Gi Flashcards
(180 cards)
1
Q
The stomach is mainly for?
A
Storage
2
Q
What is the composition/texture of food before it gets to the stomach
A
food mixed with gastric fluids,move with slow and strong contractions and becomes chyme b4 the stomach
3
Q
Small intenstine is made up of the sections namely
A
Duodernum
jejunum and illeum
4
Q
What are the characteritics of the parts of the small intestine and ehat functions do they engage in?
A
duodernum….short….secretions process chyme in the small intestine
jujenum(8ft)…most adsorption..more than half adsorption of chyme done.
ileum..adsorption of chyme continues(10ft)
5
Q
What tract leads into the colon
A
illiocecal sphincter
6
Q
What are the characteristic part of the colon and what arthe functions
A
Colon…ascending,transverse/descending colon and sphincters
For storage,slow movement of chyme and to reclaim salt and h2o….making faeces harder in the descending colon so it can be excreted…slow movement here
7
Q
Gi Tract composde of smooth muscles except
A
The GI tract is composed of smooth muscle(ANS), except in mouth, upper espohagus and external anal sphincter..voluntary muscles present here..skeletal muscles.….
8
Q
What contributes to increase surface area in the Gi
A
Villus lining/micro villi also on each cell… increases surface area up to 300times.
9
Q
Whats the function of brushborder enzymes
A
helps to digests nutrients and help with absorption
10
Q
The Gi tract has
A
Enterocyte…epithelial cells that are in the luminal side of the small intestine.
Highly vascularized and highly metabolic so it needs a lot of energy/increase in blood flow also in Gi tract to process things
Lymphatics running through it….collect fluid
Longitudinal(outside) and circular(inside) muscles to squeezing chyme…move and mix..
Myenteric plexies (nerve nets)—-muscle movement..}Both of these make up the enteric nervous system…with the one below.
Submucosal plexus(nerve nets)…secretions} Get signals from receptors and get stimulated by having the chyme present. Making the gi tract function as an independent system,.
11
Q
If the Enteric nerves stops working what happens
A
If the Enteric nerves stop working…or there is an area that does not have the nerves in it..everything stops ..illeus occur
12
Q
Replacement of cells happen every couple of days in the Gi system,what cell facilitate this?
A
Stem/Progenitor.
13
Q
What produces mucus in the Gi tract
A
Goblet cells
14
Q
What is the Firstpass effect
A
The splanchnic circulation encases the intestines; blood flows from the intestines through the portal vein to the liver. This is the first pass effect
Processed by liver before it gets put out into the systemic circulation.
Happens to all the nutrients except lipids.lipids go into systemic circ first then the liver
The lipids take a long time to preocess.
15
Q
Functions of the Gi tract
A
Digestion– Enzymes and HCl
Endocrine– LOTS of hormones which act on GI tract and other tissues
Elimination– rids body of undigested waste
Protection– HCl….rents food into small pieces..increases surface area for specific enzymes to work on and get to the nutrients and digest it, IgAs, opsonins, and other immune cells
Motility– propels and mixes chyme down
Absorption– of almost everything you eat,needs that absorption to be facilitated
Secretion– buffers mucus, hormones, enzymes
Storage– stomach and colon
Hormones are secreted into the blood ,all other things go into the lumen
16
Q
How much fluid does the Gi tract absorb in a day.
A
You may only ingest 2 liters of fluid a day, but the GI tract SECRETES
7-8 LITERS. This means it has to absorb 9-10 LITERS of fluid each day!
17
Q
What are the usefulness of the secretions in the Gi Tract
A
The secretions help lubricate, digest (HCl, enzymes), and buffer (HCO3 buffers the acid) the chyme.
18
Q
Are Borborygmi sounds normal?
A
The movement of fluids and gases in and out of the intestines can be heard sometimes. As these fluids are being absorbed.These sounds are called borborygmi. These are normal
19
Q
Most absorbtion is done where in the Gi?
A
Small intestine
20
Q
Stomach is very acidic ,buffering needs to happen the chyme gets into the small intestine. which makes chyme in small intestine acidic or basic?
A
Basic after buffering.
21
Q
Regulation of the Gi tract happen through the plexes,namely?
A
Systemmyenteric plexus (muscle/movement) submucosal plexus (secretions)
22
Q
whats the function of the Lumenal chemo-, mechano- and osmoreceptors
A
(act on the enteric NS)….where chyme is at…does not do anything anywhere else that has no chyme
23
Q
whats the composition of the PNS
A
(mainly vagal to transverse colon, then pelvic nerves to anus)
24
Q
Whats the composition of the SNS
A
(post-ganglionic adrenergic fibers from celiac, superior and inferior mesenteric and hypogastric plexes)
25
Whats the GI composition of the the CNS
anticipatory response…smelling something delicious ..preparing the stomach for a possibility to eat…salivation starts
26
Function of hormones
.released into circulation causing motility
27
THE Gi is sympathetic slow and parasympathetic pro t/f
T
28
What time frame does the MMC begin after eating?
3-4hrs after meal.
29
What location would the Chyme be in for MMC to happen?
Jejunum
30
whats the essence of the MMC
Housekeeping movement– sweeps undigested material and bacteria into colon
31
What region is the MMC active in
Midstomach down to the terminal illeum
32
NAme and explain the phases of the MMC
Has 4 phases, with the
main propulsive movements occurring during phase III (phases I, II and IV have minor, disregulated contractions): an entire cycle lasts 75-120 min.
Phase III contractions only last about 10 min each cycle, but the series of contractions sweep material lower in the tract.
Phase III is stimulated by the hormone Motilin, secreted into blood from the M cells of the small intestine.
stimulate contractions from mid-stomach down the tract..getting any bacteria or crap materials into the colon..keeps cycling until eating again
33
In MMC what phase does the main propulsive movement happen
Phase 3
34
IN MMC what phase does is Motlin secereted and sweeps materials into the lower GI tract
Phase 3
Definitely happens overnight.keeps cycling until eat and Motlin shuts off.
Important for General health of GI tract to keep it clean and prevent from making new cells all the time
35
Explain Primary peristalsis
when a bolus of food comes down the trachea and some secretions move it down…via the Parasympathetic response through vagus nerve…controlled by the swallowing center in the medulla.
primay is more through the swallowing center and parasympathetic vagal response.
36
Explain secondary Peristalsis
Eating something dry and generating pressure will stimulate stretch,mechano receptors via enteric nerves…info sent to the plexes…secretion of mucus and contractions to move that bolus…secondary is more local through the ENS/Ans,
37
whats Achalasia
Achalasia is loosing the enteric nerves in the lower part of the esophagus
Food builds up in esophagus,may dialate and get wider,this is a smooth muscle disorder
38
Explain how Gastric Accomodation relates to fullness,vagal nerve and relaxation of the Gi
Gastric accommodation is called receptive relaxation
Stomach fills to a liter of food b4 u start feeling full
The volume of food increases and pressure increases.
Accommodation is Vagally mediated.stomach needs to relax to accommodate food.
39
What is the Principle of Bariatric Surgery
The principle of bariatric surgery is to reduce the ability of the stomach to accommodate food. Reducing the amount coming in, also by vagal mediation.
40
What does the process of gastric emptying depend on?
Dependent on what the constituent of meal includes.
If its easily digestible food. Emptying time will be rapid.
If acidity is increased, it will stay in the stomach longer.
It will take longer to empty…A high-fat meal will take the longest to empty the stomach. Oleate meal takes the longest to empty.
41
What is the Resting membrane potential for the Gi tract called
Slow wave or Basic electrical Rythm
42
Whats the Electrical threshold for contraction in The Gi tract
-40mv
43
What substances or factors can cause depolarization in the Gi tract
stretch, ACh/parasymp, gastrin, serotonin,subst. P (tachykinin,)
44
What substance or stimuli can cause relaxation/Hyper-polarization in the Gi tract
NE, sympathetics, VIP, NO
45
Waves causes contraction true or false?
False
46
What causes contraction
Depolarization above -40mv ..generates spike potentials that forms on the peak of the slow waves
47
Explain the process of depolarization in the stomach
Chyme coming down. has a Need for movement…
slow waves are ..depolarized ..you have potential happening on each peak if there is chyme there ..3 slow waves per min in the stomach…every 20secs there is contraction. and relaxation…
48
Explain the process of Depolarization in the Small intestine
In the small intestine it May be 10 contractions per min.
.when u wanna move something slow wave can be fast
Slow wave depolarized above -40mv to cause spike potential which stimulates ca and that forms ca-calmodulin complex ..which gives crossbridge formation
More depolarization,More spike,the more spike,the stronger the depolarization…
49
The vagus is always gonna be controlling any parasympathetic events in the Gi tract.
FYI
50
Explain the process of Peristalsis in the small intestine
Interneuron in the back/tachykinin neuron…depolarize slow-wave and cause contraction and will go ahead of the bolus and relax the muscle in peristalsis,
this may be under the vagal control …small intestine
51
Explain the process of Segmentation in the Small intestine
Locally mediated…ENS plays a big role…there will be paring of Contracting /mixing and movement…peristalsis can happen adjacent to segmentation.
52
Explain the process of bile contraction, when and what hormones is released?
Gall bladder contracts as soon as chyme gets into the duodenum
The contraction of the gall bladder releases bile into the duodenum, which facilitates lipid absorption.
Vagal stimulation relaxes the sphincter of Oddi (into the duodenum), and later in digestion (during the intestinal phase) the hormone CCK (in addition to vagal stimulation) will stimulate gallbladder contraction.
53
What is segmental propulsion
The taneia coli contract to make sacs in the colon (haustrae). This is
54
What is the purpose of segmental propulsion
It is SLOW, and designed for storage and dehydration of chyme to feces.The reclamation of sodium and water ,.
55
How is Haustrae formed during segmental propulsion
formed by contraction of the taneia coli.
56
What is the process of peristaltic movement and how often do they occur.
3-4 times a day the Haustra relaxes and peristaltic movement occurs which allows the chyme to move forward down and through the descending colon,collecting in the rectum. In the rectum it causes rectal stretch which is a defecation reflex or or rectosphincteric reflex).
causes urge to defecate and relaxation of the internal anal sphincter
. Anytime feces goes back into the rectum the urge to defecate comes and external anal sphincter is tightened and internal relaxed
57
What stimulates peristaltic movement
These are peristaltic contractions that are stimulated by GI hormones and the vagus nerve, in response to chyme in the upper GI tract
58
What is Gastrocolic Reflex
When u eat the vagus is stimulated right away,gastrin is in circulation which stimulates ,motility…
hormonal and neural effects are only active when u feed…so we can get rid of waste.
And need to get rid of food after eating is called gastrocolic reflex.Faeces in the descending colon will stimulate the defecation reflex
Food in stomach stimulate colinic mass movement
59
Why does mass movements happen 3-4x/day
.Reason this happen 3-4 times a day is it conincides with feeding
60
What secretion do we have in the mouth
Saliva,Lingual lipase,salivary alpha-amylase,
| R-proteins =Transcobalamin-1(TC-1
61
Secretion in the Stomach
Hcl,intrinsic factor,pepsinogen,gastric lipase,mucus,gastrin,somatostatin,histamine
62
Secretions in the liver and gall bladder
Bile and buffers(Electrolytes)
63
Scecretion in the Pancrease
```
Exocrine glands:Buffers and enzymes(trypsin,chymotrypsin,procaboxypeptidase,lipase,colipase,proelastase and alphaamylase.
monitor peptide(trypsin inhibitor,stimulates cck)
```
Endocrine:Insulin,glucagon,Somatostatin
64
Secretions in the small intestine
Buffers(Mucus and elctrolytes)
| enterokinase,brushb border dissacharides,brush border peptidases,secretin,gastrin,cck,vip,gip,motlin,5HT,Somatostatin
65
WHats the direction of food fluid and elctrolytes between the gi trACT AND the Ecf
Gi tract takes fluid and electrolytes out of the Ecf and processed back into the ECf
66
Memorise slide 3
Now in lecture 3 Gi
67
How does gut peptide Regulate Hunger and Satiety
Hunger
In the fasting state, ghrelin is secreted into blood from oxnytic cells in the stomach.passes the BBB and into the arcuate nucleus of the hypothalamus ghrelin stimulates NPY, an orexigenic peptide (stimuates hunger).
Satiety
When you eat,Chyme goes into the DUO----goes to the JJ...
several peptides, including
peptide YY and GLP-1 (glucagon-like peptide) are secreted into the circulation---they suppress hypothalamic NPY, decreasing appetite
will also work faster for things that are carb based and not fat based
Leptin is produced in adipose (and other) tissues and is considered the counterpart of ghrelin– when you eat, glucose and insulin increase circulating leptin which decreases appetite by suppressing NPY in the arcuate nucleus. ]…longer process
68
What is found in the Saliva and what are its functions
Salivary alpha-amylase..starch digestion starts in the mouth(starch is glucose molecule with alpha linkages)
Lingual lipase,(lipid digestion)made in the tongue
Transcobalumin1(TCI) protein---vit b12 binding…protect B12 from proteases/pepsins in the system.
Mucus…lubricates food as it goes down into the stomach…
Saliva is dependent on the PSN..
Pro secretion pro motility
69
Explain saliva secretions as related to blood flow, electrolytes and etc.
Parotid/submandibular/sublingual produces saliva..
Saliva secretions depend on blood flow.
All glands depend on blood flow.
Pns are activated in feeding…blood flow increased……secretions into acina cells..
salivary glands are exocrine glands…
Exocrine are ductal glands..contain electrolytes and enzyme amylase that will start starch digestion, come through duct and b secreted as saliva.
Any ductal secretions has electrolytes coming back and forth
70
Whats difference btw Exocrine and Endocrine glands
Endocrine…make hormones and secrete into blood
| Exocrine make other secretions and secrete into duct
71
What's the component of Ductal secretions and how does this component relate to saliva flow and blood flow
Electrolytes
Some reabsorbed and some are not.
There is a modification of concentration.
There is a modification of secretions as it gets into duct.
sLow flow rate…electrolytes reabsorb…concentrations of electrolytes are lower because of the readsorption
Fast flow, less reabsorption (less time for absorption)Higher concentration of electrolytes
Higher potassium in saliva than blood.
Saliva is always hypotonic to plasma
Potassium is higher in saliva than plasma cos
72
do vomiting and potassium content in the saliva relate to becoming hypokalemic?explain
Yes
Vomiting will loose a lot of potassium since it has a large amount of potassium in the saliva.. and hence contribute to Hypokalemia.
73
What Controls the salivary flow between SNS and PNS, explain how? and what nerves does it work through
PNS
Saliva is dependent on parasympathetic…PNS is pro-secretion,pro-motility…
Facial(Submax and sublingual gland) and glossopharyngeal(Parotid) controls salivation….
74
What are the things that increase saliva flow in the mouth
Parasympathetic, Ach
CNS (cephalic phase)(anticipatory nerve of feeding)Sensory component…
Nausea
Esophageal distension..something stuck in ur esophagus…sends more salivation to lubricate
Chewy, flavorful foods
Dry, acidic, alkaline foods
Meats, sweets, bitter foods
75
What are the things that decrease saliva flow in the mouth
Sympathetic, NE
Hormones (ADH, Aldosterone)
Sleep
Dehydration
Drugs…chemo, barbs
Aging..pns weaken, blood flow to the gland decreases cant make a lot of salivae.
76
What does saliva do
Taste
Coagulation factors
Antimicrobial action
Protection
Digestion(Amylase and Lipase)
Lubrication..mucus to get bolus down in the stomach
Oral hygiene....low saliva in the mouth will cause cavities
77
What does the Hormone Gastrin do in the Gastric mucosa
Release from the G cells from the Antrum of the stomach and also from the duodenum.
a major function of Gastrin is to stimulate H+ secretions from the parietal cells
78
Explain the process of Gastric secretions and hormones secreted and were secreted and functions and what stimulates them to be secreted.
Having food in the stomach. Stimulates vagal action…
will secrete---Hcl( from parietal cells which is stim by Gastrin)…this will cut down the food and increase surface area)
Food Goes into the--Duo-(Intrinsic factors secreted to act as the second line of defense for vit B12
…will protect b12 from being digested…
TC1 Protects b12 in the stomach ---
P(Pepsinogen…start protein digestion, manufactured in the chief cells----They are all secreted into the lumen of the stomach…)
GL(Gastric lipase)..lipid digestion and also from chief cells)
O(other….histamine…H1 receptors..increase HCl acid,
somatostatin… modulates and decrease…hcl,
M(Mucus)…stick to the cells and trap bicarb, also lubricate.
When chyme gets into the Antrum--Gastrin is secreted into the blood which is stim by the vagus nerve and then when chyme is there, the stretch will increase response for more gastrin secretions.,
the rest goes into the lumen,,, then act on the food that comes in making it chyme.
79
What causes the Pepsinogen to activate.
Acid activates the pepsinogen to the protease.
| as soon as the acids get the PH down low the pepsinogens work
80
What happens to Tuberlae vesicles on the chromaffin cells before and after stimulation and what stimulates it.
Tuberlae vesicles invert when there is no stimulation for digestion/no active secretions
As soon as stimulated there is a physical change and the come out to increase surface area and have a lot of acid to be secreted per proton pumps come out on the membrane
81
On the Chromaffin cells,what are the 3 things or process that control secretions and release of histamine at the level of the parietal cells
Histamine(Local)..stimulates the cyclic amp pathway..proton pump is the rate limiting step …which creates the acid….hydrogen coming in.
Stimulation causes insertion of protein pump into vesicular membrane
Neural pathway}Vagal(PNS) stimulation,this will cause ach to act directly on a muscarinic receptor on the parietal cell or
indirectly by stimulating the ECL to stimulate histamine.
Gastrin input through the blood. Directly on parietal cell or indirectly through the Ecl to create histamine
82
What is the rate-limiting step in the stimulation of acid creation
The rate of creation of the proton pumps
83
Explain Parietal Cell HCL production
Co2 metabolism produces….hydrogen and h2co3.
Atp and primary pump used to get hydrogen out of the cell. Since its more h2 outside it needs atp to pump the H2 out via primary active transport and also
Exchange the potassium and bring the potassium in the cell also…this increases the conc of potassium higher in the cell….this will allow potassium leak against its conc gradient into the lumen.
Chloride comes out of the cell to balance the positive state outside…any chloride comes out is replaced by taking the bicarb…secretion of h(going out of the cell into the lumen) causes a reabsorption bicarb…..which then goes into the blood. Causing an alkaline…and hcl will make hcl acid.
84
Explain the process of Ulcer formation by H pylori
H pylori Main cause of ulcer….makes urease combines with c02 that produces NH3..toxic to cells …neutralizes the acids but all inflame the tissue by gastric proteases and effector molecules. Disrupting the mucus layer and bicarb layer. Causing mucosal death by cytotoxins and ammonia.
85
Explain the process of ulcer formation with NSAIDs
NSAIDs are prostaglandin inhibitors. (Prostaglandin inhibits histamine production and increases mucus production) which Lessens the protective effects on the stomach, allowing the acids to have more of an effect on the stomach.
86
The 3 systems that stimulate HCL production are?
Parasympathetic, ACh
Gastrin
Histamine
These 3 directly stimulate the parietal cell to produce histamine
87
Things that inhibit ACid secretion
Secretin: Duodenal hormones. Will decrease gastrin secretions not stop it at the G cells
Somatostatin…acts locally
Peptide YY…in the JJN..it will come out and decrease the system from performing actions up top..this will modulate things per acid up top.
Prostaglandins…local and act on the parietal cell to inhibit histamine production
88
What is the mechanism of action of the mucus layer in protecting against acids
Mucus layer traps bicarbonate…which will neutralize acids that come inside. Goes into water and c02 and also c02 metabolism happens to produce more bicarb.
Cells get replaced every 6days by new cells
89
Explain Neural control of Acid secretion
Smelling something stimulates the cephalic phase.
PNS excite pepsin and acid production
The vagus stimulates the parietal cells.
Neural control is upper gi.
Gastric phase kicks in....as follows
i)Local nervous secretory reflexes...Nerve plexuses kick in
ii)Vagal reflexes
iii)Gastrin Simulation...Gastrin
As soon as the chyme moves out of the location and goes into the Duodenum…the hormones secreted at those locations are turned off.
Goes into the Nervous mech and Hormonal Mechanism
90
Name the cells and process found in the small intestine mucosa
Small intestine…..DD---JJ---ILL
Brush border villus cells and crypts of liberkoon…
Absorption goes on int Brush border hydrolases side.
Brush border enzymes do the final digestion of carbs and protein…and u wont be able to absorb these things if u dont have them.
Crypts of lierberkuhn lots of secretion….CFTR is a cl channel and it secretes chloride into the lumen…sodium and water comes in …and buffering happens.. This helps alkalinize the chyme. Per buffering
This channel also presents in the lungs and pancreas of those who have cystic fibrosis. It does not work. In that situation
If no brush border,u won't get final digestion and no absorption of proteins and carbs will occur.
91
Process of chyme movement into small intestine and hormones secreted.
Into the small intestine….duodenal hormone release
Gastrin(released in response to stretch)……….into blood
Inc hcl at the parietal cell.Inc motility in the lower GI
Secretin…..secreted into blood response to low ph…responds to acid
chyme coming out..goes to inc pancreatic and intestinal buffers(7.4 -8)
Cholecystokinin(CCK)..increase pancreatic enzymes…needed to digest carbs lipid and proteins that are coming form the chyme.
The digestion in the upper gi tract..handles about 25% needed for digestion in the small enzymes.
Panc enzymes does the 75%...CCK also does Gallbladder contractions,bile production in the liver also increased by this
Glucose-insulinotropic peptide(GIP)…Inc insulin at the pancreas…..goes out to the blood early on..to be ready for glucose to start coming into the blood. When gluc in,will stimulate more insulin.
When the last of the track leaves the Duodenum everything gets shut off
92
What do the CCK and Secretin secrete in the pancreatic cells
Acini cells secrete into the duct..acini sac is where we make the secretions that go into the duct.
We make enzymes and buffer….secretin will stimulate the buffers/electrolytes…
Cck stims the acinar enzymes/cells….
The presence of CCK and secretin synergizes and potentiates the effects of each other
93
Per pancreatic enzymes, what are the proteases secreted as? and why?
Proteases secreted as zymogens
Proteases are Zymogens..it cannot be active or it would chew up the cell….once in the lumen….the zymogen will be activated to Trypsinogen
94
per pancreatic enzymes what is Tyrpsinogen activated to and by what?
trypsinogen-- activated to trypsin in the duodenum by (EK)
95
The following are activated by Trypsin
chymotrypsinogen--
pro-carboxypeptidase--
pre-co-lipase
96
What activates pancreatic lipase and what is the function of pancreatic lipase
Pancreatic Amylase-- starch digestion in the duodenum…..activated by chloride
97
All the pancreatic enzymes are in the lumen true or false
True
98
If trypsinogen autoactivates , what would be the outcome of this and what should be done
Trypsinogen can autoactivate to trypsin…..we don’t want that to happen…if it happens this creates pancreatitis..
Hence we need trypsin inhibitor(monitored peptide…trypsin activated…) in the pancreas.
99
What does pancreatic lipase need to hydrolyze lipids
Pancreatic Lipase (needs pre-co-lipase)-- hydrolyzes lipids
100
What happens at the end of a meal with secretions per pancreatic and thos lower in the tract
When the chyme is lower in the tract, pancreatic secretions cease. This occurs from the reduction in vagal stimulation (no food/chyme in the upper GI tract), as well as from multiple secretagogues, including SS, glucagon, pancreatic polypeptide, and peptide YY, which decrease pancreatic exocrine secretions.
The system shuts down after chyme moving down except the local area of the chyme.
101
Secretion of Hydrogen and bicarb into the Lumen in the illeum helps with what process
Illeum and JJ does the Nacl reabsorption
Luminal side…sodium ..hydrogen antiport(secondary transport)
Lumen…h and h2c03..helps reclaim sodium, chloride and water back into the Ecf
102
Secretion of Hco3 and K into the lumen in the colon helps with what
Storage,slow movement/Reclamation of salt and water out of the chyme and back into the ECF
Water,bicarb and potassium is the only thing left at the colon
Which is in the feces
103
Where is bile formed?
Hepatocyte cells of the liver
104
How does choloesterol get synthesised
Via HMg Coa Reductase
105
what are the 3 sources of obtaining cholesterol
Dietary
| Hmg coa Reductase
106
How does statin drugs work
they block the Hmg coa reductase thus lowering the plasma cholesterol level
107
bile is hydrophobic t/f
t, with a cholesterol backbone
108
Bile becomes amphipatic inside hepatocytes this means?
soluble in lipids and water
109
secondary bile is much more lipophillic..true or false
T
110
Where do the buffers come out from in the GI tract
Intestinal Buffers comes out of the cribs of libercoon in the small intestine and the pancrease to prevent the hcl acid high chyme from having a negative effect on the small
111
Bile salt acts like detergent and emulsifies T/F
T.
| Does not digets anything separates the lipid from each other
112
What is added to Bile salt to get Micelle salt
pancreatic lipase and prolipase
113
How do we get the Bile structure
Pancreatic lipase and prolipase added to get a micelle salt.
Most lipids come out later in the meal.
PL cant access the Lipids without the Prolipase…
Trypsin activates precolipase to prolipase(JJ on down in the lumen…this is where this all happens)
Trypsinogen is broken down to trypsin in the lumen by brush border enzymes..
Lipase can the get in and hydrolise the rest of the lipids
Bile surrounds the digested lipid.
114
What happens with illeal resection
Recycling of bile will be jeopardised
115
Why do we perform cholycystectomy
Cholecystectomy is performed in response to acute or chronic cholecystitis (inflammation of the gallbladder, with or without stones).
116
What is postcholycystectomy syndrome
postcholecystectomy syndrome, experiencing chronic GI distress and pain in the upper right abdomen.*
117
Whats the action of Cholestyramine for diarhea after cholycystectomy
Up to 20% of patients can develop diarrhea (taking years to resolve). Why? Can be treated with cholestyramine..binds to bile makes it less osmotically active
Cholestyramine sequesters and binds the bile in an insoluble complex that reduces the osmotic effects.
118
AFter cholycystectomy why do patients develop diarhea
Cholecystectomy…..Bile is osmotic ..so more bulk and more water ,more osmotic pull….diarrhea…more bile ..more diarrhea
Recycling goes down..not as effective.
119
What will be the effcets of Cholycystectomy on bile production
Liver will just keep producing bile during digestion…overall it will produce more than normal because there is no storage.
120
Effects of cholycystectomy
When the Sphincter of Oddi closes (when chyme is out of the duodenum) the recycled bile stays in the bile ducts.
Patients can have diarrhea, but usually not much of a problem
121
What happens if the ileum is removed?
Lose the bile transporters in the terminal ileum, so there is little to no recycling.
Bile secreted by the gallbladder and liver will be excreted in feces.
When the Sphincter of Oddi closes, the bile in the ducts is “vacuumed” into the gallbladder and stored. Overall the liver has to produce much more bile, since there is no recycling.
Although the increased sodium and water entering the colon will increase sodium (and water) reabsorption, overall, the increase in bile and motility will cause diarrhea,lots of discomfort…with fats….eat Low fat diet
Taking out ileum gets rid of the recycling.
Liver keeps making bile ..up produces bile if it does not see much recycling.
122
Bilirubin metabolism and excretion
Bilirubin that is secreted with bile is conjugated
w/glucuronic acid
Colonic bacteria remove the acid moiety and bilirubin is coverted to urobilinogen.
About 10-20% of the urobilinogen is recycled into portal blood (from the colon) and then systemic circulation, where it is filtered, converted to urobilin (yellow color) and excreted in urine.
123
Billi metabolism 2
Bili is biproduct of rbc metabolism…we need to get rid of it….to keep bili low..
Bili—liver conjugation…secreted with bile into small int…colonic bacteria converts to urobilinogen. Some recycles to portal blood to liver,
some gets in blood, some back into SI..majority stay in the colon as steccobilin(Brown) excrete in faeces.(70-90).Bili is Yellow(eye color)……
Color of faces depens on how much bile u have…
Both bili in blood and urobilinogen goes through the kidney…
UV light …helps break this down…ones in kidney equal urobilinogen and is excreted(10-20)
The unabsorbed bilirubin is oxidized by bacteria to stercobilin (gives feces brown color) in colon.
So “bilirubin” excretion occurs mainly in feces (as stercobilin).
124
What are the liver functions
Regulation of Protein, carbohydrate, and lipid metabolism
Regulation of cholesterol production and excretion
Beta-Oxidation of fatty acids…Energy producer,storage
Bile acid production
Degradation of hormones
Detoxification and excretion of drugs and toxins
Vitamin storage
125
Normal liver has high or low capillary venous pressures?
Low capillary pressures
126
What contributes blood to the hepatic parenchymal cells and in what volume
1L/min from portal system…(blood from intestine
Hepatic artery serves the parenchymal cells…450ml/min
About total of 1.5L /min
About 30% C.O
127
What enables hepatic veins to get blood out into the venae cava easily
Hepatic vein gets blood out into the vena cavae(low bp blood)…this enables blood to leave easily…free in ---free out..
128
Name the 3 causes of portal hypertension
pre-hepatic (portal V. thrombosis, cong. atresia)something within the portal system..no bile gets thru..extra pressure,
intrahepatic (cirrhosis, fibrosis, Wilson’s d)anything that destroys the blood flow in the liver or
post-hepatic (any obstruction between liver and right heart, eg hepatic v. thrombosis, CHF, pericarditis).
129
Whats the function of the Lymph
Lymph removes fluid and proteins from the Space of Disse, and drains the fluid into the venous blood.
130
Hepatocytes are single or double cells
Single cells
131
Does every hepatocyte have acces to blood?
Yes
132
Function of Kuffper cells
Kupffer cell…waste removal..degrade anything that is waste.
133
What is the function of the space of Disse
Space of Disse…as lymph is made (by hepatocytes)…that can't get into capillary and goes into the lymphatic through the space of disse..(big stuff goes here) other nutrients into blood
134
Where does lymph production end up at
Hepatocytes..lymph…space of disse..lymphatic……
| .or it goes to blood
135
How Does ascites form
Increased hepatic vein pressure (eg, from increased right vena cava pressure) or increased portal v. pressure (eg, portal v. thrombosis)------>
```
Pooling of blood in liver capillaries
------>
Increased HPc
------>
Increased transudation of fluid from plasma and space of Disse into the peritoneal cavity of the abdomen forming ascites (contains both fluid and proteins)
```
136
What is Hepatomegaly and its characteristics
Is an increase in liver size usually due to fluid retention (can also enlarge from excess fat)
The liver usually contains ~400 ml of blood, this can increase to ~1 liter in pathologic conditions
Inc pressure can double size of liver volume…..this removes blood from the CO and cardiovascular system or plasma, 2/2 to the loss of it to the liver.
Enlarged liver happens with liver problems
137
What is Jaundice and what are the types
Jaundice (seen as yellowing of skin, nail beds, whites of eyes, etc) is caused by increased bilirubin in the blood
Obstuctive
Hepatic
Hemolytic
Neonatal
138
Explain Obstructive Jaundice
Obstructive jaundice results from obstruction of the bile ducts (cirrhosis, gallstones, biliary atresia, cancer,liver scarring). In each case, the bilirubin that is usually incorporated into bile enters the blood, instead. Liver problem,cant secrete bile
139
Explain Hepatic Jaundice
Hepatic jaundice can result from acute or chronic hepatitis, drug hepatotoxicity and cirrhosis. This reduces the ability of the cells to metabolize bilirubin.
140
What is hemolytic Jaundice
Hemolytic jaundice results from anything that increases hemolysis of RBCs (eg, malaria, sickle cell anemia, genetic disease (spherocytosis)), and increases bilirubin production faster than bile can excrete it.
141
What is neonatal Jaundice
Neonatal jaundice usually is not pathologic, but results from metabolic changes, as the liver and GI tract start to function appropriately after birth. Congenital pathologic conditions such as G6PD deficiency and spherocytosis(Pathologic) can also cause neonatal jaundice. Uv light…breaks this down for kidney to excrete unchanged
142
FYI
Hepatic jaundice is from inflammation..
Hemolytic jaundice…has nothing to do with the liver.
143
Explain Glycogen Storage
Excess blood glucose is converted to glycogen by glucokinase. Epinephrine and glucagon can stimulate phosphorylase, releasing molecules of glucose into the blood when needed.when sleep blood glucose remains steady from glycogen stores
144
Explain Gluconeogenesis
Amino acids and glycerol (from TGs) are converted to glucose by GNG
After all glycogen has been used Gluconeogenesis starts
145
what is GLUT2
The liver has GLUT2 family transporters which are insulin-independent, and allow for high capacity transport. These transporters are also found in brain, pancreas, kidneys and basolateral side of enterocytes.)
146
Name the processes of Liver carbohydrate metabolism
Conversion of monosaccharides to glucoseATP allows galactose and fructose to enter the glycolytic pathway and be stored as glycogen, or undergo glycolysis.little galactose and fructose in the blood
Formation of chemical compoundsThese include pyruvic acid, lactic acid, succinic acid, and acetyl CoA, which can be used in other metabolic pathways.
147
through the pfrocess of Liver Lipid Metabolism explain how High rate of -oxidation of fatty acids
occurs
TGs are hydrolyzed to fatty acids and glycerol mitochondria -oxidation to acetyl CoA citric acid cycle.
148
process of Liver lipid metabolism forming most Lipoproteins
VLDL: high TGs, some chol & PLs--take TGs to adipose tissue.
LDL: high chol & PLs, little TGs (these are bad guys) arterosclerotic plaque
HDL: 50% protein, less chol & PLs(bring fat back from adipose tissue and back to the liver for processing
149
How does liver Metabolism Synthesize of lots of cholesterol and PLs
Acetyl CoA molecules combine to form a sterol nucleus side chains added cholesterol. The HMG-CoA reductase is the enzyme that catalyzes the reaction, and is the target of statin drugs.
150
How doesLiver Metabolism Converts Unused Carbs to TG
Glucose glycolysis acetyl CoA TG polymers made using malonyl CoA and NADPH packed into VLDL adipose tissue.
151
Liver metabolism
| Urea and plasma protein Production
Deamination of amino acids makes nh3Aminotransferases remove the amino group to an acceptor substance. It can be transferred again, or released as ammonia (NH3). The excess NH3 can be removed by…
Production of ureaNH3 combines with CO2 to form urea. This is a critical process to get rid of the toxic NH3.
Rid of urea by urinating it out in the kidney, made in the liver.
152
Liver Protein metabolism
| synthesis of plasma protein
90% of plasma proteins (i.e., albumin,globulins(Iga), fibrinogen) are made by the liver.binds to electrolytes and protect substances,all plasma proteins, May have edema if albumin low per liver failure.
153
Interconversion of amino acids
Transamination can convert certain amino acids to others that may be needed.
154
Liver Metabolism:
| other functions
Vitamin storage (B12, A, D)
Formation of blood coagulation products
Iron storage…in case more RBC needed
Drug, hormone, waste removal
155
Symptoms of liver failure
```
Ascites
Jaundice
Portal hypertension
Bleeding/bruising
Confusion/cognition problems (encephalopathy
Weakness
Nausea
Cholestasis (reduced/blocked bile flow)
Acidosis
```
156
Whats the final digestion for fats and protein
Brushborder enzymes
| EK..BBE also
157
What happens to the enzymes on the sloughed off cells of the Krpt of Luberkhun
Enzymes will reclaim the sloughed off cells and reabsorbed early in the process.
158
What are the components and activities of brushborder enzymes
1. final digestion for carbs and proteins
| 2. has Enterokinase that cleaves trypsinogen to trypsin
159
What are the components of krypts of leberkhun..
has secretions in the luminal membrane(cl,na and water are here.
Buffers
160
What is the process of carbohydrate digestion and what molecules do we need to get them to in order to transport them
Carbs digestion begins in the mouth
Starches and Disacharides….sucrose(Galactose and fructose) and lactose(GLC and gal)
Mouth…salivary alpha amylase…break alpha linkages in glucose.. To maltose and isomaltose…no stomach carbs digestion….small intestine carb digestion with pancreatic alpha amylase.
Brush border enzymes(brush border sacridases…….
In the SI…we have maltose and isomaltose…and lot of starch in the duo….also have sucrose and 2 disachrides and Lactose…now the Brushborder enzyme can start in the DUO and JJ….key to digest starch here will be chyme presence in the track will stim duodernal homornes and cck will stim pancreatic enzymes(proteases amylase lipase colipase) and secretin will stim buffers from the pancrease…..
Panc amylase digest startches to more maltose and isomaltose….as the chyme going down the DUO to the JJ.
Maltose will be digested by Maltase(BB Enzyme) and make a lot of glucose
The isomaltose will be digested by isomaltase and more glucose.
Discharides..lactose will be digested by lactase into 1gluc/1galactose
Sucrose will be digested by sucrase and make 1mol glucose and 1mol of fructose.
We have monosaccharides that are made at this point we can get them into the cell
161
What form do we need to get carbs to inorder to transport them...
Glucose
| Fructose and Galactose
162
How does the transport(ABsorption) of glucaose,fructosand galactose(monosaccharides) happen
Fructose will use insulin independent Glut 5 carrier(facilitated transport)
Glucose and Galactose(galactose shares the ride with glucose)…will use 2ndary active transport with sodium via the gradient through the sodium(Sglut-1) potassium Atpase….pump will pump sodium out.
You will absorb all glucose and this will be facilitated transport…cl/h20/bicarb..
all come into to cell via na glucose transporter…..
Once in the cell we get out with facilitated transport site..
Diffuse through the interstitium go through the capillaries' and then through to the liver for metabolism
163
Explain how olestra and sucralase affect absorption and form diarhea
Olestra is a sucrose polyester that is not digested or absorbed, and is used as a fat substitute (especially for fried foods).
It has no caloric content because it remains in the GI tract and is excreted… however, the carbohydrate part (sucrose) is great food for colonic bacteria… this produces gases, increased motility and reduced absorption, resulting in cramps, flatulence, and diarrhea.
Sucralose is a chlorinated sugar compound (chlorocarbon) that (for the most part) is not digested or absorbed.
Can have same type of problems as olestra (bloating, gas, diarrhea), because of the presence of sugar moiety.
We also have carb called Cellulose that is bound by beta linkages(cows ..ruminant and horses have the cellulase and also the enzymes that disgest it…
Olestra has osmotic effect because of undigested carbs…undigested carbs is food for bacteria and also since is not digestible it an becomes osmotic agent thereby causing a lot of diarrhea.
164
Explain the process of protein digestion
Begins in the stomach with pepsinogen from chief cells …cleaved to pepsin via acid secretions…..
If acids is suppressed,you can digested the protein well..
Pepsinogen---pancreatic proteases----Brushborder proteases(peptidases).
In the duo…undigested proteins…about 75% and some Oligopeptides(25%)…
Pancreatic Proteases comes in also(trypsinogen,chymotrypsinogen and pro-elastase,precolipase)these are zymogens.
Brushborder enzymes (EK) will cleave trypsinogen and into trypsin…ansl activate the other proteases all in the lumen.. They can now start working on the proteins….which will make more oligopeptides…..
Break the oligopeptides with BB peptidases and will digest them to lots of amino acids and some di/tri-peptides and lots of amino acids around…Those are the only constituents that can get in …not the oligopeptides.
165
What form of protein products can be absorbed or transported
Di and tri-peptides and the Amino acids
166
Explain the process of protein absorption from the products of digestion
The 3 constituents will transport into the cell through
sodium dependent …di and tri peptides..have facilitated transport
Amino acids…sodium dependent(facilitated)
Once in the cell only amino acids get out of the cell…
Peptidases in the cytoplasm cleave the di and tripeptides into amino acids..
Then they can go out by facilitated diffusion into the liver through the portal system….
167
Explain the process of lipid digestion
Lipid digestions starts in the mouth
Lingual lipase in the mouth…continues in the stomach with gastric lipase….in the SI with pancreatic lipase….we need the colipase here…..cos of the bile so we can get past the unstirred water layer….
In the DUO---Now we have digested lipids and blubs..fatty acids,cholesterol…
CCK released as soon as digestion begins..opens the sphincter body so bile can come in and wait for the lipid…
Works on the big blob…to have tiny lipid particles through emulsification…
Now the colipase is also here that will come in and bind the hydrophilic sides
Of the bile and the pancreatic lipase will digest these to monoglycerides free fatty acids….
…now we have digested lipids surrounded by bile…this is the micelle….this gets through unstirred water
…….lipids will go to the enterocytes this way…
Micelles drops lipids off
…they will diffuse through cell wall and into enterocytes…
Bile goes to the terminal ileum to the be recycled through portal blood
back to the liver
through liver…secreted into the canaliculi through the bile duct into the duodenum when needed..
Cycle continues until meal out of DUO…hormones shut down…also depends on how much fat u have in your meal
168
Explain the absorption of lipids
Once inside the cytosol we have to process the Lipids or fats to go into the lymph…
(lipids)--SER---esterlinkages made with Free fatty acids to remake what we ate….. tryglicerides,phospholipids and cholesterol
They are packaged into chylomicron…inside the enterocyte ..coded with beta lipase protein…allows exocytosis this way….through the lacteal.(too big to get into the capillaries so it uses the lacteal to the lymph) Through lymph and then into systemic blood ..in thoracic duct…in the CO…to the liver for processing….this takes hours to do.
This wont be processed fast..
Drugs that are lipophollic comes in through the fat pathway..
They don’t go to the liver first..
So bioavailability depends on going through systemic circ first and more available immediately.
169
What is the only way to loose cholesterol
The only way to loose cholesterol is with bile.through normal excretion of bile daily
170
Where do we have bile salts and where are they absorbed
Bile salts stay in the lumen, and are absorbed in the terminal ileum
171
What route does the bile salts return to the liver
through portal circulation
172
If bile accidentaly goes into cell
| what happens to it
Unconjugated bile is lipophilic and hydrophobic…..this can be reconjugated in the liver…if it accidentally goes into the cell….
173
Explain the Process of water absorption
Water absorption occurs primarily in the jejunum and ileum. The colon reclaims ~ 0.5 L while dehydrating the chyme to feces.
Absorption of sodium and glucose….water comes with sodium/glucose and bile as its being absorbed in the colon…
Colonic salvage happens in the colon where we reabsorb the sodium and it becomes water …this is the final step.
Does not matter how much water u drink ..it will be absorbed.
174
What does sodium absorption in jejunum stimulate
water and chloride absorption
Hydrogen out and makes co2 and water..
Na/h antiport continues and reabsorbs sodium and sodium potassium Atpase will feed the ECF……sodium stimulates the water absorption
175
explain the Process of Iron absorption
Menstruating women are in a positive balance…..
Iron must be bound always..
Bound to protein…and stored as ferritin in the enterocytes
Transported with transferrin
When enterocytes are regenerated…and replaced,we looses iron in the process also.
176
Explain the process of calcium absorption
It needs to be bound intracellularly because ….low calcium conc intracellularly..
Calbindin binds calcium and allows it to come into cell…can be taken out via ca atpase or sodium calcium transporter.VitD promotes absorption of calcium, by increasing calbindin and ability to get it out of the enterocyte..40% bound /60% is free.
177
Explain the process of vitb12 absorption
B12 binds to intrinsic factor in the duodenum, and then the complex dimerizes. The B12/IF receptors on cells in the terminal ileum recognize this complex.
Once in the cytosol, the B12 binds to transcobalamin II and enters the blood.
notes
Vit b12 binds to TC1 in the mouth……in the stomach….b12+Tc1 and pepsin cant digest B12..now add intrinsic factors from parietal cells and will bind to a different site on the b12…..needs to be in this 3 complex b4 it gets to the SI…in the SI TC! Will be cleaved by trypsin….which will now be dimerized to to b12+IF(IF protected from Pancreatic proteases)…..
Goes to the terminal ileum……transporter on luminal side takes it into the cell ..b12 goes in the blood and the b12 in the blood is bounf to TC2…which is a binding protein in the blood that will take it to the liver for storage or to the bone marrow for maturation for the RBC
If u loose ur terminal ileum it will affect bile recycling and B12 absorption…b12 shots.
178
Explain dehydration of chyme to make faeces
Sodium out,stim by aldosterone…water follows…chloride comes out…we dry out feaces until it is formed..if eat a lot of fibre ..less water will come out.
179
Name things that cause diarhea and the process of diarhea
Can be caused by viral or bacterial infection (or antibiotics)
Can be caused by irritation to the intestines (spicy, garlic-laden foods?!, or inflammation (as with inflammatory bowel diseases)).
Can be caused by osmotic agents (substances that pull water with them and aren’t absorbed). Examples are undigested carbohydrates (as with lactose intolerance), bile, and laxatives.
In each case, the increase in fluid and pressures lower in the intestines increases motility and reduces absorption. This reduces the ability to make solid feces (which occurs in the colon by absorption of most all the sodium and water out of the chyme), resulting in diarrhea.
180
composition of faeces
Electrolytes in the faeces will be potassium and bicarbonate
Sodium and chloride has been absorbed into the ECF
Sodium potassium chanell established because of the aldosterone.
Water…75%
Solids…..25%
Cellulose and indigestible fibre…variable
Bacteria….30%
Inroganic material…15%
Fat and fat derivatives…5%
