BSF Flashcards
Where is the feeding or hunger center located in the hypothalamus? What pathway is involved?
Lateral hypothalamic area. NPY edited pathway
Where is the satiety center located? What pathway is involved?
Ventromedial nuclei, melanocortin pathway (POMC)
What is the clinical effect of insulin?
Decrease appetite, increase metabolism
What is the source and effect of leptin?
Source: Fat cells, endocrine cells of the stomach
Effect: Decrease appetite, increase metabolism, decrease ghrelin release
What is the effect of CCK? Where is it released from?
Decrease appetite, decrease gastric emptying. CCK is released from I cells of the duodenum
What is the effect of PYY? What stimulates PYY?
Decrease appetite, increase metabolism, decrease gastric emptying and secretion
Stimulated by fat
What is the effect of ghrelin? Where is it released from?
Ghrelin increases appetite, decrease metabolism, decrease leptin release. It is released from endocrine cells (stomach), hypothalamus, and small & large intestines
What secretes gastrin? Where is it secreted? How is it stimulated? What are its actions?
G cells. Secreted in stomach, duodenum, all the way to the jejunum (diminished).
Stimulated by vagus nerves (direct), stomach distention and proteins.
Increases H+ and pepsinogen secretion, increases gastric distensibility. Stimulates growth of gastric mucosa
What secretes secretin? Where is it secreted How is it stimulated? What are its actions?
S cells of duodenum. Stimulated by presence of H+ and fatty acids in the duodenum.
Effect: stimulates bile and pancreatic duct secretion of H2O and bicabonate to neutralize pH. Increases pepsinogen secretion, inhibits gastric acid secretion and gastric motility.
What secretes CCK? Where is it secreted? How is it stimulated? What are its actions?
I cell, duodenum, jejunum, all the way to the ileum (diminishing). Fat/protein/vagal stimulation.
Increase enzyme secretion by pancreatic acinar cells, increase contraction of the gallbladder, inhibits gastric emptying
What secretes GIP? Where is it secreted? How is it stimulated? What are its actions? What does GIP stand for?
K cell, duodenum, jejunum. Released in response to high serum glucose in stomach.
Stimulates the release of insulin (or potentiates glucose-stimulated insulin secretion) and decreases gastric motility. Inhibits gastric secretion and emptying. GIP is why oral glucose is more effective than IV glucose at increasing insulin levels.
GIP = Glucose-dependent Insulinotropic Polypeptide
What secretes motilin? Where is it secreted How is it stimulated? What are its actions?
M cell, duodenum, jejunum, unknown stimulation
Increases motility and initiates MMC
What stimulates the release of pancreatic peptide? What is its action?
Stimulated by protein, fat, and glucose. It decreases bicarbonate and pancreatic enzyme secretion
What is the stimulus for enteroglucagon? What is its action?
Stimuli are fat and hexose. Primary action is to decrease gastric secretion and emptying, increases insulin release
Swallowing, pain, and defecation are what type of reflexes?
Long reflexes
What is the effect of parasympathetic stimulation on GI smooth muscle?
Mucosal secretory and/or endocrine cells?
Vascular smooth muscles?
Increase GI motility, decrease tone of GI smooth muscle sphincters
Increase secretion
Vasodilation, increase blood flow
What is the effect of sympathetic stimulation on GI smooth muscle?
Mucosal secretory and/or endocrine cells?
Vascular smooth muscle cell?
Decreased GI motility, increased tone of GI smooth muscle sphincters
Decreased secretion activity
Vasoconstriction, decreased blood flow
What does the submucosal plexus innervate? What action does it control
It innervates the glandular epithelium, intestinal endocrine cells, and submucosal blood vessels
It primarily controls GI secretion and local blood flow
It also regulates the contraction o fate muscular mucosa
What does the myenteric plexus control?
It primarily controls the GI movements
It regulates local and inter-regional motility activity through regulation of contraction/relaxation of circular and longitudinal smooth muscle layers
What is the purpose of interneurons (both inhibitory and excitatory)
Mainly responsible for integrating information, transmit signals from sensory to secretomotor neurons
What is VIP? What is its action?
It is a peptide neurotransmitter of the enteric nervous system . It relaxes the gut smooth muscle and stimulates intestinal and pancreatic secretion. Inhibits gastric secretion
VIP = vasoactive intestinal peptide
What do short reflexes (local) control?
Secretion, peristalsis, mixing contraction
How do pain reflexes affect the GI tract?
It is a general inhibitor of the entire GI tract
What regulates the longitudinal and circular muscles?
They are regulated by neural pathways integrated through the myenteric plexus
What is the function of mucosal muscle (usually longitudinal)?
It alters the mucosal surface area. It regulates lymph flow through the central lacteal into the lymphatic system
What is the difference between phasic and tonic contraction?
Phasic – contraction-relaxation cycles
Tonic – sustained. Found in GI sphincters and latch mechanisms
What is the major determinant of the phasic nature of contraction?
ICCs
What do slow waves determine?
SWs determine the maximum frequency and direction propagation
What are the different types of ICC and their actions?
Myenteric plexus level (ICC-MY) – generate slow waves, propagate, and coordinate propagation of slow waves
Smooth muscle layer (ICC-IM) – mediators of enteric motor neurotransmission, essential for cholinergic (ACh) excitatory and nitric (NO) inhibitory neurotransmission
Within the sepae (ICC-SEP) – convert and coordinate the spread of pacemaker activity
Which region has the highest frequency of slow waves?
Duodenum at 12 cycles/minute
What creates the depolarization of slow waves? Repolarization?
Depolarization – Na+ influx, T-type Ca2+ channels, Ca2+ activated Cl- efflux
Repolarization – K+ efflux
What causes depolarization that leads to action potential
L-type Ca2+ channels
Between tonic and phasic contractions, which is associated with BER?
Phasic is associated with BER
Does sphincter relaxation causes an increase or decrease in GI motility? What about contraction?
Sphincter relaxation causes an increase in GI motility while contraction decreases GI motility
Is the upper pharynx a part of voluntary control?
Yes
When you have a sympathetic stimulation, what happens to the motility? Sphincter?
Sympathetic stimulation contracts the sphincter, which decreases GI motility
Parasympathetic stimulation relaxes the sphincter and increases GI motility
What action of what muscle is responsible for segmentation (mixing)? Does this move the particle along the GI tract?
Focal contraction of the circular muscle layer. This does not result in significant net movement of material along the tract
What is the function of paneth cells?
They synthesize and secrete several antimicrobial agents such as secretory IgA
They are in the bases of small intestinal crypts and continually sense the microbiota to induce the production of antimicrobial peptides
What is the function of Goblet cells?
They produce mucin, which is organized into a dense, highly cross-linked inner proteoglycan gel that forms an intestinal epithelial cell-adherent inner mucous layer and a less densely cross-linked outer mucous layer
In the stomach, when is the acidity the lowest? Highest?
Acidity is lowest after digestion. It is highest after meals
What characteristic must probiotics have?
They must be non-pathogenic and non-toxic, they must have a large number of viable cells
What happens during the chewing reflex?
Bolus of food in the mouth inhibits contraction of the muscles of mastication, allowing the lower jaw to drop. The drop will induce a stretch reflex of the jaw muscles that leads to a rebound contraction
What occurs during the voluntary stage and involuntary stage of swallowing?
Voluntary is only the oral phase
Involuntary begins at the beginning of the pharyngeal stage, which lasts for less than 1 second, esophageal lasts for about 8-10 seconds
When swallowing, is respiration possible? Why or why not?
It’s not, the nasopharynx is closed as well as the epiglottis
Propulsion through which sphincter occurs during the end of the pharyngeal phase?
Propulsion through the upper esophageal sphincter
When does the esophageal phase begin?
It begins as the upper esophageal sphincter opens
What initiates primary peristalsis? What controls it?
It is initiated through pharyngeal receptor contact (swallowing) and controlled by the vagus nerves in connection with the esophageal myenteric plexus
What initiates secondary peristalsis? What controls it?
It is initiated by the distention (due to food bolus) of the esophagus. It is partly controlled by both intrinsic (myenteric) and extrinsic nervous systems
In between swallows, how is regurgitation prevented? How is pressure involved?
Largely prevented through tonic constriction of the UES and LES, which produces greater pressure than their adjacent compartments
What happens to the UES during and after swallowing?
During swallowing, it relaxes, immediately after, it constricts, which prevents air reflux
Relative to peristaltic wave, describe the contraction or relaxation of the orad stomach and LES
What causes the receptive relaxation?
LES and orad stomach relaxes shortly before the peristaltic wave arrives. They constrict after the bolus passes into the FUNDUS in order to prevent acid reflux
Receptive relaxation is mediated by a vagovagal inhibitory reflex due to a release of inhibitory NTs (NO and VIP) from intrinsic nerves
What causes pyrosis (heartburn)
Weak secondary peristalsis, increase in gastric pressure, low LES tone, causing gastric acid reflux
What causes achalasia?
Degeneration of the postganglionic inhibitory neurons (NO/VIP) in the myenteric plexus
Loss of peristalsis, elevated resting LES pressure
Loss of LES relaxation in response to swallowing
What level of pressure is maintained during eating? Why?
Low intragastric pressure is maintained during eating (stomach filling). This minimizes gastric reflux into the esophagus and prevents excessive stomach distention (which leads to vomiting)
What can increase gastric distensibility during the gastric phase of digestion?
Ants such as VIP and NO, as well as GI hormones CCK and gastrin. This increases gastric distensibility during the gastric phase of digestion
Describe gastric content mixing
Contraction begins in the mid-region of the stomach.
As contraction increases in force and velocity, some of the contents are passed over and forced back into the body of the stomach.
Contraction force and velocity are great enough to cause rapid and almost complete closure of the distal antrum.
Before and after this contraction, some of the contents is propelled into the duodenum but most stays in the stomach
During these contractions, there is no gross movement of gastric content
Where do contractions begin in gastric content mixing? Emptying?
Mid-region in mixing
Stomach antrum in emptying
What conditions of the stomach favors gastric emptying?
Increased tone of the orad region of the stomach
Forceful peristaltic contraction of the caudad region of the stomach
Relaxation of the pylorus, absence of segmenting contractions of the duodenum
What are the effects of motilin, somatostatin, and GIP in motility?
Motilin increases contraction of the caudad stomach (increases motility)
Somatostatin and GIP suppress motility
What is the role of pH in relation to gastric emptying?
The lower the gastric pH, the slower the gastric emptying
Greater pyloric sphincter resistance increases or decreases the rate of gastric emptying?
What happened when duodenal pressure is increased?
It decreases the rate of gastric emptying
It slows gastric emptying
If material is present in the small intestine, how is the stomach affected when it comes to parasympathetic and sympathetic responses?
Parasympathetic – decreased
Sympathetic – increases
What can be a result of slow digestion? Rapid?
Slow digestion interrupts flow of nutrients to the body, it may also stimulate excess gastric acid secretion. This results in poor digestion and absorption
Rapid digestion overwhelms the digestive and absorptive capacity of the small intestine. It fails to fully buffer acidic chyme
What can inhibit or stimulate BER waves?
Neural and hormonal controls
Inhibition – epi, VIP, NO, secretin, and glucagon
Stimulation – gastrin, CCK, motilin, and serotonin
What are the complications due to vomiting?
Loss of gastric contents – loss of fluid, H+, and ions (K+), metabolic alkalosis, and hypokalemia
Loss of small intestine – additional loss of ions, fluid, bicarbonates, bile, and metabolic acidosis
Nutritional deficiency, ulceration, weakening of UES, and LES, tooth decay
What is the function of haustrations? How are their contractions in comparison to those in the small intestine?
Mixing, used for segmenting contractions
Contraction is more forceful and longer (12-60 seconds)
It performs mass movements toward the rectum, less frequent but longer duration (20-30 seconds) and distance than SI
What activates the ileocecal reflex? What does it do?
It is activated by the distention of the ileum. It increases the motility of the ileum and relaxes the ileocecal sphincter, allowing chyme to pass from the ileum to the cecum
What activates the colonoileal reflex? What does it do?
It is activated by the distention of the colon. It causes the ileocecal sphincter to contract, preventing the emptying of ileal content into the colon, and providing protection against reflux of colonic contents
What activates the gastroileal reflex? What mediates it? What does it do?
It is activated by a distended stomach. It is mediated by gastrin and CCK. It increases ileal motility and movement through the ileocecal sphincter
Which reflex is responsible for the defecation sensation?
Which reflex stimulates a colonic mass movement?
Duodenalcolic reflex
Gastrocolic reflex and duodenalcolic both augment colonic mass movement
What is relaxed and what is contracted during defecation?
BOTH IAS and EAS are relaxed. This is accompanied by a peristaltic contraction f the rectum and distal colon
Contraction of the chest muscles against a closed glottis and full lungs (valsalva) and contraction of abdominal muscle raise intrathoracic and intra-abdominal pressure and enhances the propulsion of feces
Relaxation of the pelvic floor allows the increased abdominal pressure to force the floor downward. It straightens the rectum and facilitates the passage of feces
When does fasting motor activities occur during fasting?
Where do MMCs originate from?
After about 90 minutes and are associated with MMCs
They originate from the mid-stomach region
What is the difference between phase I, II and II of MMC?
Phase I – no spikes, no contractions
Phase II – irregular spikes and contractions (~50% of slow waves are associated with contractions)
Phase III – bursts of regular spikes and contractions (~100% of SWs are associated with contractions), gastric material is moved to longer distances
What is the character of MMC in the stomach? Where is it initiated?
It is vigorous and prolonged peristaltic wave
It is initiated at the mid-body of stomach and moves distally over the caudad region and through the pylorus
What is the function of MMC?
Clear the stomach of debris between meals. It keeps the SI clean of indigestible meal residua, bacteria, and desquamated cells only during fasting
What happens to the ileocecal sphincter as the MMC approaches?
It relaxes
Is saliva isotonic, hypotonic, or hypertonic?
It is INITIALLY isotonic with neutral pH, then because of electrolyte modification, it becomes HYPOTONIC with pH between 6-7
What is the effect of PSNS and SNS in salivary secretion rate?
What is the difference in the two secretions?
Both increase salivary secretion rate, however, PSNS is dominant
PSNS is watery and causes vasodilation
SNS is viscous and thick, causes vasoconstriction
What is the difference between oxyntic glands and pyloric glands?
Oxyntic – parietal cells (HCl, IF), chief cells (pepsinogen), mucus (mucus)
Pyloric glands – mucus cells (mucus), G cells (gastrin)
What converts pepsinogen to pepsin?
HCl, pH has to be less than 5
How is H+ and HCO3- produced in parietal cells? What enzyme is used?
They are produced from CO2 and water using the enzyme carbonic anhydrase
In the H,K+ ATPases in parietal cells, in which direction does H+ go and in which direction does K+ go?
H+ goes out to the lumen to form HCl
K+ goes inside the parietal cell
In the parietal cell, between gastrin and ACh, which one binds to M3 and which one binds to CCK receptors?
What do they activate?
Gastrin binds to CCK, ACh binds to M3 receptors
Their binding activates the PLC pathway through Gq, which opens calcium channels from the ER
Eventually activates H+/K+ pumps
What receptor does histamine bind to in the parietal cell? What does it activate?
What are its antagonists? Through which pathway
Histamine binds to H2 receptors, which activate the Gs protein, which activates adenylyl cyclase, activating PKA. It eventually activates H+/K+ ATPase
Its antagonists are somatostatin and prostaglandins. Both activate Gi, which inactivates adenylyl cyclase
What secretes somatostatin?
What happens during this cell’s vagal stimulation?
D cells
Vagal stimulation inhibits its release
How does the vagus nerve stimulate parietal cells? G cells?
Directly by releasing ACh and also through ECL cells
Stimulates G cells through GRP, promoting gastrin release
What is the effect of luminal H+ on D cells?
It directly stimulates the D cells to release somatostatin, which inhibits gastrin release from G cells, thereby reducing gastric acid secretion
What is the effect of somatostatin on gastric secretion?
It inhibits gastrin secretion
During which time of day is gastric acid secretion the highest? Lowest?
Lowest in the morning and highest in the evening
In the cephalic phase, what stimulates gastric secretion? Gastric phase? Intestinal phase?
Cephalic – chewing and swallowing, smell, and sight of food
Gastric – mechanically through wall distention, chemically through partially digested protein products in chyme
Intestinal – distention of the intestinal wall, circulating amino acids (major stimulus)
What happens to gastric secretion during the first hour of a meal?
Gastric secretion increases and reaches maximum, pH reaches maximum
How is gastrin secretion affected by low pH?
Low pH inhibits gastrin release, stipulates release of somatostatin, which directly inhibits acid secretion
What stimulates the release of secretin? What is its primary effect?
It is triggered by acidic pH such as HCl in the duodenum. It increases the release of bicarbonate from pancreatic ductal cells and liver
