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Physiology > Gi > Flashcards

Gi Flashcards

1
Q

The stomach is mainly for?

A

Storage

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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

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3
Q

Small intenstine is made up of the sections namely

A

Duodernum

jejunum and illeum

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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)

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5
Q

What tract leads into the colon

A

illiocecal sphincter

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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

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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.….

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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.

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9
Q

Whats the function of brushborder enzymes

A

helps to digests nutrients and help with absorption

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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,.

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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

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12
Q

Replacement of cells happen every couple of days in the Gi system,what cell facilitate this?

A

Stem/Progenitor.

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13
Q

What produces mucus in the Gi tract

A

Goblet cells

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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.

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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

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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!

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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.

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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

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19
Q

Most absorbtion is done where in the Gi?

A

Small intestine

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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.

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21
Q

Regulation of the Gi tract happen through the plexes,namely?

A 
Systemmyenteric plexus (muscle/movement)
submucosal plexus (secretions)
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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

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23
Q

whats the composition of the PNS

A

(mainly vagal to transverse colon, then pelvic nerves to anus)

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24
Q

Whats the composition of the SNS

A

(post-ganglionic adrenergic fibers from celiac, superior and inferior mesenteric and hypogastric plexes)

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25
Q

Whats the GI composition of the the CNS

A

anticipatory response…smelling something delicious ..preparing the stomach for a possibility to eat…salivation starts

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26
Q

Function of hormones

A

.released into circulation causing motility

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27
Q

THE Gi is sympathetic slow and parasympathetic pro t/f

A

T

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28
Q

What time frame does the MMC begin after eating?

A

3-4hrs after meal.

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29
Q

What location would the Chyme be in for MMC to happen?

A

Jejunum

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30
Q

whats the essence of the MMC

A

Housekeeping movement– sweeps undigested material and bacteria into colon

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31
Q

What region is the MMC active in

A

Midstomach down to the terminal illeum

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32
Q

NAme and explain the phases of the MMC

A

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

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33
Q

In MMC what phase does the main propulsive movement happen

A

Phase 3

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34
Q

IN MMC what phase does is Motlin secereted and sweeps materials into the lower GI tract

A

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

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35
Q

Explain Primary peristalsis

A

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.

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36
Q

Explain secondary Peristalsis

A

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,

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37
Q

whats Achalasia

A

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

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38
Q

Explain how Gastric Accomodation relates to fullness,vagal nerve and relaxation of the Gi

A

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.

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39
Q

What is the Principle of Bariatric Surgery

A

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.

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40
Q

What does the process of gastric emptying depend on?

A

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.

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41
Q

What is the Resting membrane potential for the Gi tract called

A

Slow wave or Basic electrical Rythm

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42
Q

Whats the Electrical threshold for contraction in The Gi tract

A

-40mv

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43
Q

What substances or factors can cause depolarization in the Gi tract

A

stretch, ACh/parasymp, gastrin, serotonin,subst. P (tachykinin,)

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44
Q

What substance or stimuli can cause relaxation/Hyper-polarization in the Gi tract

A

NE, sympathetics, VIP, NO

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45
Q

Waves causes contraction true or false?

A

False

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46
Q

What causes contraction

A

Depolarization above -40mv ..generates spike potentials that forms on the peak of the slow waves

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47
Q

Explain the process of depolarization in the stomach

A

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…

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48
Q

Explain the process of Depolarization in the Small intestine

A

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…

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49
Q

The vagus is always gonna be controlling any parasympathetic events in the Gi tract.

A

FYI

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50
Q

Explain the process of Peristalsis in the small intestine

A

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

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51
Q

Explain the process of Segmentation in the Small intestine

A

Locally mediated…ENS plays a big role…there will be paring of Contracting /mixing and movement…peristalsis can happen adjacent to segmentation.

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52
Q

Explain the process of bile contraction, when and what hormones is released?

A

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.

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53
Q

What is segmental propulsion

A

The taneia coli contract to make sacs in the colon (haustrae). This is

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54
Q

What is the purpose of segmental propulsion

A

It is SLOW, and designed for storage and dehydration of chyme to feces.The reclamation of sodium and water ,.

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55
Q

How is Haustrae formed during segmental propulsion

A

formed by contraction of the taneia coli.

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56
Q

What is the process of peristaltic movement and how often do they occur.

A

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

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57
Q

What stimulates peristaltic movement

A

These are peristaltic contractions that are stimulated by GI hormones and the vagus nerve, in response to chyme in the upper GI tract

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58
Q

What is Gastrocolic Reflex

A

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

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59
Q

Why does mass movements happen 3-4x/day

A

.Reason this happen 3-4 times a day is it conincides with feeding

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60
Q

What secretion do we have in the mouth

A

Saliva,Lingual lipase,salivary alpha-amylase,

R-proteins =Transcobalamin-1(TC-1

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61
Q

Secretion in the Stomach

A

Hcl,intrinsic factor,pepsinogen,gastric lipase,mucus,gastrin,somatostatin,histamine

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62
Q

Secretions in the liver and gall bladder

A

Bile and buffers(Electrolytes)

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63
Q

Scecretion in the Pancrease

A 
Exocrine glands:Buffers and enzymes(trypsin,chymotrypsin,procaboxypeptidase,lipase,colipase,proelastase and alphaamylase.
monitor peptide(trypsin inhibitor,stimulates cck)

Endocrine:Insulin,glucagon,Somatostatin

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64
Q

Secretions in the small intestine

A

Buffers(Mucus and elctrolytes)

enterokinase,brushb border dissacharides,brush border peptidases,secretin,gastrin,cck,vip,gip,motlin,5HT,Somatostatin

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65
Q

WHats the direction of food fluid and elctrolytes between the gi trACT AND the Ecf

A

Gi tract takes fluid and electrolytes out of the Ecf and processed back into the ECf

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66
Q

Memorise slide 3

A

Now in lecture 3 Gi

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67
Q

How does gut peptide Regulate Hunger and Satiety

A

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

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68
Q

What is found in the Saliva and what are its functions

A

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

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69
Q

Explain saliva secretions as related to blood flow, electrolytes and etc.

A

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

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70
Q

Whats difference btw Exocrine and Endocrine glands

A

Endocrine…make hormones and secrete into blood

Exocrine make other secretions and secrete into duct

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71
Q

What’s the component of Ductal secretions and how does this component relate to saliva flow and blood flow

A

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

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72
Q

do vomiting and potassium content in the saliva relate to becoming hypokalemic?explain

A

Yes

Vomiting will loose a lot of potassium since it has a large amount of potassium in the saliva.. and hence contribute to Hypokalemia.

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73
Q

What Controls the salivary flow between SNS and PNS, explain how? and what nerves does it work through

A

PNS
Saliva is dependent on parasympathetic…PNS is pro-secretion,pro-motility…
Facial(Submax and sublingual gland) and glossopharyngeal(Parotid) controls salivation….

74
Q

What are the things that increase saliva flow in the mouth

A

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
Q

What are the things that decrease saliva flow in the mouth

A

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
Q

What does saliva do

A

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
Q

What does the Hormone Gastrin do in the Gastric mucosa

A

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
Q

Explain the process of Gastric secretions and hormones secreted and were secreted and functions and what stimulates them to be secreted.

A

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
Q

What causes the Pepsinogen to activate.

A

Acid activates the pepsinogen to the protease.

as soon as the acids get the PH down low the pepsinogens work

80
Q

What happens to Tuberlae vesicles on the chromaffin cells before and after stimulation and what stimulates it.

A

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
Q

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

A

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
Q

What is the rate-limiting step in the stimulation of acid creation

A

The rate of creation of the proton pumps

83
Q

Explain Parietal Cell HCL production

A

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
Q

Explain the process of Ulcer formation by H pylori

A

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
Q

Explain the process of ulcer formation with NSAIDs

A

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
Q

The 3 systems that stimulate HCL production are?

A

Parasympathetic, ACh
Gastrin
Histamine
These 3 directly stimulate the parietal cell to produce histamine

87
Q

Things that inhibit ACid secretion

A

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
Q

What is the mechanism of action of the mucus layer in protecting against acids

A

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
Q

Explain Neural control of Acid secretion

A

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
Q

Name the cells and process found in the small intestine mucosa

A

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
Q

Process of chyme movement into small intestine and hormones secreted.

A

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
Q

What do the CCK and Secretin secrete in the pancreatic cells

A

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
Q

Per pancreatic enzymes, what are the proteases secreted as? and why?

A

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
Q

per pancreatic enzymes what is Tyrpsinogen activated to and by what?

A

trypsinogen– activated to trypsin in the duodenum by (EK)

95
Q

The following are activated by Trypsin

A

chymotrypsinogen–
pro-carboxypeptidase–
pre-co-lipase

96
Q

What activates pancreatic lipase and what is the function of pancreatic lipase

A

Pancreatic Amylase– starch digestion in the duodenum…..activated by chloride

97
Q

All the pancreatic enzymes are in the lumen true or false

A

True

98
Q

If trypsinogen autoactivates , what would be the outcome of this and what should be done

A

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
Q

What does pancreatic lipase need to hydrolyze lipids

A

Pancreatic Lipase (needs pre-co-lipase)– hydrolyzes lipids

100
Q

What happens at the end of a meal with secretions per pancreatic and thos lower in the tract

A

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
Q

Secretion of Hydrogen and bicarb into the Lumen in the illeum helps with what process

A

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
Q

Secretion of Hco3 and K into the lumen in the colon helps with what

A

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
Q

Where is bile formed?

A

Hepatocyte cells of the liver

104
Q

How does choloesterol get synthesised

A

Via HMg Coa Reductase

105
Q

what are the 3 sources of obtaining cholesterol

A

Dietary

Hmg coa Reductase

106
Q

How does statin drugs work

A

they block the Hmg coa reductase thus lowering the plasma cholesterol level

107
Q

bile is hydrophobic t/f

A

t, with a cholesterol backbone

108
Q

Bile becomes amphipatic inside hepatocytes this means?

A

soluble in lipids and water

109
Q

secondary bile is much more lipophillic..true or false

A

T

110
Q

Where do the buffers come out from in the GI tract

A

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
Q

Bile salt acts like detergent and emulsifies T/F

A

T.

Does not digets anything separates the lipid from each other

112
Q

What is added to Bile salt to get Micelle salt

A

pancreatic lipase and prolipase

113
Q

How do we get the Bile structure

A

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
Q

What happens with illeal resection

A

Recycling of bile will be jeopardised

115
Q

Why do we perform cholycystectomy

A

Cholecystectomy is performed in response to acute or chronic cholecystitis (inflammation of the gallbladder, with or without stones).

116
Q

What is postcholycystectomy syndrome

A

postcholecystectomy syndrome, experiencing chronic GI distress and pain in the upper right abdomen.*

117
Q

Whats the action of Cholestyramine for diarhea after cholycystectomy

A

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
Q

AFter cholycystectomy why do patients develop diarhea

A

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
Q

What will be the effcets of Cholycystectomy on bile production

A

Liver will just keep producing bile during digestion…overall it will produce more than normal because there is no storage.

120
Q

Effects of cholycystectomy

A

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
Q

What happens if the ileum is removed?

A

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
Q

Bilirubin metabolism and excretion

A

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
Q

Billi metabolism 2

A

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
Q

What are the liver functions

A

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
Q

Normal liver has high or low capillary venous pressures?

A

Low capillary pressures

126
Q

What contributes blood to the hepatic parenchymal cells and in what volume

A

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
Q

What enables hepatic veins to get blood out into the venae cava easily

A

Hepatic vein gets blood out into the vena cavae(low bp blood)…this enables blood to leave easily…free in —free out..

128
Q

Name the 3 causes of portal hypertension

A

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
Q

Whats the function of the Lymph

A

Lymph removes fluid and proteins from the Space of Disse, and drains the fluid into the venous blood.

130
Q

Hepatocytes are single or double cells

A

Single cells

131
Q

Does every hepatocyte have acces to blood?

A

Yes

132
Q

Function of Kuffper cells

A

Kupffer cell…waste removal..degrade anything that is waste.

133
Q

What is the function of the space of Disse

A

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
Q

Where does lymph production end up at

A

Hepatocytes..lymph…space of disse..lymphatic……

.or it goes to blood

135
Q

How Does ascites form

A

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
Q

What is Hepatomegaly and its characteristics

A

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
Q

What is Jaundice and what are the types

A

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
Q

Explain Obstructive Jaundice

A

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
Q

Explain Hepatic Jaundice

A

Hepatic jaundice can result from acute or chronic hepatitis, drug hepatotoxicity and cirrhosis. This reduces the ability of the cells to metabolize bilirubin.

140
Q

What is hemolytic Jaundice

A

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
Q

What is neonatal Jaundice

A

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
Q

FYI

A

Hepatic jaundice is from inflammation..

Hemolytic jaundice…has nothing to do with the liver.

143
Q

Explain Glycogen Storage

A

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
Q

Explain Gluconeogenesis

A

Amino acids and glycerol (from TGs) are converted to glucose by GNG

After all glycogen has been used Gluconeogenesis starts

145
Q

what is GLUT2

A

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
Q

Name the processes of Liver carbohydrate metabolism

A

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
Q

through the pfrocess of Liver Lipid Metabolism explain how High rate of -oxidation of fatty acids
occurs

A

TGs are hydrolyzed to fatty acids and glycerol mitochondria -oxidation to acetyl CoA citric acid cycle.

148
Q

process of Liver lipid metabolism forming most Lipoproteins

A

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
Q

How does liver Metabolism Synthesize of lots of cholesterol and PLs

A

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
Q

How doesLiver Metabolism Converts Unused Carbs to TG

A

Glucose glycolysis acetyl CoA TG polymers made using malonyl CoA and NADPH packed into VLDL adipose tissue.

151
Q

Liver metabolism

Urea and plasma protein Production

A

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
Q

Liver Protein metabolism

synthesis of plasma protein

A

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
Q

Interconversion of amino acids

A

Transamination can convert certain amino acids to others that may be needed.

154
Q

Liver Metabolism:

other functions

A

Vitamin storage (B12, A, D)
Formation of blood coagulation products
Iron storage…in case more RBC needed
Drug, hormone, waste removal

155
Q

Symptoms of liver failure

A 
Ascites
Jaundice 
Portal hypertension
Bleeding/bruising
Confusion/cognition problems (encephalopathy
Weakness
Nausea
Cholestasis (reduced/blocked bile flow)
Acidosis
156
Q

Whats the final digestion for fats and protein

A

Brushborder enzymes

EK..BBE also

157
Q

What happens to the enzymes on the sloughed off cells of the Krpt of Luberkhun

A

Enzymes will reclaim the sloughed off cells and reabsorbed early in the process.

158
Q

What are the components and activities of brushborder enzymes

A
  1. final digestion for carbs and proteins

2. has Enterokinase that cleaves trypsinogen to trypsin

159
Q

What are the components of krypts of leberkhun..

A

has secretions in the luminal membrane(cl,na and water are here.
Buffers

160
Q

What is the process of carbohydrate digestion and what molecules do we need to get them to in order to transport them

A

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
Q

What form do we need to get carbs to inorder to transport them…

A

Glucose

Fructose and Galactose

162
Q

How does the transport(ABsorption) of glucaose,fructosand galactose(monosaccharides) happen

A

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
Q

Explain how olestra and sucralase affect absorption and form diarhea

A

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
Q

Explain the process of protein digestion

A

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
Q

What form of protein products can be absorbed or transported

A

Di and tri-peptides and the Amino acids

166
Q

Explain the process of protein absorption from the products of digestion

A

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
Q

Explain the process of lipid digestion

A

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
Q

Explain the absorption of lipids

A

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
Q

What is the only way to loose cholesterol

A

The only way to loose cholesterol is with bile.through normal excretion of bile daily

170
Q

Where do we have bile salts and where are they absorbed

A

Bile salts stay in the lumen, and are absorbed in the terminal ileum

171
Q

What route does the bile salts return to the liver

A

through portal circulation

172
Q

If bile accidentaly goes into cell

what happens to it

A

Unconjugated bile is lipophilic and hydrophobic…..this can be reconjugated in the liver…if it accidentally goes into the cell….

173
Q

Explain the Process of water absorption

A

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
Q

What does sodium absorption in jejunum stimulate

A

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
Q

explain the Process of Iron absorption

A

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
Q

Explain the process of calcium absorption

A

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
Q

Explain the process of vitb12 absorption

A

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
Q

Explain dehydration of chyme to make faeces

A

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
Q

Name things that cause diarhea and the process of diarhea

A

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
Q

composition of faeces

A

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%

Physiology (11 decks)

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