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LO 1

Anathomy, Histology, and


biochemicals from upper
GASTROINTESTINAL TRACT

• Mouth
• Esophagus
• Gaster UPPER
GASTROINTESTINAL
• Duodenum TRACT:

• Treitz ligament
• Jejunum LOWER
• Ileum GASTROINTESTINAL
TRACT:
• Colon
• Anus
Anatomy of Abdomen

Upper GI Tract

Lower GI Tract
MOUTH
Esophagus
• The largest part of thorax
• Pars thoracalis (behind trachea)
• Pars abdominalis : enter to the gastric cardia ventriculi
• transition  ostium cardiacum/ cardiac orificium/ junctio gastroesophagei
• It has LES and its function for preventing reflux
• The closing of spincter is controlled by vagal and amplified by gastrin ,and
decreased by secretin response, cholecystokinin, glucacon
• vascularitation:
– a. gastrica sinistra
– Cabang a. phrenica inferior
– V. azygos
– V. gastrica sinistra
• nerves : N. vagus (parasimpatis), N. splanchnici (simpatis)
Small Intestine
• Small intestine comprises the duodenum,
jejunum, and ileum .
Hepar
HISTOLOGY OF UPPER GIT
Labium Oris / Lips
• 3 layers:
–Pars cutanea/outer layer:
–Pars Intermedia/Vermillion border: A
–Pars oral mucosa: B
Pars cutanea
1. Stratified keratinizing squamous cell epithelium
2. Hair follicle with sebaceous and sweat glands
3. Orbicularis oris muscle
Pars intermedia (A)
Pars oral mucosa (B)
1. Stratified nonkeratinizing squamous cell epithelium
2. Tunica propria
a. Labialis glands
3. Orbicularis oris muscle
4. Labialis artery
5. Small chorium
Tongue/Lingua
• There are 3 forms of papillae:
–Circumvalata papillae
–Filiform papillae
–Fungiform papillae
Circumvalata Papillae
A. Circumvalata papillae:
1. Secondary papillae
2. Taste bud
B. Ebneri glands
Filiriform (A) and Fungiform Papillae (B)
Teeth
1. Dental cement
a. Sharpey’s fiber
2. Tomes granular layer
3. Dentine + dentine canals
ESOPHAGUS
GASTER
Duodenum
A. T. mucosae
1. Vili
2. Columnar surface epithelium +
goblet cell
3. Crypt/of lieberkuhn
4. T.M. Mucosae
B. T. submucosae
C. T.muscularis
BIOCHEMISTRY OF UPPER GIT
The Digestive Enzymes
Digestive enzymes are enzymes which help break down food
substances into forms that can be absorbed and assimilated by
the body.
Digestive enzymes are normally secreted :
1) in the mouth (as part of the saliva),
2) by the stomach
3) released into the small intestines from the liver and pancreas.
The major enzymes are:
• Amylase, also called ptyalin, is an enzyme that aids the
breakdown of starches. It is secreted in the saliva and the
pancreatic juices.
• Mycozyme is an enzyme that also digests starches.
• Lipase, secreted by the pancreas, refers to any of several enzymes
that increase the breakdown of fats (lipids).
• Protease, an enzyme that helps the breakdown of protein, is also secreted by the
pancreas. Enzymes that breakdown protein are known as a proteolytic enzymes.
• Pepsin is an enzyme released in the stomach that also helps with the breakdown
of protein.
• Pancreatin refers to pancreatic enzymes. Pancreatin is often obtained from cows
or pigs and used as a dietary supplement.
• Bile, also called gall, is a bitter, yellow-green secretion of the liver, stored in the
gallbladder, and released during digestion when fats enter the first part of the
small intestine (duodenum). Bile emulsifies fats preparing them for further
digestion and absorption in the small intestine.
• Cellulase is an enzyme that breaks down cellulose, the carbohydrate that is the
main part of the cell walls of plants. Cellulose is non-digestible by humans
because we do not produce the enzyme cellulase. Cellulase is produced by
grazing animals such as cows (with the aid of the beneficial bacteria that reside
in the animal's digestive tract), and is the reason why they can get nutrition from
plants such as grasses. The human body does not produce cellulase, however, it
is sometimes included in enzyme supplements since it can help us break down
the cell walls of plants better, thereby getting the most nutrition from the herbs
and other plants that we eat.
Function or
Source Enzim Activator Substrat
katalitik product

Hidrolisis bond 1:4


@-Amilase Flour @; produce dextrin
Saliva gland Cl-
Saliva essence @limit, maltotriosa,
and maltosa

Lipid acid plus 1,2


Lingual gland Lingual lipase Trigliserida
- diasilgliserol

Decompose
Pepsin
Protein and peptida chain
(pepsinogen)
polipeptida which closer with
aromatic amino
Gaster Hcl-
acid
Gaster lipase
Trigliserida Lipid acid and
gliserol
Function and catalitic
Source Enzim Activator Substrat
produce

Decompose peptida bond


Pancreas Tripsin Enteropeptida Proein and
to karboksil various amino
eksocrine (tripsinogen) se polipeptida
acid basic (arginin or lisin)

Proein and Decompose peptida chain


Kemotripsin Tripsin polipeptida to karboksil aromatic acid
amino
Elastin other
Decompose karboksil
Elastase Tripsin protein
amino acid alifatik chain

Decompose karboksil
Proein and
Karboksipept teminal acid amino chain
Tripsin polipeptida
idase A which aromatic chain or
bifurcate alifatik

Proein and Decompose karboksil


Karboksipept
Tripsin polipeptida terminal acid amino chain
idase B
which alkali chain
Kolipase Tripsin Lipid items To open a part of active
lipase pancreas

Pancreas Trigliserida Monogiserida and fatty acid


Lipase

Lipase Choesteril ester Cholesterol

Ester Cholesteril ester Cholesterol


Kolesteril
hidrolase

Panckreas Cl- Starch @-amilase saliva


@-amilase

Ribonukleas RNA Nukleotida


e
Deoksiribonu DNA Nukleotida
klease

Fosfolipase Tripsin Phosfolipid Fatty acid and lisophosfolipid


A2
Function and katalitik
Source Enzim Activator Substrat
produce

Small intest
Enteropeptidase Tripsinogen Tripsin
mucous

Decompose to amino chain


Aminopeptidase Polipeptida acid amino terminal from
peptide
Decompose to amino chain
acid amino terminal from
Karboksipeptidase Polipeptida
peptide

Decompose to residue
Endopeptidase Polipeptida
between middle of peptide

Dipeptidase Dipeptida 2 amino acid

Maltosa,
Maltase maltotriosa, Glucose
Function and
Source Enzim Activator Substrat katalitik
produce

Small intest Galaktosa and


Laktase Laktosa
mucous glucose

Sukosa; maltotriosa Fruktosa and


Sukrase*
and maltosa glucose

@-dekstrin, maltosa,
@-Dekstrinase* Glucose
maltotriosa

Threhalase Trehalosa Glucose

Nuklease and Pentosa,purin


Nukleat acid
other enzims and pirimidin

Cytoplasma Various Di,tri, and


Amino acid
cell mucous peptidase tetrapeptida
Organ
Hormon Sasaran Fungsi

Motility control, support absorption


Exocrine glands
and digestion process
Stomach Gastrin and smooth
muscle

Sekretin,
Digestive tract, Motility control, support absorption
kolesistokinin,
Duodenum pancreas, liver, and digestion process
gastric inhibitor,
vesica velea
peptide

Bones, Soft
Liver Somatomedin Growth trigger
Tissues

-Insulin (B cell) Almost all cell


Supporting absorption, using and
saving nutrients by cell for maintain
nutrient level after absorption phase
Pancreas; -Glukagon Almost all cell
Inhibit digestion and absorption
langerhans (sel A)
island
-Somastatine Digestive system
Inhibit all pancreatic hormones
(sel D) Pancreatic cell;
secretion
langerhans island
Gastric Acid Production
1. CO2 and Cl- diffuse from blood into the stomach cell

2. CO2 combined with H2O to form H2CO3

3. H2CO3 dissociates into bicarbonat (HCO3-) and H+

4. H+ combines with Cl- in duct of gastric gland to form HCl

5. An ATP pump is necessary to pump the HCl into the duct since
the concentration of HCl is about million times more
concentrated in the duct
Digestion and Absorption
• The diet must provide metabolic fuels :
– Mainly carbohydrates and lipids
– protein (for growth and turnover of tissue proteins)
– fiber (for bulk in the intestinal lumen)
– minerals ( containing elements with spesific
metabolic functions)
– vitamins and essential fatty acids (organic
compounds needed in smaller amounts for other
metabolic and phsiologic functions)
A = SGLT 1 transported protein KH
B = GLUT 5 Na+ independent facilitative
transporter
C = GLUT 2 facilitative transporter Starch/ polysaccharide

α amylase of saliva
α amylase of pancreas
Laktosa Sukrosa
Maltosa

Laktose Thelase Sukrose

Glucosa and Glucosa and


Glucosa and
Galactosa Glucosa
Fructosa

Glucosa
Galactosa Fructosa
A
Intestinal
epithelium B
C
Capiller
Exogen of
protein Endogen
(from food) of protein

Pepsin in stomach
Proteolityc enzimes of pancreas

Small
Amino acid
Peptide
Aminopeptides
Dipeptides
Dipeptides
Tripeptides
Amino acid

Capiller
Fat TAG
bile salt

Lipase of pancreas hydrolyzed

MAG FFA

Micelle
TG

Chylomicron

Centre of Lacteal Capiller


• Minerals
– Macrominerals and trace elements are mainly absorbed from the
small intestine, but the large intestine may also take part in the
absorption processes.
– Active calcium absorption is subjected to regulatory mechanisms
that are mediated by vitamin D, parathyroid hormone and
calcitonin.
– Phosphorus is less well studied and seems to be regulated by
similar mechanisms.
– Magnesium is absorbed without homeostatic regulation so that
the blood magnesium levels have a higher variation.
– Sodium, potassium and chloride are mainly absorbed in the small
intestine and the absorption rates normally exceed 90 per cent.
– The absorption rates of zinc, iron and manganese are subjected to
regulatory mechanisms. Active transport systems have been
demonstrated for manganese and copper. Other elements are
absorbed by passive diffusion.
• Vitamins
– Lipid-soluble vitamins (A, D, E and K) are
dissolved in mixed micelles, and passively
absorbed across the MVM.
– Water-soluble vitamins, most notably B
vitamins, are absorbed by passive diffusion,
facilitated transport or active transport.
IRON

Intestinal lumen Duodenal mucosal cell Capiller

Heme transporter
Transferrin
Heme Heme Fe3+

Heme
oxygenase Ferroporin

Fe2+ Fe2+ Fe2+ Fe3+

(-) (+)

Fe3+ Fe3+ Apotransferrin


LO 2

Physiology of swallowing
PHYSIOLOGY
Physiology - Digestive System
• The functions of the digestive system are:
– Ingestion - eating food
– Digestion - breakdown of the food
– Absorption - extraction of nutrients from the food
– Defecation - removal of waste products
• The digestive system is a group of organs that breakdown
the chemical components of food, with digestive juices,
into micromolecul nutrients which can be absorbed to
generate energy for the body
The bucal cavity (mouth) and salivary glands

• Food enters the mouth and is chewed by the


teeth, turned over and mixed with saliva by the
tongue.
• Mouth: the salivary glands. Saliva produced by
these glands contains an enzyme that begins to
digest the starch from food into smaller
molecules  ptyalin enzyme
The Stomach
• It is the widest part of the alimentary canal and acts as a reservoir
for the food where it may remain for between 2 and 6 hours.
• Here the food is churned over and mixed with various hormones,
enzymes including pepsinogen which begins the digestion of
protein, hydrochloric acid, and other chemicals
• The stomach has an average capacity of 1 liter, varies in shape,
and is capable of considerable distension.
• At regular intervals a circular muscle at the lower end of the
stomach, the pylorus opens allowing small amounts of food, now
known as chyme to enter the small intestine.
Duodenum
Small Intestine
• The small intestine measures about 7m in an average
adult and consists of the duodenum, jejunum, and ileum.

• Both the bile and pancreatic ducts open into the


duodenum together.

• The small intestine, because of its structure, provides a


vast lining through which further absorption takes place.
LO 3
Explain difficulty of swallowing
( Dysphagia & Odynophagia, Oral
Candidiasis, Chest Pain, Heart Burn,
Regurgitation )
Physiology
• The lower esophageal sphincter (LES) must have a normal
length and pressure and a normal number of episodes of
transient relaxation (relaxation in the absence of swallowing).

• The gastroesophageal junction must be located in the


abdomen so that the diaphragmatic crura can assist the action
of the LES, thus functioning as an extrinsic sphincter. The
presence of a hiatal hernia disrupts this synergistic action and
can promote reflux (see image below).
Physiology
• Esophageal clearance
must be able to neutralize
the acid refluxed through
the LES. (Mechanical
clearance is achieved with
esophageal peristalsis.
Chemical clearance is
achieved with saliva.)
• The stomach must empty
properly.

Barium swallow indicating hiatal hernia.


Definition

• Gastroesophageal reflux disease, commonly referred to as


GERD or acid reflux, is a condition in which the liquid content
of the stomach regurgitates (backs up or refluxes) into the
esophagus. The liquid can inflame and damage the lining of
the esophagus although visible signs of inflammation occur in
a minority of patients
• The regurgitated liquid usually contains acid and pepsin that
are produced by the stomach. The refluxed liquid also may
contain bile that has backed-up into the stomach from the
duodenum.
• Acid is believed to be the most injurious component of the
refluxed liquid. Pepsin and bile also may injure the esophagus,
but their role in the production of esophageal inflammation
and damage is not as clear as the role of acid.
Risk factor
• Obesity
• Hiatal hernia
• Pregnancy
• Smoking
• Dry mouth
• Asthma
• Diabetes
• Delayed stomach emptying
• Connective tissue disorders, such as scleroderma
• Zollinger-Ellison syndrome
• Apart from incompetent barriers, gastric
contents are most likely to reflux :
– When gastric volume is increased

– When gastric contents are near the


gastroesophageal junction

– When gastric pressure is increased


Pathophysiology
However, if this valve relaxes abnormally or weakens 
stomach acid can flow back up into esophagus heartburn 
acid can irritate the lining of esophagus inflamed
(esophagitis).  can erode the esophagus bleeding or
breathing problems.
Pathophysiology
• A functional (frequent transient LES relaxation) or mechanical
(hypotensive LES) problem of the LES is the most common
cause of gastroesophageal reflux disease (GERD).
• Certain foods (eg, coffee, alcohol), medications (eg, calcium
channel blockers, nitrates, beta-blockers), or hormones (eg,
progesterone) can decrease the pressure of the LES.
• Obesity is a contributing factor in gastroesophageal reflux
disease (GERD), probably because of the increased intra-
abdominal pressure.
Complication
• Narrowing of the esophagus (esophageal stricture). Damage to
cells in the lower esophagus from acid exposure leads to formation
of scar tissue. The scar tissue narrows the food pathway, causing
difficulty swallowing.

• An open sore in the esophagus (esophageal ulcer). Stomach acid


can severely erode tissues in the esophagus, causing an open sore
to form. The esophageal ulcer may bleed, cause pain and make
swallowing difficult.

• Precancerous changes to the esophagus (Barrett's esophagus). In


Barrett's esophagus, the color and composition of the tissue lining
the lower esophagus change. These changes are associated with an
increased risk of esophageal cancer. The risk of cancer is low, but
your doctor will recommend regular endoscopy exams to look for
early warning signs of esophageal cancer.
Diagnose
An X-ray of upper digestive system.
• Sometimes called a barium swallow or upper GI series, this procedure
involves drinking a chalky liquid that coats and fills the hollows of
digestive tract.
• Then X-rays are taken of upper digestive tract.

Endoscopy

A test to monitor the amount of acid in esophagus.


• Ambulatory acid (pH) probe tests use an acid-measuring device to identify
when, and for how long, stomach acid regurgitates into esophagus.

A test to measure the movement of the esophagus.


• Esophageal impedance measures movement and pressure in the
esophagus.
Treatment and drug
• Antacids that neutralize stomach acid. Antacids, such as Maalox, Mylanta, Gelusil,
Rolaids and Tums, may provide quick relief. But antacids alone won't heal an
inflamed esophagus damaged by stomach acid. Overuse of some antacids can cause
side effects such as diarrhea or constipation.
• Medications to reduce acid production. Called H2 receptor blockers, these
medications include cimetidine (Tagamet HB), famotidine (Pepcid AC), nizatidine
(Axid AR) or ranitidine (Zantac 75). H2 receptor blockers don't act as quickly as
antacids, but they provide longer relief. Stronger versions of these medications are
available in prescription form.
• Medications that block acid production and heal the esophagus. Proton pump
inhibitors block acid production and allow time for damaged esophageal tissue to
heal. Over-the-counter proton pump inhibitors include lansoprazole (Prevacid 24 HR)
and omeprazole (Prilosec OTC).
Heartburn
• Heartburn or pyrosis, is characterized by burning retrosternal
discomfort that may move up and down the chest like a wave.
• Heartburn is characteristic symptom of reflux esophagitis and
may be associated with regurgitation or a feeling of warm
fluid climbing up the throat.
• Heartburn is produced by heightened mucosal sensitivity and
can be reproduced by infusion or dilute HCl or neutral
hyperosmolar solutions into the esophagus.

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