Digestion of CHOs Flashcards
1
Q
What are CHOs digested to
A
Simple sugars
2
Q
Proteins are hydrolysed to
A
Di & tripeptides and free AAs
3
Q
TAG metabolism
A
4
Q
Primary function of salivary glands
A
Production of fluid & digestive enzymes for homogenisation, lubrication & digestion of CHO (amylase) and lipid (lingual lipases)
5
Q
Primary function of stomach
A
Secretion of HCl and proteases to initiate hydrolysis of proteins
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
7
Q
Primary function of liver/gall bladder
A
Secretion and storage of bile acids for release to SI
8
Q
Primary function of SI
A
Final intraluminal digestion of food, digestion of CHO dimers and specific absorptive pathways for digested material
9
Q
Primary function of LI
A
Absorption of fluid and electrolytes and products of bacterial action in the colon
10
Q
Names and functions of the 3 pairs of salivary glands
A
- Parotid
- Submandibular
- Sublingual
alpha-amylase
-> lubrication
11
Q
Function of exocrine liver
A
Produces bile - important for fat digestion & absorption
ALSO excretion of waste metabolites and drugs
12
Q
Function of saliva
A
Lubrication - enables chewing & swallowing
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
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
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
16
Q
How much gastric juice is secreted a day
A
2 litres
17
Q
What is the intrinsic factor of gastric juice important for
A
Vit B12
- absence leads to pernicious anemia
18
Q
What is peptin responsible for
A
20% protein digestion
19
Q
Endopeptidase degrades…
A
Proteins -> peptides
20
Q
What is pepsin formed from
A
Inactive precursor pepsinogen
21
Q
What is the optimal pH of pepsin
A
- 5
- implicated in acid-induced ulceration
22
Q
What lines the stomach to protect it from damage by acid and pepsin
A
Mucus
23
Q
Endocrine function of pancreas
A
Insulin and glucagon
24
Q
Exocrine function of pancreas
A
Secrete pancreatic juice via pancreatic duct
25
What cells of the pancreas provide the most important digestive enzymes
Acinar cells
26
What cells of the pancreas provide HCO3- t adjust to appropriate pH for enzymes
Duct cells
27
@ what pH does the absorption of fat (requiring micelle formation) take place
Neutral or higher pH
- protects intestinal mucosa against excess acid
28
What is acute pancreatitis
Disease in which pancreatic tissue is destroyed by digestive enzymes
29
Where are digestive enzymes produced and secreted
* Gastric mucosa - chief cells
* Pancreas - acinar cells
30
What are digestive enzymes produced as
Proenzymes/zymogens (inactive)
31
Where are digestive enzymes stores
Zymogen granules which fuse with plasma membrane to release contents
\*\* Activation of enzyme activity occurs after release from cells
32
Exocrine secretion of digestive enzymes
33
What are secretagogues
Cells of different glands possess different sets of receptors
34
What does the binding of secretagogue activate
IC pathways leading to release of zymogen granules
35
1st pathway of release of zymogen granules (activated by binding of secretagogue)
Activation of PLC liberates IP3 & DAG
IP3 triggers release of Ca2+ from ER and activation of PKC
36
2nd pathway of release of zymogen granules (activated by binding of secretagogue)
Activation of AC results in increase in cAMP levels
37
Plant starch polysaccharides (2)
1. Amylose - alpha(1-4)
2. Amylopectin - alpha(1-4) & alpha(1-6)
38
Animal polysaccharide
Glycogen - branched with alpha(1-4) & alpha(1-6) linkages
39
Indigestible polysaccharide
Fibre - cellulose beta(1-4)
40
Which is the only disaccharidase that is inducible
Lactase
41
What is the principal digestive enzyme
alpha-amylase
42
Where is alpha-amylase secreted
Salivary glands and pancreas
endosaccharidase (works on inside)
43
what does alpha-amylase do
Splits alpha(1-4) glycosidic linkages in amylose to yield mainly maltose (2 x glucose)
44
What does alpha-amylase act on
Glycogen and amylopectin at alpha(1-4) linkages
45
1. What alpha-amylase enzyme is produced in larger amounts
2. What pH is it active at
1. Pancreatic enzyme
2. Neutral/slightly alkaline pH
46
Action of salivary and pancreatic alpha-amylase
47
Digestion of amylopectin by salivary and pancreatic alpha-amylase
48
What are brush border enzymes
Intestinal isomaltase splits alpha(1-6) linkages in glycogen and amylopectin
49
4 pathways of degradation of disaccharides
What is released onto the surface of membrane adjacent to transporters
* 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
How are
* D-glucose
* D-galactose
* D-fructose
absorbed
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
What GLUTs are present on enterocytes
* GLUT 1
* GLUT 2
* GLUT 5
52
What GLUT delivers sugars to portal circulation
GLUT 2
53
How are glucose and fructose transported in the intestinal epithelial cells
By facilitated glucose transporters on the luminal and serosal sides of the absorptive cells
54
Glucose and galactose transported
by Na+/glucose cotransporters on the luminal/mucosal side of the absorptive cells
55
Digestion and absorption of CHOs
56
Symptoms of CHO malabsorption syndromes
Abdominal distension
Gassiness
Cramping
Diarrhea
57
Detection of CHO malabsorption syndrome
Administer the sugar and determine if it is in the faeces and not in blood
58
Deficiency where patient is sucrose intolerant
Sucrase-isomaltose deficiency
59
What is coeliac disease characterised by
What happens to absorptive surface
Autoimmune condition characterised by malabsorption and specific diagnostic features exhibited by intestinal mucosa
Absorptive surface is markedly reduced (resulting indigestion/malabsorption is severe)
60
What are the histological changes with coeliac disease due to
Interaction of gluten, principal protein of wheat, with the epithelium
61
What antibodies are frequently present in cases of coeliac disease
CIrculating antibodies to wheat gluten and its fractions
62
How to screen for coeliac disease
e.g. endomysial antibodies of IgA subclass has shown that coeliac disease is under-diagnosed (especially in patients with unexplained anaemia)
63
Cause of coeliac disease
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
What is Cystic Fibrosis characterised by
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
What is lactose intolerance caused by
* Primary deficiency of lactase production
* Secondary to an injury to the intestinal mucosa where it is usually produced
66
What happens to the lactose that isn't absorbed
Converted by colonic bacteria to
1. Lactic acid
2. Methane gas
3. H2 gas
67
What is the osmotic effect in the bowel of the lactose and lactic acid responsible for
Diarrhea often associated with this syndrome
68
What happens to undigested CHO
Moves into LI - osmotically active (draws water in =\> osmotic diarrhea)
Bacterial fermentation of lactose to lactic acid, methane and H2 gas =\> flatulence
69
What do some people develop regarding lactose
Ability to ingest small amounts of lactose - probably through increase in poulation of colonic bacteria that can cleave lactose
70
What are starch blockers
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
Postulated mechanism of action of starch blockers
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
Why are starch blockers ineffective
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
