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Flashcards in GI III & IV Deck (58)

Describe the cephalic phase.

What are stimuli?

Activation of the GI tract in readiness for the meal.

The stimuli are cognitive and include:
Idea of food
Visual stimuli
Auditory stimuli

All of these can trigger responses in the GI system in the absence of food ingestion.


Describe the stimulation for the GI tract to receive and digest food. Start with sensory inputs (smell). What is the response from stimulation?

Sensory inputs (smell) to cortex and hypothalamus

lower pons/upper medulla (Dorsal motor vagal nucleus): cell bodies of vagal preganglionic neurons...

parasympathetic (vagus) stimulation

then salivary secretion increases (via 9th cranial nerve)
gastric secretion increases
pancreatic secretion increases
gallbladder contraction increases
relaxation of sphincter of oddi increases

(need gallbladder to contract- bile comes in
relax oddi- so pancreatic secretion and bile can come in)
salivary - both glossopharyngeal and facial nerves will innervate.


Describe the oral phase.

Many of the responses are same as in Cephalic phase, only difference is – food if present in the mouth.

Additional activation of GI from sensory inputs from taste buds (tongue) and mechanical receptors in the mouth and upper pharynx.

mech. of stimulation similar to cephalic phase

(chemical receptors now activated and mechanical (pressure activated) so additional to cephalic but have all cephalic components as well )


Describe the process of chewing.

Food is mixed with what? Which enzymes?

Does absorption take place in mouth?

What nerves contribute to activating the GI system?

What are some clinical applications?

Breaking of food into small pieces – mechanical disruption.

Mixing of food with enzymes - salivary amylases and lingual lipase (modest digestion in healthy). salivary amylase- inactivated by time reaches stomach bc low pH. can initiate process of carb. digestion. lipase- fat digesting enzyme, can initiate but by time gets to stomach its all inactivated
stomach has some enzymes it can produce

Mixing of food with Salivary Mucin (glycoprotein, lubrication of bolus- helps in chewing, swallowing).

No absorption in mouth except for alcohol and some drugs (clinically relevant).

Enhancement of activation of GI system. (mostly activation of GI system, now bolus coming. most stimulation through Vagus (parasym.) or IX and facial)

In the Clinic: Xerostomia or dry mouth – impaired salivary secretion – congenital or autoimmune. The decrease in secretion reduces pH in the oral cavity – tooth decay, esophageal erosions, difficulty swallowing.


What are the muscles involved in chewing? What innervates them?

What is the muscles' action?

Temporalis (Most Important)
Lateral Pterygoids
Medial Pterygoids

Muscles are innervated by distinct branches (mandibular division) of Trigeminal Nerve

Muscles elevate, protract and retract jaws

In addition, Pterygoids individually move mandible laterally and front-back


Where do secretions in the GI tract come from?

Secretions in the GI tract come from:

The glands associated with the tract:
Salivary glands, pancreas, liver

From the glands formed by the gut wall itself:
Example: Brunner’s glands in the duodenum, all throughout gut wall have glandular structures that secrete mostly mucus and bicarb

Intestinal mucosa itself. - columnar cells, also secrete mucus


What do secretions include?

What initiates secretions? What elicits them?

Secretions include water, electrolytes, protein and humoral agents.

Secretion is initiated by multiple signals associated with meal: chemical, osmotic, mechanical.

Secretions are elicited by secretagogues (any substance that stimulates secretion) acting on secretory cells- work as endocrine, paracrine or neurocrine modulators.


Describe salivary secretion. What are the 3 pairs of major salivary glands?

Considerable stimulation of salivary secretion occurs during the Cephalic and Oral phase of a meal

There are 3 pairs of major salivary glands:
Sublingual (sublingual is smallest)
Additional smaller glands are found in the oral and buccal mucosa.


Describe the types of secretions.

There are two types of secretions:

Serous (water, electrolytes, enzymes) –Parotid glands

Mucous (Mucin glycoprotein) – Sublingual Glands

Mixed – Submandibular Glands


Describe the tubuloalveolar structure of secretory glands in the GI tract.

Acinar: single cell
Acinus: a group of acinar cells
Acini: > 1 acinus

slide 10

structure.. same structure set up in almost all glands of GI tract (except liver)
structure where blind end, sac like structure, acini cells (in case of salivary glands, acini cells are units of secretion. they prod. secretion)
ductal modify but don't really secrete separately ( in pancreas its different)

acini secretion transported by network of tubes, 3 types (intercalated, striated, )


What are the two main anatomical structures by which salivary glands are formed??

acinus (secretory unit)

and a network of collecting ducts that empty the secretory juice into the gut.

Slide 13.

pouch like acinus prod. salivary secretion, then see intercalated striated and excretory and main collecting ducts collects from everyone and pours into oral cavity


What is the acinus?

What do acinar cells produce?

Describe what the initial saliva passes through. How is final saliva produced?

The acinus is the blind end of the branching duct system, lined with acinar cells.

The acinar cells produce initial saliva composed of water, ions, enzymes, mucus.

The initial saliva passes through – intercalated duct – then striated duct – lined with ductal cells.

The ductal cells modify initial saliva and produce final saliva by altering electrolyte concentrations.

Slide 14.

(salivary secretion- one being initial the other being final.. initial secretion is whatever secreted by acini cells as saliva transported through ducts, the ducts can modify salivary secretion.. final product will be final saliva.)


Describe myoepithelial cells. Where are they present? What do they contain? How are they stimulated and what happens when stimulated?

Are present in the acini and intercalated ducts.

These cells contain actin and myosin fibers, which allows them to contract.

When stimulated by neural input, they contract to expel saliva in the forward direction.

line acini cells, can contract and that will move salivary secretion out of cells and into duct.

Slide 15


Describe parotid glands histology and pathology.

What do they secrete?
How are lobule structure separated?

Slide 16.

parotid are largest glands. almost exclusively serous secretion
if stain by hemotoxin

adipose tissue, ducts collecting.. then entire gland, salivary gland covered by dense connective tissue
-divides glands into lobes, septa
box A -interlobular tube, lined by columnar epithelial cells and connective tissue


Describe histology of submandibular gland.

Striations are folding of membranes rich in pumps, ion and fluid transport. Lobular structure.

Slide 18

(mixed of serous and mucous)


Describe histology of sublingual gland.

Lobular structure. Nuclei of mucous cells are darker than serous cells.

sublingual- mucus secreting mostly
if compare histology of parotid gland.. mostly mucus (light staining) sometimes see acini. mostly present as demilunes in cap-like structure

Slide 21


Describe adenoma. Where do they usually occur?

Adenoma. Benign, rapid growth. Surgical. Here (and bottom) patients notice difficulties in swallowing, poor salivation (dry mouth, bad breath, chewing, speaking).
Slide 23

80 percent happens in parotid glands
usually removed by surgery
after removal if returns can become malignant
structure becomes diff, parotid gland but lose serous type of structure
can cause lots of problems bc parotid not properly secreting..

Fluid-filled cavity (trauma, infections, tumors). Swelling in clinics. Surgical procedure.


Describe inflammation. How occurs? How treated?

Inflammation (happens in all types of salivary glands). Injuries, viral and bacterial invasion, and autoimmune. Gland destruction. Antibiotics/surgery.


Describe the main functions of saliva.

How much is produced per day?

Functions of Saliva:
Saliva is produced by the salivary glands at the rate of 1L per day (secretes its own weight).

Functions of saliva are:

Lubrication of ingested food with mucus to aid its movement through the esophagus – salivary mucus is also required for speech. (lubrication- mucin that comes in in salivary secretion so important for mixing food so bolus can move forward.)

Protection: By diluting and buffering of ingested foods. During vomiting it buffers and neutralizes the gastric acid and pepsin that comes to the mouth. It also maintains healthy oral tissue – washes away pathogenic bacteria and contains Lysozyme (enzyme), which lyses bacterial cell walls.

Initial digestion of starches and lipids by salivary enzymes – not a major contribution.


Describe how saliva can protect. 2 ways.

2 ways salivary can protect. brings enzyme that can destroy cell wall of bacteria. use in lab. lysozyme -imp. for bacteria, infectious things coming in w food.
thats why poor salivary secretion can lead to some infection in oral cavity

protection also by vomitting (stimulation for salivary secretion) profuse increase in salivary secretion. volume increased.. reverse peristalsis- high pepsin, high acid..buccal mucosa, and esophageal area has almost no protection against.. so in order to protect secrete saliva (a lot of it) which provides huge volume to dilute out acid and corrosive things also bicarb is there and can partially neutralize the contents


Describe the inorganic composition of saliva.

Inorganic Composition is entirely dependent on the stimulus and rate of salivary flow.
The major components are:
Water, bicarbonate, Na+, K+, Ca++, Mg++ and Cl-
Fluoride can be secreted - this forms the basis of oral fluoride treatment for the prevention of dental caries.


Describe the organic constituents of saliva.

The major Organic Constituents include:
Salivary α-amylase (initiates starch digestion)

Lingual Lipase (important for lipid digestion)

Glycoprotein (mucin forms mucous when hydrated)

Lysozyme (attacks bacterial wall)

Kallikrein (which converts plasma protein into bradykinin, a potent vasodilator).

bradykinin-vasodilator, so during active salivary secretion, have more blood flow so more salivary secretion


Describe the osmolarity of saliva.

In humans, salivary secretion is hypotonic (i.e. has lower osmolarity), has
higher K+ and HCO3- concentrations
lower Na+ and Cl- concentrations.


Describe the 2 step process of formation of saliva.

The first step is the formation of an isotonic plasma-like solution by the acinar cells – known as the primary secretion or initial saliva.

The second step is modification of this plasma-like solution by the ductal cells to produce hypotonic final saliva.

hypotonic secretion.. saliva initially secreted by acini cells- usually isotonic
initial secretion similar to plasma
but second step when transformed to final saliva, that usually becomes hypotonic… dep. on rate its very hypotonic or slightly. but never isotonic. at all flow rates its hypotonic.


Describe the second step of forming final saliva.

What modifies the initial saliva? How?

What transporters are present in the luminal/basolateral membranes.

What is the result of the combined action of all channels?

Is there net absorption or secretion? Of what?

The ductal cells modify initial saliva via complex transport mechanisms.

The luminal membrane here contains three transporters:
Na+-H+ exchange
Cl- - HCO3- exchange
H+-K+ exchange

The basolateral membrane contains the Na+-K+ ATPase and Cl- ion channels.

The combined action of all these results in absorption of Na+ and Cl- and secretion of K+ and HCO3-.

More NaCl is absorbed than KHCO3 is secreted, so there is a net absorption of solute.

Slide 29

The ductal cells are relatively water-impermeable, thus water is not absorbed along with solute.

As indicated earlier, there is net absorption of solute.

The combination of these two makes the final saliva hypotonic.


Describe the effect of flow rate on the composition of saliva.

How does flow rate affect ionic composition? Highest flow rates will final saliva be more or less similar to plasma? At low flow rates?


What is the exception? Why?

The ionic composition of saliva changes with flow rate.

At highest flow rates (4mL/min) the final saliva is almost similar to plasma (or initial secretion).

At the lowest flow rates ( less than 1mL min) the final saliva is most dissimilar to plasma

Exception - HCO3- secretion is selectively stimulated when saliva production is stimulated (e.g. parasympathetic stimulation).


Why is the flow of K different than the other ions?

bc K ion secreted, little higher but not major..

K ion bc secreted, follows opposite profile, starts higher then see decrease (all exchange mech. that work when low secretion rate to really absorb Na and Cl ions and secrete K and bicarb.) don't function fast bc saliva in duct for short time and not enough time to modify the saliva so composition of final saliva is more like initial, will have more Na bc not enough time to be absorbed..more Cl.. less K ion bc it cannot be secreted. bicarb profile doesn't follow that.. Bicarb not going down (exception bc parasym. stimulation that can directly stimulate bicarb secretion)
salivary secretion is hypotonic always. less hypotonic at high rate. more hypotonic at low rate.


Describe control of salivary secretion; neural, hormonal, endocrine?

How is salivary secretion stimulated?

Parasympathetic/sympathetic? Which is dominant?

What will stimulation of salivary cells result in?

Control of salivary secretion is exclusively neural (exception in the GI system- other GI secretions both neural and hormonal).

Salivary secretion is stimulated by both sympathetic and parasympathetic subdivisions of autonomic nervous system, although parasympathetic stimulation is dominant.

There is both parasympathetic and sympathetic innervation of acinar and ductal cells.

Stimulation of salivary cells results in increased saliva production, increased HCO3- and enzyme secretions, and contraction of myoepithelial cells.


Describe parasympathetic innervation of salivary secretion.

What innervated by? What released? What type of receptors? Describe second messenger.

Parasympathetic Innervation: branches of Facial (CN VII) and Glossopharyngeal (CN IX): post-ganglionic neurons release Ach – interacts with muscarinic receptors –production of IP3 and increased intracellular Ca++ - increased saliva secretion.

Slide 33

NOT VAGUS here..salivary is by VII and IX.


Describe sympathetic innervation of salivary secretion.

What innervated by? What released? What type of receptors? Describe second messenger.

Sympathetic Innervation:
originates in thoracic segments T1-T3 - preganglionic nerves synapse in the superior cervical ganglion - postganglionic neurons release NE – interacts with β-adrenergic receptors – production of cAMP - increased saliva secretion

Slide 33


Describe the swallowing reflex.

Swallowing can be initiated voluntarily, and after that it is almost entirely under reflex control.

The Swallowing reflex – propel food from mouth to pharynx – and then to stomach. It inhibits respiration – inhibits food entrance into trachea while swallowing.

reflex control, controlled by swallowing reflex. swallowing reflex regulated by swelling center (medulla and pons area- where vagal nerves and other CN are that are req. for activity)

carry bolus from pharynx through sphincters, through UES, to LES then finally to stomach. many steps will take place, mostly under control of swallowing center until lower end of esophagus when we start vagal supply. before that, its all swallowing center.


Describe the afferent limb of the reflex.

Afferent limb of the reflex – begins when touch receptors near the opening of pharynx are stimulated – sensory impulses transmitted to the swallowing center (in the medulla and lower pons) .

so afferent limb- all touch receptors, toward back of oral cavity, in pharynx, as stop swallowing these stretch receptors get activated, send info to swallowing center, swallowing center is activated. there is coordination to higher centers like respiratory and speech centers. when swallow respiration is stopped briefly. cant breathe and swallow at same time. speak center is inactivated. don't speak when swallow


Describe motor impulses from swallowing center. Where do they go?

Motor impulses from swallowing center travel to the pharynx and upper esophagus (via cranial nerves) and to the remaining esophagus (via vagal motor neurons).

sends efferent info through motor neurons (IX bc upper region of esophagus and pharynx area-no vagus there) regulates activity of muscular activity and w that move bolus forward.


Draw a flow chart of reflex control involving swallowing center..what info does it send out where, from where does it receive info?

Slide 36.

when start swallowing, stretch receptors activated.
swallowing coordinates w respiratory and speaking centers..

pharynx under control of swallowing center
some input of vagus to lower end of esophagus
this coordinated activity makes chyme move forward.


What are the three phases in swallowing?

Describe the 2 openings and how/when they are closed during swallowing.

There are 3 phases in swallowing:
oral, pharyngeal and esophageal.

swallowing, activating swallowing center, main goal to close down 2 diff openings in pharyngeal area. nasopharynx area must be closed (connection toward auditory tube) also trachea is other opening- don't want food to enter there so tracheal opening must be closed so food doesn't go in wrong tube,
soft palate-closes nasopharynx area. moves into pharyngeal area, bolus moves forward see epiglottis and larynx try to close down and close tracheal opening. swallowing most effective when both openings closed totally
v coordinated response.. can try to go into wrong tract, cough so try to move food back to proper place
nasopharynx closed, bolus moves into pharynx area, as tries to go to pharyngeal area, epiglottis closes tracheal opening. now bolus moves toward esophagus…pharynx contracts strongly and moves pharyngeal opening. area behind bolus now closed.

coordination w respiratory center, so respiration stopped but v short response. swallowing is fast. usually swallow in short phases..


Describe the oral phase of swallowing.

Oral phase (voluntary):
This is initiated when tongue forces a bolus of food back towards pharynx - activates stretch receptors - initiates involuntary swallowing reflex.


Describe the pharyngeal phase of swallowing.

Pharyngeal phase (involuntary, less than 1 sec)
The soft palate is pulled upward and palatopharyngeal fold moves inward, creates narrow passage – prevents reflux into nasopharynx, food moves into pharynx.

Epiglottis moves to cover the opening to larynx, larynx moves upward against epiglottis – prevents food entry to trachea. Respiration is inhibited (interactions between respiratory & swallowing centers).


Describe the UES.
When does it relax/contract/why?

The upper esophageal sphincter (UES) relaxes to receive food bolus.

Pharynx contracts, further enhancing the propulsion of food into the esophagus. A peristaltic wave of contraction is initiated, which forces the bolus through the relaxed UES.

After the bolus crosses the UES (pharyngeal phase) the swallowing reflex closes the sphincter – prevents reflux into the pharynx.

swallowing center organizing in esophagus, almost starts esophageal phase, UES not stopped yet.
pharynx as closes down sends info for UES to relax so food has space to enter.
more and more contraction from pharynx..contraction of muscles in pharynx that moves food from pharyngeal area through UES and in esophageal area… wave of peristaltic strong contractions in muscles of pharynx one after another, so peristaltic waves, forces food through UES so enters esophageal area

as soon as bolus crosses UES, closed back again.
pharynx contracts, and same time signal to UES to be open so pharyngeal contractions will move it through UES as soon as crosses UES, UES tonically contracted again and is closed so food cannot go back to pharynx.


Describe the esophageal phase of swallowing. What is it controlled by?

What are the 2 main functions of UES and LES?

Controlled by both swallowing reflex and enteric nervous system.

The esophagus, the UES and the lower esophageal sphincter (LES) serve two main functions:

They propel food from pharynx to stomach.
The sphincters protect the airway from swallowed material. They also protect the esophagus from acidic gastric reflux.

UES and LES - both have propulsive functions. after UES closes, allows movement of bolus to next stage. protective function. usually tonically closed- which guards airway and helps food during swallowing phase so no entry of food into trachea. UES participates in making sure airway protected from swallowing material


What happens if LES is leaky? Can reflux go all way back to trachea?

if gastric material reflux (shouldn’t happen bc LES also tonically closed so gastric contents cant come back to esophagus) if any condition where LES leaky then there could be reflux of gastric contents back into esophagus.. in that condition or case UES is another protection. so gastric material in esophagus but UES doesn't allow those gastric contents to enter the trachea.


Describe esophageal phase of swallowing:

What happens after bolus crosses UES?

Describe the types of contractions and what purpose they serve.

Slide 40.
After the bolus crosses the UES (pharyngeal phase) the swallowing reflex closes the sphincter – prevents reflux into the pharynx.

A primary peristaltic contraction (coordinated by swallowing reflex) occurs, involves a series of coordinated sequential contractions (peristaltic wave) - propels food down the esophagus.

Distension of the esophagus by the moving bolus initiates another wave called secondary peristalsis – (mediated by enteric nervous system) – repetitive secondary peristalsis clears the esophagus of the bolus.

pharyngeal contraction (last box), also have relaxation already in lower esophageal sphincter..same thing happens in stomach next stop after crosses LES, goes to stomach. relaxed bc food is coming and relaxation is req.
after bolus crosses, relaxation of LES, bolus enters, contraction and LES closes back.
propulsive contractions move chyme forward
primary peristaltic contracts not enough to move it into stomach so secondary come in as well (secondary under control of ENS) up until primary peristaltic part we had swallowing center still working. as bolus toward end of esophagus- ENS come in and generate more contractions.


What happens as peristaltic wave and food bolus approach LES?

How does food enter the stomach?

As the peristaltic wave and food bolus approach the LES, the sphincter opens (relaxation) - mediated by peptidergic fibers in the vagus nerve that release VIP.

At the same time the LES relaxes, the orad region of the stomach also relaxes – a phenomenon called receptive relaxation. (not just LES..the proximal part of stomach in close contact to LES also is relaxing.. if stomach didnt relax w it, then food couldn’t go through.)

Receptive relaxation reduces pressure in orad stomach – helps in movement of bolus into stomach.

When bolus enters orad stomach, LES contracts, returns to its high resting tone. At resting tone, the pressure at the sphincter is higher than esophagus or orad stomach.


What is relaxation of LES mediated by?

What happens as soon as food crosses LES and is in stomach? Why?

relaxation of LES is mediated by vagus nerve.. agents we have are peptides, VIP, also have NO as one of relaxing agents. (for relaxation of LES and proximal part of stomach)

as soon as food crosses LES and is in stomach now LES will go back to normally resting tone of being contracted so food cannot go back into the esophagus.


Describe the intraesophageal pressure vs abdominal pressure. What problems does this create?

What are UES and LES doing?

Due to the anatomical position of the esophagus, the intraesophageal pressure is lower than abdominal pressure.

This creates two problems:
Keeping air out at the upper end of esophagus (done by UES).
Keeping gastric acidic contents out at the lower end of esophagus (done by LES).

Both UES and LES are closed, except when food enters esophagus or leaves esophagus.

Increase in intra-abdominal pressure can lead to gastroesophageal reflux.

for most of esophagus =thoracic area which is intrathoracic pressure which usually is less than atmospheric pressure and intraabdominal pressure so there is a lot of push for gastric materials to go back into there bc of the pressure drop and that is guarded against by LES strongly (UES protects against reflex and swallowed material down wrong tube)


What will an increase in intra-abdominal pressure result in? When might this happen?

intra-abdominal pressure can pregnancy intra-abdominal pressure can change, if becomes higher than the LES pressure then LES becomes leaky (why in pregnancy people complain of heart burn)

obesity intra-abdominal pressure also increases and LES can become leaky

Increase in intra-abdominal pressure can lead to gastroesophageal reflux.


Describe the histological features of upper, middle, and lower esophagus.

Slide 45

very well designed… esophagus just transport (no absorption, no secretion) just transports food from oral area to stomach. well designed histology for transport (lots of contraction going on) bolus not changed at all. does not reduce in size any more until stomach

frictional force as bolus tries to move through must be counteracted by esophagus.. see that in mucosal layer of esophagus. also see musculature, see upper part of esophagus. mucosa not that well developed, as go deeper into esophagus see thick mucosal structure

muscular layer-inner circular layer, outer longitudinal and see initially skeletal muscle here.. as go deeper again see skeletal muscle changing toward smooth muscle type.
epithelial cells we see, type of robust epithelial cell structure, skeletal muscle cell structure only see in initial part of esophagus and anal structures..both designed for transportation

initial swallowing voluntary, the skeletal muscles in this area also, under voluntary control. not much glands in esophageal area until goes towards stomach and some glands appear…not a lot of secretion going on so esophagus has to be v robust structure.


Describe the typical mucosal layer. What type of cell? What happens with gastric changes?

Slide 46.
typical mucosal layer - v thick and cell type in here is stratified squamous epithelium. only here we find this and in anal sphincter we find this- to handle frictional force thats happening

there are pathologies related to this. stratified squamous epithelium in gastric changes to simple columnar epithelium.
pathology- esophagus normally should have stratified squamous epithelium

middle portion has mixture-smooth muscle and skeletal as go to next part becomes completely smooth

Mucosa - covered by a thick layer of squamous epithelium (protection from abrasion & friction).


When does gerd occur? Why? How is it treated?

What is absent in patients with this condition?

Conditions that lead to increased intra-abdominal pressure may cause gastroesophageal reflux:
Example pregnancy, morbid obesity

This happens when LES is unable to prevent the gastric acidic contents reflux back into the distal part of the esophagus.

This region of the esophagus does not have robust protection of the mucosal lining. The acid will activate pain fibers – resulting in pain, discomfort – can happen in healthy individuals also.

Long term – continual reflux can damage the esophageal mucosa, which is called GERD.

Treated with
H2 receptor antagonists- e.g. ranitidine to reduce gastric acid secretion
Or proton pump inhibitors – example omeprazole.

if prolonged gird, squamous epithelial cells are v irritated, v sensitive, then change from squamous to simple columnar that we see in stomach
change from squamous to columnar- thats emitplagia?

in more advanced cases simple columnar cells become intestinal type of cells..intestinal have secretory cells (called goblet..mucus producing cells, don't see those in stomach)
that is typical pattern of intestinal epithelial cells. transformation from squamous into intestinal type metaplagia…change further than gastric change to intestinal type- lesion for esophageal malignancy.. doctors careful to not allow gird for prolonged period so less acidity, can’t control LES if too leaky but can suppress acid secretion.

esophageal cardiac glands-secretory cells coming in, all throughout stomach is all diff secretory cells.. all over gastric mucosa. but don't see too much of those in esophageal area

Esophageal cardiac glands (close to stomach) release mucous . Patients with chronic gastroesophageal reflux have the squamous epithelia absent.


What do you call changes from stratified squamous to simple columnar? What about changes to intestinal?

when changes from stratified squamous to simple columnar-we call metaplagia. only when change to intestinal we call intestinal metaplagia (Barrett’s)!


How does pepsin become activated?

Describe the environments of stomach, duodenum, esophagus, how do they handle acidic environment?

LES really guarding gastric contents (gastric contents just have acid, bring in pepsin …secreted as pepsinogen but in acidic environment its converted pepsin-active form of proteolytic enzymes…) secrete all in inactive form -idea is these are proteolytic enzymes, they would chew and destroy cell membrane if syn. in active form.

acidic environment converts to active form.. bringing in lots of activated pepsin. and pepsin activity highest in acidic environment. pH neutral or above then pepsin activity lowered

gastric contents -not just acid, its also pepsin and both are equally corrosive

not different in case of duodenum, next segment that comes after the stomach.. gastric contents (both pepsin and high acidity) but duodenum has protection (stimulates pancreas to release a lot of bicarb that neutralize) as pH goes up, pepsin activity low.

problem in duodenum only happens if pancreatic secretion not functioning properly so cant neutralize it properly or gastric contents emptying too fast nd cant handle it.

duodenum controls gastric emptying. not fast process. little emptying then closes, duodenum handles it, then moves forward


What happens if pyloric sphincter not functioning properly?

How do you treat?

pyloric area- at end of stomach, pyloric sphincter not functioning then problem w duodenal acidity
normal is have a little gastric reflux. LONG term is Gerd. 2 main therapeutic approaches

H2 receptor blocking only blocking one access so gastric secretion can still go on (there are many accesses)
proton pump more complete inhibition of gastric acid secretion


Describe hiatal hernia.

What happens anatomically? Why?

What are major symptoms?

What can be common causes?

Upper portion of stomach protrudes into the chest cavity through an opening of the diaphragm called the esophageal hiatus. This opening usually is large enough to accommodate the esophagus alone.

With muscle weakening and enlargement however, the opening (or herniation) can allow upward passage or even entrapment of the upper stomach above the diaphragm.

Pain, acid reflux (heartburn) are the major symptoms. The LES no longer works properly.

Genetic predisposition, obesity, weight lifting, and constipation appear to be common causes of hiatal hernia.

It is estimated that 60% of the population over 60 years of age has some degree of hiatal hernia.

esophageal hiatus-small opening in diaphragm for esophagus to go through
in people if muscles don't work properly/weakened, hiatus size increases and stomach proximal part tries to escape and go beyond diaphragm and gets trapped in that region..then LES doesn't work properly. so symptoms same as see in GERD (problem w reflex, heartburn, can become GERD)
usually surgery… or proton pump inhibitor and H2 receptor inhibitor.


What is achalasia?

What are common symptoms? What is the treatment?

The SMOOTH MUSCLE LAYER of esophagus does not have normal peristalsis and the LES does not relax normally in response to swallowing.

Dysphagia, regurgitation, chest pain are common symptoms.

Treatment is surgical (myotomy along esophagus). Meanwhile patients must be treated with Ca2+ channel blockers, BOTOX injection in the LES, and other muscle relaxants.


In achalasia a major problem is that LES doesn't work properly. Describe what is going on.

Where does pain come from? Describe how to treat the pain.

major problem is LES doesn't work properly so has to be relaxation of LES that starts right from where pharynx contracts. pharynx contract, UES opens at same time, and LES opens at that time. in those patients, that coordination is gone. in these patients LES is tonically contracted.
peristaltic movements but cannot move through LES… if LES doesn't open then you can’t swallow properly. regurgitation.. chest pain, all common symptoms. usually bc of damage of nerve plexus in myenteric plexus.. surgery is usually only procedure that can help. usually after surgery they’re okay.. at that time if for temporary relief given atropin-inhibitor of muscarinic receptors (ach binding muscarinic receptors)

2 things happening…LES not opening so food no place to go, so food in esophageal area, extenstion of esophageal smooth muscle, stimulate pain receptors so pain coming from smooth muscle on esophageal wall. these have ach-muscarinic receptors. if inhibit those then pain sensation will be gone and relief from pain. problem of LES- not relaxing bc nerve is damaged and VIP and NO needed to relax it is not coming. also sometimes LES tonically constricted, usually under control of ach-muscarinic receptors, so the atrophine can help open up LES in some patients too ( in cases it doesn't help the myenteric plexus damaged to such an extent that those receptors not available either)
if atropine works on relieving pain that would mean that the smooth muscle muscarinic receptors are functional so pain gone but still cannot swallow bc LES did not respond.. so LES prob lost muscarinic receptors-myenteric plexus damaged to that extent


Describe vomiting. What are common causes?

Mouth ejection of gastric or gastroduodenal contents.

Preceded by nausea, irregular heartbeat, dizziness, sweating, retching, etc..

Causes of Vomiting:
Tactile: stimulation of back of throat

Irritation/distension of stomach and duodenum

Elevated intracranial pressure (e.g. cerebral hemorrhage)

Rotation/acceleration of the head (e.g. motion sickness)

Intense pain

Chemical agents (e.g. emetics): act on upper portions of the GI tract or on specialized chemoreceptors in the brain

Emotional factors.


Describe the vomiting reflex, vomiting center, vomiting act.

Vomiting center (reticular formation in pons): integration of sensory inputs and coordination of vomiting act.

Vomiting act: reverse peristalsis of small intestine, relaxation of pyloric sphincter and stomach (to receive intestinal contents). Forced inspiration (against closed glottis) decreases intra-thoracic pressure and increases intra-abdominal pressure.

Forceful contraction of abdominal muscles increasing intra-abdominal pressure. Relaxation of esophagus, both UES and LES and contraction of pylorus and antrum facilitate expulsion of intestinal contents.

Autonomic discharge - salivation, dilation of pupils, sweating, pallor, rapid and irregular heart beat.


Describe UES and what is happening during retching.

In retching, the UES remains closed, gastric content is forced into esophagus but does not enter pharynx; often precedes vomiting.

retching.. UES still closed. in case of retching, UES not relaxed yet.. so haven’t thrown out yet.
saliva secretion goes up to neutralize and dilute gastric contents.


Describe sphincter activity during vomiting.

sphincter guarding between stomach and intestine- pyloric sphincter usually case of vomiting see pyloric sphincter will be relaxed, allows intestinal contents to enter into stomach and there will be increase in intra-abdominal pressure, then intra-ab. muscles contract. so forward moving peristalsis UES and all contracted.. remaining part of esophagus and LES contracted. now complete reverse and all is relaxed so passage free. UES, esophagus, LES, and proximal part of stomach all relaxed

increase in pressure in intra-abdominal area by abdominal muscles increases pressure in distal area so it contracts and moves everything up toward reverse peristalsis