Vander's GIT Flashcards
1
Q
Only substance that can cross the epithelium of the gastric wall
A
Water
2
Q
Intake vs output in digestive system
A
3
Q
CNS receives info from GIT
A
Afferent input
4
Q
CNS has an influence on GIT
A
Efferent input
5
Q
Structure of GIT wall
A
6
Q
Contraction of circular muscle
A
Produces a narrowing of the lumen
7
Q
Contraction of longitudinal muscle
A
Shortens the tube
8
Q
Function of Peyer’s Patches and immune cells in SI
A
Secrete inflammatory mediators (e.g. cytokines) and alter motility
9
Q
Where do carboxypeptidases come from
A
The pancreas
10
Q
Where are aminopeptidases found
A
On the luminal membranes of epithelial cells
11
Q
How do free AAs enter the epithelial cells
A
// Secondary active transport coupled to Na+
12
Q
How are short chains of 2 or 3 AAs absorbed
A
By a secondary active transport coupled to H+ gradient
Within the epithelial cell, these di- and tri-peptides are hydrolysed to AAs, which then leave the cell and enter the blood through a facilitated diffusion carrier in the basolateral membranes
13
Q
Difference between CHO and protein absorption
A
With CHO absorption, molecules larger than monosaccharides are not absorbed
With protein absorption, short chains of 2/3 AAs are absorbed by a secondary active transport coupled to H+ gradient
14
Q
How do the SMALL NUMBER of intact proteins cross the intestinal epithelium and gain access to interstitial fluid
A
Endocytosis & exocytosis
(absorptive capacity for intact proteins is much greater in infants than in adults - antibodies)
15
Q
Action of lipase
A
catalyses the splitting of bonds linking FAs to the 1st and 3rd C atoms of glycerol
16
Q
Action of phospholipids on fat digestion
A
They are amphipathic molecules consisting of 2 non-polar FA chains attached to glycerol with a charged phosphate grp located on glycerol’s 3rd carbon
EMULSIFYING AGENT
17
Q
What are bile salts formed from
A
Cholesterol in the liver - amphipathic
18
Q
How do we over come the empairment of the accessibility of water-soluble lipase to its substrate
A
- COLIPASE from pancreas, which is amphipathic, lodges on the lipid droplet surface
- COLIPASE binds the lipase enzyme, holding it on the surface of the lipid droplet
19
Q
Components of micelles
A
- Bile salts
- FAs (low solubility in water)
- Monoglycerides (low solubility in water)
- Phospholipids
20
Q
- During their passage through the epithelial cells, what are FAs and monoglycerides re-synthesised to
- How is a diffusion gradient for these molecules maintained
- What is the function of these packages
A
- Triglycerides
- This process lowers the conc of cytosolic free FAs and monoglycerides and thus maintains a diffusion gradient for these molecules into the cell
- The re-synthesised fat aggregates into small droplets coated with amphipathic proteins that perform an emulsifying function similar to that of bile salts
21
Q
How are the fat droplets released into IS fluid
A
Vesicles containing the droplet pinch off the ER, are processed through the golgi apparatus and eventually fuse with the plasma membrane
These are known as CHYLOMICRONS
22
Q
Content of chylomicrons
A
Triglycerides
Other lipids
23
Q
Where do the chylomicrons pass into
A
- Chylomicrons released from epithelial cells pass into the lacteal rather than the blood capillaries because the BASEMENT MEMBRANE (an EC glycoprotein layer) at the outer surface of the capillary provides a BARRIER to the diffusion of large chylomicrons
- Lacteals have large, slit like pores between their endothelial cells
- Lymph eventually empties into system veins via thoracic duct
24
Q
Overview of fat digestion and absorption
A
25
What will a vit D malabsorption result in
Decrease in calcium absorption in GIT
26
How is vit B12 absorbed
With intrinsic factor by ENDOCYTOSIS
- erythrocyte formation
- pernicious anaemia
27
What accounts for much of the actively transported solute
Na+ ions - most abundant solute in chyme
* Na+ absorption is a primary active process using the Na+/K+ ATPase pumps
* Cl- and HCO3- are absorbed with Na+ ions
28
How is iron transported into intestinal epithelial cells
Fe is incorporated into ferritin, the protein-iron complex that functions as an IC Fe store
Most of Fe bound to ferritin in the epithelial cells is released back into the intestinal lumen when the cells at the tips of the villi disintegrate, and the iron is then excreted in the faeces
29
What happens to the absorbed iron that does not bind to ferritin
It's released on the blood side where it circulates throughout the body bound to plasma protein TRANSFERRIN
30
What does iron absorption depend on
Types of food ingested because it binds to many -vely charged ions in food which can retard its absorption
e.g. iron in ingested liver is much more absorbable than iron in egg yolk, due to the phosphates that bind the iron to form an insoluble and unabsorbable complex
31
Absorption typical of most trace metals
* Cellular storage proteins and plasma carrier proteins are involved
* The control of absorption, rather than urinary excretion is the major mechanism for homeostatic control of the body's content of Fe
32
Luminal stimuli that initiate GI reflexes
1. Distension of wall by the volume of the luminal contents
2. Chyme osmolarity (total solute conc)
3. Chyme acidity
4. Chyme concentration (of digestive products)
33
2 nerve networks of the enteric nervous system
1. Myenteric plexus – SM activity
2. Submucosal plexus – secretory activity
34
2 types of neural reflex arcs
1. Short reflexes – from receptors through the nerve plexuses to effector cells
2. Long reflexes from receptors in the tract to the CNS by way of afferent nerves, and back to the nerve plexuses and effector cells by way of autonomic nerve fibres
35
What stimulates the secretion of CCK
Presence of FAs and AAs in the SI triggers CCK secretion from cells in the SI into blood
36
Effect of CCK
Circ CCK stimulates the pancreas to increase secretion of digestive enzymes
CCK causes the gallbladder to contract, delivering to the intestine the bile salts required for micelle formation
37
How is the stimuli for CCK release removed
Fat and AAs are absorbed
38
Potentiation of secretin and CCK
* Secretin strongly stimulates pancreatic bicarbonate secretion WHEREAS CCK is a weak stimulus of bicarbonate secretion
* HOWEVER both hormones together stimulate pancreatic bicarbonate secretion more strongly than would be predicted by the sum of their individual stimulatory effects
39
What does leptin stimulate
Satiety (fullness)
40
What does ghrelin stimulate
Hunger
41
Effect of GIT hormones on tissues in general
Trophic (growth-promoting) effects on various tissues
42
How is secretion of saliva controlled (greatest exocrine gland)
By both sympathetic and parasympathetic neurons, although PS has a greater response
NO HORMONAL REGULATION OF SALIVARY SECRETION
43
SJÖGREN’S SYNDROME
* Immune disorder
* Renders different exocrine glands non-functional by infiltration of WBCs and immune complexes
44
Composition of muscle in the oesophagus
UPPER 1/3RD - Skeletal muscle (efferent activity in somatic nerves)
LOWER 2/3RDS - Smooth muscle (autonomic nerves)
45
Secondary peristalsis
if a large food particle does not reach the stomach during the initial peristaltic wave, the maintained distension of the oesophagus by the particle activates receptors that initiate reflexes, causing repeated waves of peristaltic activity
46
How does the LOS remain closed when swallowing is not taking place
the last portion of the oesophagus lies BELOW the diaphragm and is subject to the same abdominal pressures as the stomach =\> pressures rise together, and a pressure gradient cannot be formed
47
What does acid in the oesophagus trigger
A secondary peristaltic wave + increased salivary secretion, which helps to neutralise acid and clear it from the oesophagus
48
How to pump H+ ions into the lumen of the stomach
Primary H+/K+ ATPases in the luminal membrane of the PARIETAL cells
49
What electrolyte is lost in excessive vomiting
K+ - pumped out with H+ but leaks back into lumen through K+ channels
50
HCl secretion overview
* The H+ secreted into lumen by primary active transport are derived from the breakdown of water molecules, leaving OH- behind
* carbonic anhydrase is present in high concentrations in parietal cells
51
WHY DOESN’T HIGH CONC OF H+ IN THE STOMACH LUMEN DESTROY LINING OF STOMACH WALL
* Mucus secreted by the cells in the gastric pit creates a protective coating and traps bicarbonate
* This gastric mucosal barrier protects the stomach from the luminal acidity
52
4 chemical messengers that regulate the insertion of H+/K+ ATPases into plasma membrane
1. Gastrin – gastric hormone
2. ACh – NT
3. Histamine – paracrine
4. Somatostatin – paracrine (only 1 to inhibit)
53
Function of histamine
Stimulates acid secretion by markedly potentiating the response of ACh and gastrin
54
H+ secretion stimulation overview
55
Apart from hormonal input, how is H+ secretion stimulated
* Distension from the vol of ingested material and presence of peptides and AAs released by digestion of luminal proteins
56
Factors in SI that inhibit gastric acid secretion
1. Acid
2. Distension
3. Hypertonic solutions
4. Solutions containing AAs
5. FAs
57
What are enterogastrones
What do they include
Hormones released by the intestinal tract that reflexly inhibit gastric activity
INCLUDING
Secretin
CCK
58
Pepsinogen secretion parallels...
Acid secretion
59
Control of HCl during a meal
60
Pepsin's role in protein digestion
Not essential
Enzymes in SI digest protein
Pepsin is important in digestion of collagen contained in the CT matrix of meat
61
What is receptive relaxation
How is it mediated
* When a meal is swallowed, the SM in the fundus and body relax before the arrival of food, allowing the stomach’s vol to increase to as much as 1.5 L with little increase in P
* Mediated by PS nerves to stomach’s enteric nerve plexuses, with co-ordination provided by AFFERENT input from the stomach via the vagus nerve and by the swallowing centre in the brain
* NO and serotonin released by enteric neurons mediate this relaxation
62
What happens as the peristaltic wave of the stomach approaches the antrum
* A more powerful contraction is produced which both mixes the luminal contents and closes the pyloric sphincter, a ring of SM and CT between the antrum and duodenum
* As a consequence of the sphincter closing, only a small amount of chyme is expelled into duodenum with each wave
* Most of the antral contents are forced backward toward the body of the stomach, thereby contributing to the mixing activity in the antrum
63
How are the gastric peristaltic waves produced
Rhythm (3/min) is generated by PACEMAKER CELLS in the longitudinal SM layer
64
How is the SM brought closer to threshold
* SM cells undergo spontaneous depolarisation-repolarisation cycles (slow waves)
* Excitatory NTs and hormones act upon the SM to further depolarise the membrane, thereby bringing it closer to threshold
65
What is the frequency of contraction determined by
Intrinsic basal electric rhythm and remains essentially constant
66
What is the force of contraction (amt of gastric emptying/contraction) is determined by
Reflexly by neural and hormonal input to antral SM
67
How are the reflexes affecting gastric motility intiated
* Gastrin, in sufficiently high concentrations, increases the force of antral smooth muscle contractions
* Distension of the stomach also increases the force of antral contractions through long and short reflexes triggered by mechanoreceptors in the stomach wall
* After a large meal, the force of initial stomach contractions is greater, resulting in greater emptying per contraction
68
What is gastric emptying inhibited by
* Distension of the duodenum
* Presence of fat
* Low pH
* Hypertonic solutions in the lumen of the duodenum
69
How do hypertonic solutions in the lumen of the duodenum inhibit gastric emptying
* This reflex prevents the fluid in the duodenum from becoming too hypertonic, by SLOWING the rate of entry of chyme and thereby the delivery of large molecules that can rapidly be broken down into many small molecules by enzymes in the SI
* An extremely hypertonic solution could cause enough water to flow by osmosis into the SI from the blood to lower blood vol and produce circulatory complications
* The large distension of the intestine by the entering fluid can also trigger vomiting in these patients
70
What is dumping syndrome
Rapid entry of large quantities of ingested material into SI
71
What do gland cells of the pancreas secrete
Enzymes
72
What do epithelial cells (lining ducts) of the pancreas secrete
HCO3-
73
Pancreatic secretion
74
What is HCO3- secretion identical to
HCl secretion in the stomach except reversed
75
Pancreatic enzymes
76
Effect of enterokinases on pancreatic enzymes
77
What is the stimulus for secretin
HCO3- secretion
78
What is the stimulus for CCK
FAs and AAs in the duodenum
79
What is the primary ion determining the magnitude of fluid secretion
Cl-
* Water movement into the lumen also occurs when chyme entering the SI from the stomach is hypertonic because of a high conc of solutes in the meal, and because digestion breaks down large molecules into many more small molecules
* This hypertonicity causes the osmotic movement of water from the isotonic plasma into the intestinal lumen
80
How is the large net absorption of water from SI achieved
By transport of primary Na+ from the intestinal lumen into the blood, with water following by osmosis
81
How is segmentation intiated
By electrical activity generated by pacemaker cells in or asscoiated with the circular SM layer
* As with the slow waves in the stomach, this intestinal basic electrical rhythm produces oscillations in the smooth muscle membrane potential. If threshold is reached, action potentials are triggered that increase muscle contraction
82
Contractions/min in:
1. Duodenum
2. Ileum
1. 12
2. 9
83
How does cephalic phase stimuli alter intestinal motility
Like the stomach, these inputs produce changes in the force of SM contraction but do NOT significantly change the frequencies of the BASIC ELECTRIC RHYTHM
84
What is Migrating Myoelectric Complex
* After most of a meal has been absorbed, the segmenting contractions cease and are replaced by a pattern of peristaltic activity
* Beginning in the lower portion of the stomach, repeated waves of peristaltic activity travel about 2 feet along the small intestine and then die out
* The next MMC starts slightly farther down the small intestine so that peristaltic activity slowly migrates down the small intestine, taking about two hours to reach the large intestine
* By the time the MMC reaches the end of the ileum, new waves are beginning in the stomach, and the process repeats
* The MMC moves any undigested material still remaining in the small intestine into the large intestine and also prevents bacteria from remaining in the small intestine long enough to grow and multiply excessively
* Upon the arrival of a meal in the stomach, the MMC rapidly ceases in the intestine and is replaced by segmentation
85
Initiation of MMC
* Rise in plasma conc of MOTILIN
Feeding inhibits the release of motilin
Motilin stimulates MMCs via both the enteric and autonomic nervous systems
86
What is the gastroileal reflex
Segmentation intensity in the ileum increases during periods of gastric emptying
87
What is the intestino-intestinal reflex
Large distensions of the intestine, injury to the intestinal wall and various bacterial infections in the intestine lead to a complete CESSATION of motility
88
What do the secretions of the LI contain
HCO3- and K+
89
Primary absorptive process in the LI
Active transport of Na+ from lumen to blood, with the accompanying osmotic absorption of water
90
How is K+ moved from blood into LI lumen
Probably due to an active mechanism stimulated by cAMP
(Severe depletion of total-body K+ can result when large volumes of fluid are excreted in the faeces)
91
How is HCO3- transported into lumen
* There is also a net movement of HCO3- into the lumen coupled to Cl- absorption from the lumen – loss of HCO3- in patients with prolonged diarrhoea can cause metabolic acidosis
92
How is the segmentation motion of the LI produced
Contractions of the circular SM in the LI produce a segmentation motion with a rhythm considerably slower (one every 30 min) than that in the SI
93
How is mass movement carried out
A wave of intense contraction spreads rapidly over the transverse segment of the LI towards the rectum
* Usually coincides with the ***GASTROILEAL REFLEX***
* Unlike a peristaltic wave, in which the smooth muscle at each point relaxes after the wave of contraction has passed, the smooth muscle of the large intestine remains contracted for some time after a mass movement
* PS input increases segmental contractions
* S input decreases colonic contractions
94
What is the anus composed of
Internal anal sphincter - SM
External anal sphincter - skeletal muscle, voluntary control
95
What initiates the defecation reflex
The sudden distension of the walls of the rectum produced by the mass movement of faecal matter into it
96
How do brain centres control the defecation reflex
* Brain centres can, however, via descending pathways to somatic nerves to the external anal sphincter, override the reflex signals that eventually would relax the sphincter, thereby keeping the external sphincter closed and allowing a person to delay defecation
* In this case, the prolonged distension of the rectum initiates a reverse peristalsis, driving the rectal contents back into the sigmoid colon
