Digestion In Depth Flashcards
1
Q
Digestion’s Major Goal
A
- Major goal: energy in macronutrients is in Carbon-carbon bond; take macronutrients and digest down to macromolecules but leave C-C bonds intact; if break in digestion then loose energy
- Take substrate – Protein and break down w/enzymes and then break into a.a. and small peptides
- Enzymes we use are: exopeptidases (attacks protein at end), endopeptidases (attacks protein in interior)
•Carbohydrates as glucose, glycogen and starch and use amylases, glycosidases and break down into disaccharides; membrane of small intestine we take disaccharides and break down into monosaccharides
- Sucrose is disaccharide and is broken in to glucose and fructose, etc.
- Goal is to get to monosaccharides and we take those up too
•Lipids – most lipids we take in are triglycerides and cholesterol (don’t do much) use lipases w/triglycerides from pancreas; break into free fatty acids
2
Q
Digestive Tract Map
A
- Digestion begins in the mouth – mastication (manipulate and grind food) input from salivary secretions for this for lubrication and amylase enzyme is secreted in saliva (minimal effect); minimal lipase too but minimal effect; most in mouth is lubrication
- Move food through esophagus – channel to stomach, sphincter muscle; smooth muscle forms a sphincter since so tight and have to actively push food through there at top and bottom of esophagus, chest cavity at pressure lower than atm pressure so separate GI tract w/sphincter muscle to not get pressure issues in other parts of GI tract; use peristalsis to get through esophageal sphincter and then lower sphincter
- Stomach – storage organ for your meal; involved in protein digestion esp – secrete hydrochloric acid which will denature proteins and helps to kill foreign bacteria (protection) in the stomach and pepsin to help digest proteins; not much you can absorb in stomach except alcohol
- Small Intestine – digestion and absorption (24 ft); for digestion need help from pancreas and pancreatic secretions involve HCO3- (bicarbonate) to neutralize pH to give pH of 7-8; pancreas also secretes digestive enzymes for carbohydrates, for lipids, for protein secreted into small intestine
- Lower end of stomach where enter small intestine there is another sphincter muscle
- Large Intestine – 6 ft, ascending portion, transverse portion, descending portion and then rectum and anus; water balance – food moving through is in aquatic environment and want to start conserving body water and pull water out; dehydration leads to constipation; but illness w/diarrhea you get dehydrated via the gut; bacterial reservoir – E. coli and entire microbiome
3
Q
Stomach Anatomy
A
- three sections based on structural and functional distinctions—the fundus, body, and antrum. The mucosal lining of the stomach is divided into the oxyntic mucosa and the pyloric gland area based on differences in glandular secretion.
- Fundus stomach and then major body and then pyloric gland area and then pyloric sphincter before you get to the small intestine
- Duodenum is the 1st part of the small intestine
- Stomach has lots of folds so has ability to expand – when stomach is empty you have volume of 200 mL when you eat huge dinner, it can expand up to 2 L
- Couple stomach stapling w/limiting eating
4
Q
Gastric emptying from stomach
A
- Gastric emptying and mixing as a result of antral peristaltic contractions (mammalian stomach).
•Mixing food in stomach – once food mass is in stomach it’s called chyme and there are peristaltic contractions to mix the food in the lower part of the stomach
5
Q
Enervated stomach
A
The enteric nervous system of a rat’s stomach. By injecting a tracer derived from a horseradish enzyme into the vagus nerve, which connects the brain to the esophagus and stomach, researchers were able to reveal the extent of the nerve network. As nerve fibers fray out into the tiny endings across the stomach, information concerning food volume, hunger, discomfort, and satiety are sent back the brain.
- Rat stomach – have tons of nerves in the stomach
- GI tract is one of the most highly enervated so signals relayed back to central nervous system
- Satiety, ability to feel full, is one of them
6
Q
How to make acid in stomach?
A
- gastric pits with various cell types
- One cell type are the parietal cells which make HCl, and they also make intrinsic factor, which helps us absorb vitamin B12
- In gastric pits we have chief cells which make pepsinogen (which is inactivate pepsin) – when pepsinogen gets released into the stomach HCl cleaves it into pepsin which is the active enzyme
- Pepsinogen Is a zymogen – which is an enzyme precursor
- Digestive enzyme inside a cell you don’t want it active inside that cell because it will act on proteins, so we make it as zymogen so its inactive, precursor form and then we active it
- Same is true of digestive enzyme from the pancreas - made as zymogens, released, and then activated
- Stomach is heavy w/goblet cells as protection from HCl
- Make Gastrin in G cells which turn on Gastric pits to help us make HCl in particular to generate pepsin; gastrin gets into local circulation
- HCl denatures proteins since its acid
7
Q
Gastric Pit and epithelial cells
A
- Gastric pit w/lumen and epithelial cells and then inside the pits are variety of cells, parietal cells and chief cells and mucus cells are in gastric pits and along cell walls
- G cells are separate
- Layer of stomach called mucosa and then gastric pits and then submucosa
8
Q
Mucous cells, Chief Cells, Parietal cells, and ECL cells
A
- Mucous cells, chief cells, parietal cells, and then ECL cells
- ECL stands for enterochromaffin-life cells: which make the compound histamine which stimulates gastric pits and helps give you acid secretion as well
- Histamine is mediator of immune response ;
histamine receptor in gastric pit is different than histamine receptor for other immune responses – same signaling compound but receptors are different
9
Q
Acid Secretion
A
Mechanism for how H+ ions are secreted by the parietal cells of the stomach.
water and carbon dioxide make H+ for HCL in stomach and bicarbonate for blood
10
Q
Making of Stomach Acid
A
- H2O + CO2— H2CO3 — H+ + HCO3-
- To generate stomach acid we take water and CO2 and use the enzyme CA (carbonic anhydrase)
- Generate hydrogen ion which gets put into the stomach and Cl- follows through ion channel
- Bicarbonate goes into the blood
- When eat meal have acid secretion in stomach and bicarbonate in the blood – so your blood flow goes a little bit alkaline call it the alkaline tide
- Excess acid secretion with stress
11
Q
Pancreas and Duodenum
A
Schematic representation of the exocrine and endocrine portions of the mammalian pancreas. The exocrine pancreas secretes into the duodenal lumen a digestive juice composed of digestive enzymes secreted by the acinar cells and an aqueous NaHCO3 solution secreted by the duct cells. The endocrine pancreas secretes the hormones insulin and glucagon into the blood.
- Food digested in stomach w/pH of 2 or 3
- 2 hours to empty stomach after meal in rhythmic fashion
- Food goes into duodenum – and need secretions from pancreas to help out
- In pancreas: like 2 diff organs that are put together: endocrine pancreas are little islets of tissue called islets of Langerhans which makes major metabolic hormones – insulin and glucagon, secrete into blood; and exocrine pancreas– secrete into ducts the bicarbonate and digestive enzymes and go into duodenum to neutralize pH and digestive enzymes finish digestive process
12
Q
Liver and Gull Bladder
A
- Liver: Focused on bile which is made by liver to emulsify fats
- Gull bladder – stores bile and w/appropriate signals it releases bile which comes down and joins the pancreatic duct and enters the duct right before secretions go in
- w/out gull bladder may have issues w/high fat meals since release of bile not as well timed
13
Q
Liver Blood Flow in Mammal
A
- Circulation to stomach
- Nutrients we absorb in GI tract are put into that structure – hepatic portal vein and first stop is the liver
- What ever nutrition you take in, the liver gets first crack at those nutrients and will regulate what happens next
- Exception here is fat – which gets taken up by lymph system and bypasses the liver; at end fat enters venous system and gets circulated
- Liver regulates what rest of circulation can’t
14
Q
Bile Salts
A
- Bile salts are put into duodenum as needed and they do their job and then as we absorb fats we also absorb some bile salts and the bile salts go back through hepatic portal circulation back to the liver but fats go to lymph system
- Ability to make bile is not that great so important to be able to recycle
15
Q
Liver Functions
A
- Liver has over 500 diff functions – key in glucose and fat metabolism and makes urea
- Bile salts made in liver and absorb some bile salts and other nutrients in GI tract
- Liver ships out glucose, proteins, vitamin D etc., liver metabolizes most of our drugs
16
Q
Small Intestine
A
- Small intestine – digestion and absorption
- Promote digestion by releasing bicarbonate and put in digestive enzymes
- Much of anatomy of small intestine has to deal with that mesentery to body wall
- Serosal side, mucosal side and layers of smooth muscle for peristalsis (all you need to know)
17
Q
Generalized Intestine
A
- Villi are going to increase surface area dramatically
- Folding inside too to increase SA
- Folds of Keckering
- Action is in the villi
18
Q
Mucosal Side of Intestine
A
- Mucosal side is where the villi are
- Layers of smooth muscle and then submucosal w/circulation
- SA is 200-300 m2
19
Q
Enterocytes and Crypts
A
- At base are the crypts – crypts of Liber Kuhn, production/ our source of epithelial cells which migrate up onto the villi, 2 x 1010 cells/day made in our GI tract, lots of cell division since that is where we take up the nutrients
- Carbs go into villi and away into the venous system and lymph system for lipids
- Epithelial cells on villi are called Enterocytes
- chemotherapy - agents attach rapidly dividing cells but don’t distinguish btwn cancer and normal cells – side effect of chemo is that it can effect the gut and give people very sick because trouble in GI tract since not making proper number of epithelial cells
- Celiac disease – allergic rxn to gluten which interacts w/membrane and immune system gets involved and can reek havoc and immune system sluffs off villi and so trouble absorbing nutrients since looks like people are malnourished
- Enterocytes have brush border membrane so surface area is > again by the tiny fingerlike projections
20
Q
Villi
A
- Lots of mito and ATP in theses cells since very active cells
- Microvilli which on them have glycoproteins called glycocalyx
- Glycocalyx off of microvilli which slows down the mvmt of all of fluid in digestive tract
- Stomach And the small intestine (digestion and absorption)
21
Q
Regulation of Cephalic Phase (1st phase)
A
- Turn on GI tract for bit then turn off for a bit
- First part of digestion is Cephalic Phase – presentation and presence of food in the mouth; when food present in mouth and presentation visually will activate the salivary glands and a couple neurotransmitters (Ach = acetyl choline; VIP = vasoactive intestinal polypeptide) use nervous system to turn this on and vagus nerve to turn on parietal cells and chief cells and generate HCl and pepsinogen even before food gets to stomach
22
Q
Regulation of Gastric Phase (2nd phase)
A
•When you eat food enters the stomach – its called gastric phase – presence of food in stomach sets up and stimulates things –> turn on the G cells and get gastrin release which stimulates the gastric pits via circulation; and histimine release from ECL cells which also turns on the gastric pits
•Vagus can stimulate the ECL cells and the G cells a bit so dual control mechnisms
- Enorvating gastric pits and also stimulating ECL etc.
- Multiple control mechanisms on gastric pits to ensure proper acid production
23
Q
Regulation of Intestinal Phase (3rd phase)
A
- As push food into duodenum start on 3rd phase called intestinal phase - causes release of 2 hormones - secretin and CCK-cholecystokinin from duodenum (CCKPZ - initially thought there were 2 hormones w/pancreozymin too but same hormone)
- Secretin causes release of bicarbonate;
-(1)CCK causes release of digestive enzymes (zymogens)- stimulate pancreas here
- (2)CCK causes release of bile and (3) slows down release of acid from gastric pit
- CCK and secretin enter blood stream ; GI tract is an endocrine gland
- Intestinal tract communicates w/stomach via CCK which says has food so can slow contractions and allow digestive process to start in intestine w/out more food coming in
- Intestine communicates back to to the stomach via CCK
- Gut is highly enervated so signals from nervous system which communicate from intestine to stomach – called enterogastric reflex
24
Q
H. Pylori
A
- Helicobater pylori (H. Pylori) – something that can cause ulcers – bacteria that can invade the stomach, generates ammonia so can live in acid environment and create microenvironment; some cause stomach ulcers and strong risk factor for gastric cancer, can treat it w/antibiotics
- > allergy and asthma in kids may be correlated w/kids treated w/antibiotics early on have > incidence of asthma and allergy; asthma may have protective effect in first few years to keep kids from getting H. pylori
25
Q
Inhibition/Activation of secretion of H+ from parietal cells
A
- Cells have number of diff receptors and respond to diff compounds
- Vagus releases acytyl choline and stimulate receptor to stimulate acid production
- Gastrin stimulates receptor for acid production
- Histamine stimulates receptor and gives acids production too
- Too much acid production in stomach can generate – GERD (gastro-esophageal reflux disease) - too much acid backs up into esophagus which isn’t made for acid (pain)
- To control – first line of defense use drug that blocks histamine (zantac) which bind the histamine receptor in stomach and keep it from being stimulated by histamine
- Second line of defense is use omeprazole – blocks hydrogen ion pump and it’s a stronger medication
- Acid secretion increases probability of getting an ulcer which can occur in stomach or duodenum (easily damages)
26
Q
REgulation of HCl secretion
A
27
Q
Absorption in Small Intestine of Carbs
A
Absorption takes place in small intestine (villi w/epithelial cells/enterocytes that are responsible)
- Digestion in lumen and want to absorb in blood
- Process of digestion we get down to monosaccharides
- Have a transporters called SGLT1 – NA+-glucose transporter #1 (moves sodium and glucose at same time and is symporter, Na+ is down concentration gradient taking glucose with it)
- On basal membrane we have GLUT2 - glucose transporter, uniport and allows glucose out of cell and then it can go into blood; each villi has own circulation
- Where expend energy
- Sodium –potassium exchange pump; pump sodium out of cell to < Na+ inside cell which allows the sodium gradient to exist but this uses ATP
- Fructose transporter is different from glucose and galactose; its transporter is GLUT5 for fructose which goes through GLUT5 into cell
- And then transported out using GLUT2
- In portal blood glucose – 10-15mmol, will be high and first stop from intestine is the liver which has lots of GLUT2 (low affinity transporter, w/Km of about 15-20 mmol) but move lots of glucose through it and bidirectional ; after meal the GLUT2 gets saturated and allows liver to take up sugar it needs and then it stores glucose as glycogen to put sugar into blood between meals if necessary
- Fructose and glucose can use GLUT2 in the liver cell
- After need to use glycogen to > glucose in blood then goes out GLUT2 in liver and into blood
- Blood Glucose (5mM)
- GLUT1 and GLUT3 which have kM of 1-3 mM
- Nervous system and blood vessels w/sugar available normally in the blood their transporters can be saturated and transport to the body in way they need to
- If not enough glucose it will bypass the liver and go to blood vessels and nervous system
29
Q
Absorption of aa in small intestine
A
- Amino acid-Na+ co-transporter
- Amino acids go out another transporter on other side
- What powers this is the sodium-potassium pump; lower Na+ inside cell and help drive a.a. in and then take them out
- Sodium co-transport: w/diff symporter types
- (1) symporter for neutral a.a.
- (2) transporter for acidic a.a. (glutamic and aspartic acid)
- (3) transporter for basic a.a. (Lys, Arg, His)
- (4) transporter for glycine, proline, hydroxyproline – these few neural a.a. have these 2 options
- Membrane can also take up di and tri-peptides w/a go transporter coupled w/H+
- Endocytosis of entire polypeptide
30
Q
Absorbtion of Lipids
A
- Meal with fats, then you will release bile which is made in liver and stored in gull bladder
- Bile emulsifies fats
- Bile has bile salts which have cholesterol on one end and a.a. like glycine or taurine on other end; cholesterol end that is lipid soluble and a.a. end that is water soluble
- Bile salts get together in micelles w/25-50; and inside this micelle you have triglyceride and lipases
- Micells can emulsify since hydrophilic end is outside and hydrophobic end is inside
- Allows for digestion of triglycerides into free fatty acids and a monoglyceride
- Micelle is ferry to get fats to wall of epithelial and release free fatty acids and monoglyceride into the cell
- TG are too bit to go into epithelial cell so you break it down first before enter
- In epithelial cell reforms FFA+ monoglyceride to form triglyceride and adds cholesterol and put together into protein coat called chylomicron
- And via exocytosis chylomicron goes out of cell and into the lymph system which allows you to bypass the liver
- Lymph goes into venous system and then through heart and then arterial system and gets distributed to tissues
- Distribute fat as chylomicron to diff tissues
- In adipose or skeletal muscle tissues – they have enzymes in their capillaries called lipoprotein lipase which act on chylomicron and begin to extract the fat out of the chylomicron and can be incorporated into the tissue
- Fat you eat in a meal is distributed this way; don’t overburden the liver w/fat; fat is distributed to tissues where we can use it in muscle or store it in fat
