

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5
Q

Primary function of stomach

A

Secretion of HCl and proteases to initiate hydrolysis of proteins

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6
Q

Primary function of pancreas

A

Secretion of HCO3-, proteases and lipases to continue digestion of proteins/lipids and amylase to continue digesting starch

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7
Q

Primary function of liver/gall bladder

A

Secretion and storage of bile acids for release to SI

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8
Q

Primary function of SI

A

Final intraluminal digestion of food, digestion of CHO dimers and specific absorptive pathways for digested material

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9
Q

Primary function of LI

A

Absorption of fluid and electrolytes and products of bacterial action in the colon

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10
Q

Names and functions of the 3 pairs of salivary glands

A
  1. Parotid
  2. Submandibular
  3. Sublingual

alpha-amylase

-> lubrication

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11
Q

Function of exocrine liver

A

Produces bile - important for fat digestion & absorption

ALSO excretion of waste metabolites and drugs

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12
Q

Function of saliva

A

Lubrication - enables chewing & swallowing

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13
Q

Functions of amylase

A

Major digestive enzyme

  • Hydrolyses alpha 1,4 glycosidic linkages in starch
  • Continues even after food has reached the stomach
  • Gastric juice inactivates it but not immediately
  • Starch in potatoes or bread may be 75% digested before inactivation of enzyme
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14
Q

What are the other enzymes in saliva

A
  • Lysozyme (beta 1,4 glycosidic bonds in bacterial cell wall polysaccharide peptidoglycan)
  • Sialoperoxidase (bacteriostatic)
  • Lingual lipase
  • Ribonuclease
  • Deoxyribonuclease
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15
Q

Function of stomach

A

Store ingested food and regulate release into duodenum

  • Chyme
  • exocrine secretions - gastric juices
  • paracrine secretion - histamine which stimulates gastric secretion
  • endocrine secretion - hormone gastrin
  • Stimulates gastric motility & acid secretion
  • Acts on intestines, pancreas and liver
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16
Q

How much gastric juice is secreted a day

A

2 litres

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17
Q

What is the intrinsic factor of gastric juice important for

A

Vit B12

  • absence leads to pernicious anemia
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18
Q

What is peptin responsible for

A

20% protein digestion

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19
Q

Endopeptidase degrades…

A

Proteins -> peptides

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20
Q

What is pepsin formed from

A

Inactive precursor pepsinogen

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21
Q

What is the optimal pH of pepsin

A
  1. 5
    - implicated in acid-induced ulceration
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22
Q

What lines the stomach to protect it from damage by acid and pepsin

A

Mucus

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23
Q

Endocrine function of pancreas

A

Insulin and glucagon

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24
Q

Exocrine function of pancreas

A

Secrete pancreatic juice via pancreatic duct

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25
Q

What cells of the pancreas provide the most important digestive enzymes

A

Acinar cells

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26
Q

What cells of the pancreas provide HCO3- t adjust to appropriate pH for enzymes

A

Duct cells

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27
Q

@ what pH does the absorption of fat (requiring micelle formation) take place

A

Neutral or higher pH

  • protects intestinal mucosa against excess acid
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28
Q

What is acute pancreatitis

A

Disease in which pancreatic tissue is destroyed by digestive enzymes

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29
Q

Where are digestive enzymes produced and secreted

A
  • Gastric mucosa - chief cells
  • Pancreas - acinar cells
30
Q

What are digestive enzymes produced as

A

Proenzymes/zymogens (inactive)

31
Q

Where are digestive enzymes stores

A

Zymogen granules which fuse with plasma membrane to release contents

** Activation of enzyme activity occurs after release from cells

32
Q

Exocrine secretion of digestive enzymes

A
33
Q

What are secretagogues

A

Cells of different glands possess different sets of receptors

34
Q

What does the binding of secretagogue activate

A

IC pathways leading to release of zymogen granules

35
Q

1st pathway of release of zymogen granules (activated by binding of secretagogue)

A

Activation of PLC liberates IP3 & DAG

IP3 triggers release of Ca2+ from ER and activation of PKC

36
Q

2nd pathway of release of zymogen granules (activated by binding of secretagogue)

A

Activation of AC results in increase in cAMP levels

37
Q

Plant starch polysaccharides (2)

A
  1. Amylose - alpha(1-4)
  2. Amylopectin - alpha(1-4) & alpha(1-6)
38
Q

Animal polysaccharide

A

Glycogen - branched with alpha(1-4) & alpha(1-6) linkages

39
Q

Indigestible polysaccharide

A

Fibre - cellulose beta(1-4)

40
Q

Which is the only disaccharidase that is inducible

A

Lactase

41
Q

What is the principal digestive enzyme

A

alpha-amylase

42
Q

Where is alpha-amylase secreted

A

Salivary glands and pancreas

endosaccharidase (works on inside)

43
Q

what does alpha-amylase do

A

Splits alpha(1-4) glycosidic linkages in amylose to yield mainly maltose (2 x glucose)

44
Q

What does alpha-amylase act on

A

Glycogen and amylopectin at alpha(1-4) linkages

45
Q
  1. What alpha-amylase enzyme is produced in larger amounts
  2. What pH is it active at
A
  1. Pancreatic enzyme
  2. Neutral/slightly alkaline pH
46
Q

Action of salivary and pancreatic alpha-amylase

A
47
Q

Digestion of amylopectin by salivary and pancreatic alpha-amylase

A
48
Q

What are brush border enzymes

A

Intestinal isomaltase splits alpha(1-6) linkages in glycogen and amylopectin

49
Q

4 pathways of degradation of disaccharides

What is released onto the surface of membrane adjacent to transporters

A
  • Maltose alpha(1-4) -> 2 glucose// maltAse
  • Isomaltose alpha(1-6) -> 2 glucose // isomaltAse
  • Sucrose -> glucose and fructose // sucrAse
  • Lactose -> galactose and glucose // lactAse

Release of monosaccharides occurs on surface of membrane adjacent ot transporters

50
Q

How are

  • D-glucose
  • D-galactose
  • D-fructose

absorbed

A

Absorbed by passive diffusion

Mostly by transporters in enterocytes if duodenum and jejunum

  • Na+/glucose cotransporters
  • SGLT1 present in SI
  • Na+-independent facilitative hexose transporters
51
Q

What GLUTs are present on enterocytes

A
  • GLUT 1
  • GLUT 2
  • GLUT 5
52
Q

What GLUT delivers sugars to portal circulation

A

GLUT 2

53
Q

How are glucose and fructose transported in the intestinal epithelial cells

A

By facilitated glucose transporters on the luminal and serosal sides of the absorptive cells

54
Q

Glucose and galactose transported

A

by Na+/glucose cotransporters on the luminal/mucosal side of the absorptive cells

55
Q

Digestion and absorption of CHOs

A
56
Q

Symptoms of CHO malabsorption syndromes

A

Abdominal distension

Gassiness

Cramping

Diarrhea

57
Q

Detection of CHO malabsorption syndrome

A

Administer the sugar and determine if it is in the faeces and not in blood

58
Q

Deficiency where patient is sucrose intolerant

A

Sucrase-isomaltose deficiency

59
Q

What is coeliac disease characterised by

What happens to absorptive surface

A

Autoimmune condition characterised by malabsorption and specific diagnostic features exhibited by intestinal mucosa

Absorptive surface is markedly reduced (resulting indigestion/malabsorption is severe)

60
Q

What are the histological changes with coeliac disease due to

A

Interaction of gluten, principal protein of wheat, with the epithelium

61
Q

What antibodies are frequently present in cases of coeliac disease

A

CIrculating antibodies to wheat gluten and its fractions

62
Q

How to screen for coeliac disease

A

e.g. endomysial antibodies of IgA subclass has shown that coeliac disease is under-diagnosed (especially in patients with unexplained anaemia)

63
Q

Cause of coeliac disease

A

Possible due to defect in yet to be identified peptidase in brush border that results in the incomplete digestion of gluten

Genetic pre-disposition - HLA-DQ2 and HLA-DQ8, genes that give rise to proteins that display gluten fragments to immune system cells

Environmental trigger

Highly permeable gut - junctions come apart, allowing a large amt of indigestible gluten fragments to seep into the underlying tissue and incite immune system cells

64
Q

What is Cystic Fibrosis characterised by

A

Accumulation of abnormal concentration of salt in the body

Formation of thick sticky mucus

Mucus blocks airways

Repeated infections lead to lung damage

Muck blocks digestive ducts - liver, pancreas, (possibility of diabetes) SI

Mucus blocks reproductive tract

Malfunction of sweat glands - increase of salt in sweat is diagnostically useful

65
Q

What is lactose intolerance caused by

A
  • Primary deficiency of lactase production
  • Secondary to an injury to the intestinal mucosa where it is usually produced
66
Q

What happens to the lactose that isn’t absorbed

A

Converted by colonic bacteria to

  1. Lactic acid
  2. Methane gas
  3. H2 gas
67
Q

What is the osmotic effect in the bowel of the lactose and lactic acid responsible for

A

Diarrhea often associated with this syndrome

68
Q

What happens to undigested CHO

A

Moves into LI - osmotically active (draws water in => osmotic diarrhea)

Bacterial fermentation of lactose to lactic acid, methane and H2 gas => flatulence

69
Q

What do some people develop regarding lactose

A

Ability to ingest small amounts of lactose - probably through increase in poulation of colonic bacteria that can cleave lactose

70
Q

What are starch blockers

A

Marketed as a means of losing weight without exercise or reduce caloric intake

Based on a protein extracted from beans, which blocked the action of amylase

71
Q

Postulated mechanism of action of starch blockers

A

You can eat as much starch as you like with a meal and taken with the starch blocker the starch would pass through the digestive tract without being metabolised

72
Q

Why are starch blockers ineffective

A
  1. Inactivation of inhibitor by the low pH of the stomach
  2. Excess of amylase activity as compared with the amt of starch blocker ingested