Download Physiology of Digestion

Physiology
of Digestion
Dr. Yudi Herlambang
Prof dr Abdul Majid
Dr Nura
Nuraiza Meutia
Department of Physiology
School of Medicine
University of Sumatera Utara
Nutrient
Assimilated
Digestive
system
Food
Non Nutrient
P
F
Eliminated
D
S
Activity necessary:
Motility
Secretion
Digestion
Absorption
P
F
D
S
Activity necessary:
Motility
Movement of food through tract ,includes ingestion,
mastication (chewing food and mixing with saliva),
deglutition (swallowing) and peristalsis (rhythmic
contractions along GI tract that propel food)
muscular contraction.
Secretion
•Endocrine (secretion of hormones that regulate
digestive process)
•Exocrine (secretion of water, enzymes, acid,
bicarbonate, into GI tract enzyme & other digestive
juices.
Digestion
Hydrolysis reactions that break ingested polymers (large
molecules) into their smaller subunits (monomers) breakdown of substances.
– proteins into amino acids
– fats into glycerol and free fatty acids
– complex sugars into monosaccharides
Absorption
Transfer of monomer subunits across wall of small
intestine into blood or lymph
transport modified nutrients.
Histology of the Alimentary Canal
Figure 23.6
Regulation;;
Regulation
N
• There are two ‘nerve nets’ (plexuses) in GI tract that
contain neurons and interneurons
– sub mucosal (Meissner)
– Myenteric (Auerbach)
• Plexuses = brain of the gut
– stimulated by stretch (bolus of food), chemicals, and
stomach content (local stimuli)
• Activity of plexuses can be modified by central
nervous system and the autonomic nervous system
• Neural regulation via autonomic nervous system
– GI tract receives both sympathetic and
parasympathetic innervations
• Parasympathetic via vagus nerve and spinal nerves
in sacral region (to lower portion of large intestine)
→ stimulates motility and secretion; favors digestion
• Sympathetic
→ reduces motility and secretory activity and
stimulates sphincter contraction
H
.
• Paracrine regulation
– production of hormonehormone-like molecules that are
produced in one cell and travel through
interstitial fluid (not bloodstream) to affect
activity of nearby cells
• Hormone regulation
– production of hormones that are released into
the bloodstream and carried to target tissues
within digestive system where they affect
digestive activity
Nervous Control of the GI Tract
Figure 23.4
Components of Digestive System
• Organs of GI tract include:
– oral (buccal) cavity (mouth) and pharynx
– esophagus
– stomach
– small and large intestine
– rectum and anus.
• Accessory digestive organs include:
– teeth, tongue, and salivary glands
– liver and gall bladder
– pancreas
4 layers of the GIT wall
1. Tunica Mucosa:
•Epithelial lining cells
•Lamina propria:
loose connective tissue.
blood & lymph vessel.
immune system cells (macrophage,
lymphoid tissue, lymphocytes, IgA,
IgM)
•Muscularis mucosae
inner circular fibers.
outer longitudinal fibers.
•Villi.
•Microvilli.
2. Tunica Submucosa:
•Blood & lymphatic vessels
•Nerve plexus (enteric nervous system)
submucosal nerve plexus (Meissner)
control secretion in the GIT
control motility o/t villi
3. Tunica Muscularis:
• Innermost circular layer Ø intestinal lumen.
• Myenteric nerve plexus (Auerbach)
control of motility.
• Outer longitudinal layer shorten the tube
4. Tunica serosa (adventitia):
• Outermost layer.
layer.
• Larger nerves & blood vessels travel in a bed of
connective & adipose tissue.
Mouth:
Salivary Glands
• Terdiri dari 3 pasang extrinsic glands : parotid,
submandibular, dan sublingual
• Ditambah Intrinsic salivary glands (buccal
glands) : tersebar di mucosa oral.
Mouth:
Teeth
–
–
grind and tear food into smaller pieces
increases surface area upon which digestive enzymes work
Salivary glands
(parotid, submaxillary, sublingual)
parotid gland
secrete saliva
parotid duct
sublingual gland
lubricates and softens food; submandibular
gland
aids in swallowing
contains amylase = enzyme
that begins breakdown of
carbohydrates
SALIVARY GLANDS
Sympathetic and parasympathetic responses are not antagonistic
1. Parasympathetic system has the dominant role - continuous
2. Increased parasympathetic stimulation produces a watery saliva
rich in enzymes
3. Increased sympathetic stimulation produces a smaller volume of
thick saliva rich in mucus inhibits secretion (dry mouth when
nervous)
NB Salivary secretion is the only digestive secretion
completely under neural control
CONTROL OF SALIVARY SECRETION
cerebral cortex
salivary centre
in medulla
pressure receptors
and chemoreceptors
in the mouth
simple
reflex
other inputs
Conditioned reflex
autonomic nerves
salivary glands
↑ salivary secretion
Oropharynx
To convey food
into the
esophagus.
Important role in
swallowing.
Pharynx = throat
Cavity at back of mouth opening to
both esophagus (digestive tract)
and trachea (windpipe)
Voluntary raising of larynx to close
(epi)glottis and prevent food entry
into windpipe
Esophagus.
Hollow muscular tube
connecting pharynx and
stomach.
Bounded by sphincters.
Lined w/ stratified squamous
epithelium.
Disorder o/t LES tone major cause esophageal reflux
heart burn.(GERD)
Stomach wall
S
D
• Stomach:
– Temporary stores ingested food. sphincters prevent
backward flow of materials into esophagus and regulate
release of stomach contents into small intestine
– Churn, mixes food with gastric juice.
– Mechanical and chemical breakdown of ingested material
– Produces, mucus, HCl and pepsinogen.
– HCl converts pepsinogen into pepsin.
– Sterilization of stomach contents by acid
– Pepsin digests proteins into peptide fragments.
– Absorbs some water, alkohol, glucose.
– Binds vit. B12 allows abs. in ileum
• Pada Epitel
terdapat Goblet
cells yang
manghasilkan
lapisan mukus
alkalin .
• Pada Gastric pits
terdapat gastric
glands yang
mensekresi
gastric juice,
mukus, dan
gastrin
Variety of secretory cells :
– Mucous neck cells : acid
mucus
– Parietal cells : HCl dan
intrinsic factor
– Chief cells : pepsinogen
– Enteroendocrine cells :
gastrin, histamine,
endorphins, serotonin,
cholecystokinin (CCK), dan
somatostatin ke lamina
propria
HCl
Gastrin
Histamin
Pepsinogen
Regulation of Gastric Secretion
• Pengeluaran cairan lambung diatur oleh mekanisme
neural dan hormonal .
• Proses stimulasi atau inhibisi berlangsung
dalam 3 fase :
– Cephalic (reflex) phase: sebelum makanan masuk
– Gastric phase: ketika makanan masuk ke lambung
– Intestinal phase: ketika sebagian dari makanan
yang sudah dicerna masuk ke duodenum
1.Cephalic Phase
• Hal yang dapat merangsang :
– Melihat atau memikirkan makanan
– Stimulasi reseptor pengecap atau penghidu
• Hal yang dapat menghambat :
– Depresi atau hilang nafsu makan
– Penurunan stimulasi parasimpatetik
Figure 24.15a
2.Gastric Phase
• Hal yang dapat merangsang :
– Stomach distension
– Activation of stretch receptors (neural activation)
– Activation of chemoreceptors by peptides, caffeine,
and rising pH
– Release of gastrin to the blood
• Hal yang dapat menghambat :
– A pH lower than 2
– Emotional upset that overrides the parasympathetic
division
Figure 24.15b
3. Intestinal Phase
• Excitatory phase : low pH(keasaman
meningkat); makanan yg sebagian telah
dicerna memasuki duodenum dan mendorong
/mengaktifkan kelenjar di lambung.
• Inhibitory phase : distensi duodenum, adanya
lipid, acidic, atau kimus hipertonik, dan bahan
iritan di duodenum
(Initiates inhibition of local reflexes and vagal nuclei)
(Closes the pyloric sphincter)
(Releases enterogastrones that inhibit gastric
secretion
Figure 24.15c
Gerakan Lambung
Gastric Contractile Activity
• Peristaltic waves move toward the pylorus at
the rate of 3 per minute
• This basic electrical rhythm (BER) is initiated
by pacemaker cells (cells of Cajal)
• Most vigorous peristalsis and mixing occurs
near the pylorus
• Chyme is either:
– Delivered in small amounts to the duodenum or
– Forced backward into the stomach for further
mixing
Gastric Contractile Activity
Figure 23.18
Regulation of Gastric Emptying
• Gastric emptying is regulated by:
– The neural enterogastric reflex
– Hormonal (enterogastrone) mechanisms
• These mechanisms inhibit gastric secretion
and duodenal filling
• Carbohydrate-rich chyme quickly moves
through the duodenum
• Fat-laden chyme is digested more slowly
causing food to remain in the stomach longer
Regulation and Mechanism of HCl Secretion
• Sekresi HCl distimulasi oleh ACh, histamine,
dan gastrin melalui sistem secondmessenger
• Release of hydrochloric acid:
– Is low if only one ligand binds to parietal cells
– Is high if all three ligands bind to parietal cells
• Antihistamines block H2 receptors and
decrease HCl release
Regulation and
Mechanism of HCl
Secretion
Figure 23.17
Hormones Released During the Intestinal Phase
When acidic chyme arrives, hormones are released by
the duodenum.
1. Secretin
• stimulates pancreas to secrete bicarbonate ions
that neutralise stomach acid
• inhibits gastric secretion and motility of stomach
2. Cholecystokinin (CCK)
• stimulates production / release of pancreatic enzymes
• stimulates bile release from gallbladder
• inhibits gastric secretion and motility of stomach
Digestion in the stomach
• CHO digestion is halted because acidic pH of the
•
•
stomach inactivates salivary amylase
Little fat digestion occurs in the stomach
Protein digestion begins in the stomach
– Involves mechanical breakdown of proteins by the
churning actions of the stomach
– Involves the chemical digestion of proteins by acid and
hormones
• Gastric (stomach) acid = hydrochloric acid (HCl)
• Pepsin
Protein Digestion in the Stomach
• Parietal cells
– secrete acid (hydrochloric acid = HCL) & intrinsic
factor
– stimulated to produce acid by gastrin
• Chief cells
– secrete pepsinogen & gastric lipase
• Pepsinogen = inactive hormone
• Pepsinogen converted to pepsin (active hormone) by
•
acidic pH of the stomach
Pepsin breaks large proteins down into smaller peptides
Protein Digestion in the Stomach
• G cells
– Secrete gastrin
– Gastrin = hormone
• target tissues = chief cells and parietal cells in stomach
• stimulates gastric juice production
– HCL from parietal cells
– Pepsinogen from chief cells
• Decreases pH of stomach
– Promotes conversion of pepsinogen to pepsin
– It also activates gastroileal reflex which moves
chyme from ileum to colon
– Parasympathetic stimulation releases gastrin
releasing peptide (GRP), which stimulates G cell
release of gastrin
–
Mucus cells - secretes mucus to protect epithel
against acid and digestive enzymes
Absorption in the Stomach
• Almost all products of digestion are
absorbed in the intestine
• Notable exceptions
– alcohol and aspirin can be absorbed directly
through stomach wall
– due to their lipid solubility
– absorption of aspirin through stomach wall
associated with bleeding, may be related to
peptic ulcers in people taking large dosages
Chyme
• Food in stomach is liquified
– mixed with stomach juices to form pasty liquid
material = chyme
• Chyme = material passed from stomach to
small intestine
Small Intestine
• Functions in digestion
– CHO digestion resumes
and is completed here
– Protein digestion
continues and completes
here
– Fat digestion is initiated
and completed here
Divisions (@ 12 feet long total length)
3 segments (12 ft long, 22 ft in cadaver)
duodenum = upper portion (@ 1 foot
long) closest to stomach
jejunum = middle section
ileum = lower section closest to large
intestine
• Also functions to absorb
nutrients, fluids, and
electrolytes
• Features that increase
surface area
– Circular folds
• Project into lumen 3-10
mm
• Prominent in
duodenum and
jejunum and disappear
near mid ileum
– Villi
• 4-5 million in entire
length
• 0.5-1.5 mm long
Anatomy
– Microvilli
•
•
1.0 um long
Brush border
Physiology
•
Two primary function
– Digestion
– Absorption of nutrients and water
•
Digestion
– Mainly in duodenum – small intestine and
pancreatic enzymes
– Bicarbonate from pancreas neutralizes acids
– Mucous protects from acids
– Bile emulsifies fats
Hormones Important in Sm. Intestine
Digestive Activity
•
•
•
•
Secretin
Cholecyctokinin (CCK)
Enterokinase
Pancreatic enzymes
– Lipase, Amylase, Peptidases, Trypsinogen,
Trypsin
Physiology
– Digestive enzymes
• Salivary amylase
• Pepsin
• Pancreatic enzymes:
–
–
–
–
–
–
Trypsin
Chymotrypsin
Carboxypeptidase
Nucleases
Pancreatic lipase
Pancreatic amylase
• Intestinal enzymes:
–
–
–
–
Peptidases
Disaccharidases
Lipase
Nucleotidases
Physiology
– Hormones
•
Cholecystokinin – secretion stimulated by fat in
duodenum
– Contraction of gall bladder
– Pancreatic secretion of enzyme rich material
•
Secretin – secretion stimulated by low pH in
duodenum
– Secretion of bile from the liver
– Pancreatic secretion of HCO3- rich juice
Physiology
•
Absorption
–
–
Nutrients broken down into simple sugars, fatty acids
and amino acids
Principle sites of absorption
•
•
•
Duodenum: iron, calcium, vitamins, fats, sugars, amino acids,
vitamins
Jejunum: fat, sugar, amino acid (largely complete by mid
jejunum), vitamins
Ileum: vitamin B12 and bile salts
–
Most bile salts are absorbed and recirculated to the liver –
important in maintaining bile pool
Brush border
enzymes
reassembly
Intestinal Contractions and Motility
• 2 major types of
contractions occur in the
small intestine:
– Peristalsis:
• Slow movement.
• Pressure at the pyloric end of
small intestine is greater than
at the distal end.
– Segmentation:
• Major contractile activity of
the small intestine.
• Contraction of circular
smooth muscle.
– Mix chyme.
Insert fig. 18.14
Contractions of Intestinal Smooth
Muscles
• Occur automatically in response
to endogenous pacemaker
activity.
• Rhythm of contractions is paced
by graded depolarizations called
slow waves.
– Slow waves produced by interstitial
cells of Cajal.
– Slow waves spread from 1 smooth
muscle cell to another through
nexuses.
Contractions of Intestinal Smooth Muscles
• When slow waves above threshold, it triggers APs by opening of
VG Ca2+ channels.
• Inward flow of Ca2+:
– Produces the upward depolarization phase.
– Stimulates contraction of smooth muscle.
• Repolarization:
– VG K+ channels open.
• Slow waves decrease in amplitude as they are conducted.
• May stimulate contraction in proportion to the magnitude of
depolarization.
• Parasympathetic NS, stretch and gastrin increase the amplitude
of slow waves.
– Stimulate APs.
• SNS decrease APs.
Cells and Electrical Events in the Muscularis
Digestion
• Most occurs by hydrolysis reactions reactions that add water to break chemical
bonds
• Enzymes involved:
– amylase - breaks complex sugars to
disaccharides
– lipases - breaks down lipids
– proteases - breaks down proteins
Hormonal Control of Intestinal
Secretion
• S cells secrete secretin
– secretin target tissue = pancreatic ducts and liver
– induces release of water and HCO3- from pancreatic duct
cells and secretion of HCO3- into bile by liver
– HCO3- neutralizes acidic chyme
• Stimuli for secretin secretion
– acid (pH less than 4.5 stimulates secretion)
– secretin = nature’s antacid
Hormonal Control of Intestinal
Secretion (continued)
• I cells secrete cholecystokinin (CCK)
– CCK target tissues = pancreatic acinar cells and
gall bladder
– induces secretion of digestive enzymes from
pancreatic acinar cells
– induces contraction of gall bladder, which releases
bile into small intestine
• Stimuli for CCK secretion
– presence of protein and/or fat in chyme
CCK and Appetite Control
• CCK also thought to act on satiety center in
brain and inhibit appetite
• Butabindid = drug that interfers with
enzyme responsible for CCK degradation
(breakdown)
– keeps CCK in system longer
– boosts appetite inhibition
– used to treat obesity
Pancreatic Enzymes
• Amylase - breaks CHO starch to maltose, maltriose,
and small branched structures
• Lipase - breaks down triglycerides into fatty acids
and glycerol
• Proteolytic enzymes break peptides down to amino
acids and dipeptide fragments
• Trypsinogen
– converted to trypsin by enzyme (enterokinase) located
along inner wall of small intestine
– trypsin converts other pancreatic zymogens (inactive
forms) to their active forms within the small intestine
Pancreatic Enzymes (continued)
• Most pancreatic enzymes are produced as
inactive molecules = zymogens
• Are transported to small intestine in zymogen
form
• Protects the pancreas from ‘self digestion’
CHO Digestion in Sm. Intestine
• Pancreatic amylase secreted into duodenum in
response to secretin
Is active in the intestine because the acidic chyme
is neutralized by HCO3- also secreted from
pancreas in response to secretin
• Amylase converts complex CHOs to maltriose,
maltose, and short branched sugars
Small Intestine (continued)
• Inner surface (epithelial layer) extensively
folded and covered with smaller folds (villi)
and even smaller folds (microvilli) increase
surface area for absorption to occur
• Site of absorption of carbohydrates, lipids,
amino acids, calcium and iron in duodenum
and jejunum
• Bile salts, Vit B12, water, and electrolytes
mainly in ileum
CHO Absorption in the Sm. Intestine
• Enzymes in the brush border complete breakdown of
maltotriose, maltose, and branched sugars, lactose
and sucrose
• Lactase converts lactose to glucose and galactose
• Sucrase converts sucrose to glucose and fructose
• Isomaltase converts branched sugars glucose,
maltose and unbranched short oligosaccharides
• Maltase converts maltose to glucose
CHO Absorption in the Sm. Intestine (continued)
• Epithelial cells that line the sm. Intestine absorb
monosaccharides by active or facilitated transport
• Glucose and galactose are actively co-transported with
sodium using the same transporter and
• Fructose is absorbed by passive facilitated transport
using a different transporter protein than that used by
glucose and galactose
• Monosaccharides enter bloodstream and are transported
to liver and converted to glycogen or sent to bloodstream
for immediate, direct ultilization or storage by cells
Fat Digestion in Sm. Intestine
• Limited fat digestion occurs prior to sm. Intestine
– Some lipases in saliva and gastric secretions
• Lipase = enzyme important in fat digestion
– Secreted into sm. intestine from pancreas in response
to secretin
– breaks down triglycerides to free fatty acids and
monoglycerides
– Activity is dependent upon the amount of surface area
on which it can work
• Phospholipase A2 digests phospholipids
• Bile is essential for proper fat digestion
Digestion and Absorption of Lipids in
Small Intestine
• Fats stimulate I cell release of CCK
• CCK triggers release of bile from gall
bladder
• Bile emulsifies fats
– breaks large fat globules into smaller globules
does not actually break bonds between glycerol
and fatty acids
– Increases surface area available for pancreatic
lipase to act
Liver
• Largest organ in body
• Blood supply
– hepatic artery delivers oxygenated blood
– hepatic portal vein
• products absorbed into capillaries in the intestines do not
directly enter general circulation
• this blood is delivered first to the liver by the hepatic
portal vein, and then passed on to the general circulation
• liver has ‘first crack’ at absorbed nutrients, except lipids
Liver (continued)
• Digestive functions
– secretes bile - essential for digestion and absorption of fats
– Function - overall is to filter and process nutrient-rich blood,
not just a digestive function
• regulates carbohydrate metabolism through glycogen storage and
release
• regulates many aspects of lipid metabolism, eg., cholesterol
synthesis and release of ketones
• detoxifies blood
• urea and bile synthesis
PANKREAS
Gallbladder
Figure 24.21a, b
Large Intestine
• Divisions
– cecum = section nearest
small intestine
(appendix attached in
this region)
– colon = major portion
•
•
•
•
ascending
transverse
descending
sigmoid (leads to
rectum)
•
Functions (converts chyme to feces)
– Absorption of water and electrolytes (mainly
on right side)
•
•
Absorbs 800 ml water/day
Capacity 1500-2000 ml/day (when exceeded
results in diarrhea)
– Sigmoid colon reservoir for dehydrated fecal
mass
•
~200 g feces/day
–
–
–
–
–
Water – 80-90%
Food residue
Bacteria
Cells
Unabsorbed minerals
– Secretes mucus (no enzymes)
– Bacteria produce vitamin K and several B’s
– Flatus (NH3, CO2, H2, H2S, CH4)
• CO2 produced when fatty acids and HCl are
neutralized by bicarbonate
• Bacterial fermentation of carbohydrates produces
CO2, H2, CH4
• ~1000 ml expelled each day
• Excess occurs with aerophagia and diets high in
indigestible carbohydrates
– Rectum and anus sites of some of most
common disorders known to humans
• Constipation
• Hemorrhoids
• Abscesses and fistulas
• Bacteria live in the colon and stimulate the
production of vitamin K and some of the B
complex vitamins
• Mucus is produced but no enzymes are
secreted in the large intestine
• Mass Peristaltic Movements (2-3x day)
• Moves through in 12-24 hours
DIGESTIVE ACTIVITIES OF LARGE
INTESTINE
STRUCTURE
Mucosa
ACTIVITY
Secretes
mucus
RESULT
Lubricates colon &
protects mucosa
Absorbs water Maintains water
balance; solidifies
feces; absorbs
vitamins & some ions
DIGESTIVE ACTIVITIES OF LARGE
INTESTINE
STRUCTURE
Lumen
ACTIVITY
Bacterial
activity
RESULT
Breaks down
undigested
carbohydrates,
protein, & amino
acids into products
that can be expelled
in feces or absorbed
& detoxified by liver
Synthesizes certain B
vitamins & vitamin K
DIGESTIVE ACTIVITIES OF LARGE
INTESTINE
STRUCTURE
Muscularis
ACTIVITY
RESULT
Haustral
churning
Contractions move
contents from haustrum
to haustrum
Peristalsis
Contractions of circular
& longitudinal muscles
move contents along
length of colon
DIGESTIVE ACTIVITIES OF LARGE
INTESTINE
STRUCTURE
Muscularis
ACTIVITY
RESULT
Mass
peristalsis
Forces contents into
sigmoid colon
Defecation
reflex
Eliminates feces by
contractions in sigmoid
colon & rectum
Secretion
& H2O
absorption
2000 ml – 150 ml = ?
Ion &
Vitamin
absorption
Rectum
The
Defecation
Reflex
Defecation process
• Reflex relaxation of internal sphincter
• Valsalva maneouvre raising intraabdominal
pressure
• Relaxation of puborectalis (anorectal angle)
• Voluntary relaxation of external sphincter
Defecation reflex
> 15 mm Hg
Continence mechanism
• Rectum normally empty
• Colonic movements distend rectum - 150
mls, 25 cm H2O which activate defecation
reflex
• Voluntary inhibition (external sphincter) –
movement of faecal material back into
colon
Disorders of the GI tract
• Mouth and throat
– gingivitis - infection of the gum, can lead to
periodonititis involving the supporting bone of
the teeth
– Vincent’s disease - a kind of gingivitis caused
by a spirochete
– Leukoplakia - characterized by thickened white
patches on the mucous membranes of the
mouth - common in smokers and may be a
precursor to cancer
Symptoms of esophageal disorders
•
Dysphagia
–
–
–
–
Subjective awareness of an impairment of swallowing
Major symptom for diseases of the pharynx or esophagus
Occurs in some non-esophageal disorders resulting from
vascular or neurologic disease
May be of obstructive or motor origin
•
Obstructive causes
–
–
•
Stricture
Tumors
Motor causes
–
–
–
Impaired peristalsis
Dysfunction of UES or LES
Common motor disorders – achalasia, scleroderma, diffuse esophageal
spasm
Symptoms of esophageal disorders – cont.
•
Pyrosis (heart burn)
–
–
–
•
Caused by reflux of gastric acid or bile secretions
Persistent reflux caused by incompetent LES
results from excess stretching of the lower esophagus; not
due to hyperacidity of the stomach
Odynophagia
–
•
Pain induced by swallowing
Regurgitation
–
–
–
–
Back flow into mouth
Effortless (as opposed to vomiting)
Common in infants
Reflects both LES incompetence and failure of UES to serve as
regurgitation barrier
Disorders of esophageal motility
•
Achalasia
–
Definition = uncommon hypomotility disorder characterized by
weak and uncoordinated peristalsis or aperistalsis within the
body of the esophagus, elevated LES pressure and failure of
LES to relax completely
•
–
Exact etiology unknown
•
–
Foods and liquids accumulate in lower esophagus
May be degeneration of Aurbach’s plexus
Most common symptom is dysphagia
•
•
•
Regurgitation during meals
Nocturnal regurgitation may result in aspirations and chronic
pulmonary infections or sudden death
Food in esophagus may lead to inflammatory changes, erosions, or
cancer
Disorders of esophageal motility
•
Achalasia - cont.
– Treatment
•
Palliative, measures to relieve obstruction of lower
esophagus
– No way to restore peristalsis
•
Two forms of therapy
– Dilation of LES with pneumatic bag or mercury filled bag
(bougie)
– Surgery to open LES accompanied by pyloroplasty
Disorders of esophageal motility – cont.
•
Diffuse esophageal spasm
–
–
Definition = uncoordinated, nonpropulsive contractions in
response to swallowing
Cause unknown – more common in patients > 50
•
–
Usually asymptomatic
•
•
–
Fairly common
Sometimes dysphagia and odynophagia that are aggravated by cold
foods, large boluses and nervous tension
Sometimes chest pain that may be confused with angina
Treatment
•
•
•
Avoid cold foods and large meals
Antacids, sedatives, nitroglycerine
Esophageal dilation is symptoms persistent and distressing
Disorders of esophageal motility – cont.
•
Scleroderma
– Esophageal motor dysfunction occurs in > 2/3 of
patients with progressive systemic sclerosis
(scleroderma)
– Atrophy of smooth muscle in lower portion of
esophagus
– Incompetence of LES often leads to reflux
esophagitis and subsequent stricture formation in
lower esophagus
Esophagitis
•
•
Definition = inflammation of the esophageal
mucosa
May be acute or chronic
– Innocuous type follows ingestion of hot liquids
– Most common significant form caused by acid
reflux
– Are infectious forms – Candida albicans (thrush),
herpes virus
– Acute, severe follows ingestion of strong alkalis or
acids
This is Candida esophagitis. Tan-yellow plaques are
seen in the lower esophagus, along with mucosal
hyperemia. The same lesions are also seen at the upper
right in the stomach
The lower esophagus here shows sharply demarcated ulcerations that
have a brown-red base, contrasted with the normal pale white
esophageal mucosa at the far left. Such "punched out" ulcers are
suggestive of herpes simplex infection.
Esophagitis
•
Chronic reflux esophagitis and Hiatus Hernia
– Most common form
– Cause – incompetence of LES and reflux of gastric
or intestinal juice into esophagus
•
often associated with hiatus hernia
– Mechanisms that prevent reflux
•
•
•
Tone of sphincter in LES
Angle of entry – creates a flap valve
Intra-abdominal pressure closes segment of esophagus
below diaphragm
Esophagitis – cont.
– Hiatus (hiatal) hernia
•
•
Herniation of portion of stomach into chest
2 types
– Direct or sliding (most common)
» Gastroesophageal junctions slides into thoracic cavity
» LES opens causing reflux
» Often asymptomatic
– Paraesophageal or rolling
» Part of fundus roles through hiatus
» LES remains competent and no reflux
» Major complication is strangulation
•
Important clinical consideration is if there is reflux
Esophagitis – cont.
•
Treatment of sliding hernia
– Goal is to prevent reflux or neutralize reflux
» Frequent small meals
» H2 blockers (ranitidine)
» Protective agents (sucraflate)
» Loose weight
» Avoid stooping forward
» Elevate head during sleep
– Surgery if evidence that persistent reflux is causing esophagitis
or stricture formation
Disorders of the GI tract
• Stomach
– Hiatal hernia - a weakness in the diaphragm at the
point where the esophagus connects allowing the
stomach or other abdominal organs protrude
upwards
– nausea and vomiting - caused by an interruption of
forward movement of nutrition; reverse peristalsis
Disorders of the GI tract
• Stomach, continued
– gastritis - inflammation of the stomach mucosa;
causes include irritation by spicy food, drugs, alcohol,
or nicotine
– stomach cancer - males are more susceptible than
females; symptoms usually long standing indigestion
– peptic ulcer - most common ages 30-45; causative
factors include smoking, drinking; anti-inflammatory
drugs and bacterium, Helicobacter pylori
Gastritis – inflammation or hemorrhagic condition
of the mucosa
•
Acute superficial gastritis
– Erodes surface of epithelium in diffuse or localized
patterns
– Causes
•
•
•
–
Drugs – NSAIDS
Chemicals – alcohol, bile acids, pancreatic enzymes, caffeine,
strong spices
Helicobacter pylori
Clinical manifestations
•
•
•
•
•
Vague abdominal discomfort
Epigastric tenderness
Bleeding
Vomiting
Hematemesis
This is a typical acute gastritis with a diffusely hyperemic
gastric mucosa. There are many causes for acute gastritis:
alcoholism, drugs, infections, etc.
Gastritis – inflammation or hemorrhagic condition of the mucosa - cont.
– Usually resolves when offending agent removed
•
•
•
•
Antiemitic drugs to relieve nausea and vomiting
May need to correct fluids and electolytes
Acid blockers and antacids
Sulcrafate to coat stomach lining
Gastritis - cont.
•
Chronic atrophic gastritis
– Progressive atrophy of glandular epithelium with
loss of parietal and chief cells
•
Decreased HCl, pepsin and intrisic factor production
– Caused mainly by H. pylori
•
•
More often in elderly
Alcohol, hot tea and smoking may predispose
– May lead to gastric ulcers or carcinoma
Gastritis is often accompanied by infection with Helicobacter pylori.
This small curved to spiral rod-shaped bacterium is found in the surface
epithelial mucus of most patients with active gastritis. The rods are
seen here with a methylene blue stain.
This of gastric mucosa reveals the presence of many short, curved rod-like organisms
overlying the mucosa. These are Helicobacter pylori organisms, whose home is the
gastric mucus. The incidence of H. pylori infection increases with age, with half of
American adults infected by age 50. H. pylori organisms break down mucosal
glycoproteins and damage epithelial cells, leading to inflammation--a chronic gastritis
that is asymptomatic in most cases. Peptic ulcer disease, particularly duodenal
ulceration, is strongly associated with H. pylori infection, which may also play a role in
development of gastric carcinoma. Antibiotic treatment of H. pylori reduces these
complications
Gastritis - cont.
– Symptoms generally varied and vague
•
•
•
Feeling of fullness
Anorexia
Vague epigastric distress
– Treatment varies depending on cause
•
•
•
•
Antibiotics
Avoid irritants
Correct iron deficiency if present
Vitamin B12 supplement
Peptic ulcer disease
•
General consideration
– Definition = circumscribed breaks in the continuity
of the mucosa, extending below the epithelium
•
•
Erosions – do not extend below epithelium
Chronic ulcers have scar tissue at base, acute don’t
– Can be anywhere in GI tract exposed to acidpepsin gastric juice
•
Other factors also contribute
–
–
–
–
H. pylori
Mucosal bicarbonate secretion
Stress
Genetics
A 1 cm acute gastric ulcer is shown here in the upper
fundus. The ulcer is shallow and sharply demarcated, with
surrounding hyperemia. It is probably benign. However, all
gastric ulcers should be biopsied to rule out a malignancy.
The strongest association
with Helicobacter pylori is
with duodenal peptic
ulceration--over 85% of
duodenal ulcers. Seen
here is a penetrating acute
ulceration in the duodenum
just beyond the pylorus. An
acute duodenal ulcer is
seen in two views on upper
endoscopy in the lower
panels.
Peptic ulcer disease - cont.
•
Pathogenesis
– Two factors prevent stomach from digesting itself
•
Gastric mucosal barrier
– First line of defense
– NSAIDS cause changes in mucosa that my facilitate its digestion
by pepsin
– Destruction of barrier believed to be important factor in
pathogenesis of gastric ulcers
» Results of back diffusion of H+ injuring underlying tissues
» Antrum more susceptible to back diffusion than fundus
» Duodenum resistant to ulceration due to Brunner’s glands
which produce a highly alkaline secretion
Peptic ulcer disease - cont.
•
Epithelial barrier
– Depends on abundant vascular supply and continual,
rapid regeneration of epithelial cells (~3 days)
– Other factors
•
•
•
•
•
•
•
500,000 new cases/year (10-12 % of population affected)
Duodenal ulcers occur in much younger group than gastric
Lower incidence in women
Caffeine increases acid production
Emotional stress (how one deals with stress)
>90% of duodenal ulcers are on anterior or posterior wall
within 3 cm of pyloric ring
40-60% have family history
Peptic ulcer disease - cont.
•
Clinical features
– Principle feature is chronic, intermittent epigastric
pain – typically relieved by food
– ~25% have bleeding (more common with
duodenal)
– Other signs and symptoms
•
•
•
•
•
Vomiting
Red or “coffee-ground” emesis
Nausea
Anorexia
Weight loss
– Pain-food-relief pattern may not be typical of
gastric ulcers – food sometimes aggravates
Peptic ulcer disease - cont.
•
Benign vs malignant ulcers
– 4% of gastric ulcers are malignant
– Malignant (carcinoma) ulcers have shaggy, necrotic base while
benign have smooth, clean base
Peptic ulcer disease - cont.
•
Medical treatment
– Primary consideration is to inhibit or buffer acid to
relieve symptoms and promote healing
•
•
•
•
•
Antacids – increase pH so pepsin isn’t activated
Dietary management – small frequent meals, avoid
alcohol and caffeine
Anticholinergics – inhibit vagal stimulation
Antimicrobial therapy
Physical and emotional rest
– Ulcers caused by H. pylori are successfully treated
with antimicrobial agents, bismuth salts, and H2
blockers
– 65-95% eradication rates
Peptic ulcer disease - cont.
•
Complications
–
Hemorrhage
•
•
•
•
Most frequent complication – 15-20%
Most common in ulcers of the posterior wall of duodenal bulb due to
proximity of arteries
Symptoms depend on severity
– Anemia
– Occult blood in stool
– Black and tarry stool
– Hematemesis
– Shock
Mortality up to 10% - higher for patients over 50
Peptic ulcer disease - cont.
– Perforation
•
•
•
•
•
Approximately 5% of all ulcers perforate - accounts for
65% of deaths from peptic ulcers
Usually on anterior wall of duodenum or stomach
Thought to be due to excess acid and often a result of
NSAIDS
Characteristic presentation
– Sudden onset of excruciating pain in upper abdomen
– chemical peritonitis
– Patient fears to move or breath
– Abdomen becomes silent to auscultation and board
like rigidity to palpation
Treatment – immediate surgery
Peptic ulcer disease - cont.
–
Obstruction
•
•
•
•
•
Obstruction of gastric outlet in ~5% of patients
Due to inflammation and edema, pylorospasm or scarring
More often with duodenal ulcers
Symptoms
– Anorexia
– Nausea
– Bloating after eating
– Pain and vomiting when severe
Treatment
– Restore fluids and electrolytes
– Decompress stomach with nasogastric tube
– Surgical correction - pyloroplasty
Peptic ulcer disease - cont.
–
Intractability
•
Medical therapy fails to control symptoms adequately,
resulting in frequent, rapid recurrences
– Typically surgery is recommended
Peptic ulcer disease - cont.
•
Surgical treatment – for patients who do not respond
to therapy
–
For duodenal ulcers aim is to permanently reduce stomach’s
capacity to secrete acid and pepsin
• Vagotomy
– Cut vagal branches to stomach
– Eliminates cephalic phase
– Several techniques
•
Antrectomy
– Removal of entire antrum
– Eliminates gastric phase
•
Vagotomy plus antrectomy
– Eliminates both cephalic and gastric phases
Peptic ulcer disease - cont.
•
Partial gastrectomy
– Removal of distal 50-75% of stomach
– Gastric remnant anastamosed to duodenum (Billroth I)
or jejunum (Billroth II)
– For gastric ulcers
•
•
Usually partial gastrectomy and a gastroduodenal
anastomosis
Normally do not do vagotomy as patients have
normal to low acid production
Peptic ulcer disease - cont.
•
Postoperative Sequelae
–
Dumping syndrome ~20% of patients
•
•
•
•
•
•
Rapid emptying of hyperosmotic chyme into intestine
Rapid fluid shift from vascular compartment into intestinal lumen
Hypotension
Reflex tachycardia, diaphoresis and vasoconstriction
Feeling of fullness, nausea, vomiting and diarrhea common
Symptoms usually during or within minutes of meal
Peptic ulcer disease - cont.
–
Hypoglycemia
•
•
•
•
May occur within 2-3 hrs after eating
Due to excess release of enteroglucagon from intestine which sensitizes
beta cells
Over corrects the hyperglycemia
Treatment
– Eat frequent, small meals
– Low carbohydrate and high protein diet
– Restrict liquids at mealtime
Malabsorption – intestinal mucosal absorption of
single or multiple nutrients is impaired resulting in inadequate
movement of digested food into blood or lymphatic system
•
Causes (box page 346)
–
–
–
–
–
–
Prior gastric surgery
Pancreatic disorders
•
Chronic pancreatitis, cancer, cystic fibrosis
Hepatobiliary disease
•
Bile tract obstruction, cirrhosis, hepatitis
Disease of small intestine
•
Nontropical sprue, enteritis. giardiasis
Hereditary disorders
•
Lactase deficiency
Drug-induced malabsorption
•
Neomycin, calcium carbonate
Disorders of the GI tract
• Stomach, continued
– pyloric stenosis - more common in males than
females, causes persistent vomiting because of
the stricture in the pyloric sphincter; requires
surgery to repair
Disorders of the GI tract
• Intestinal disorders
– diarrhea - abnormal frequent watery stools;
danger is dehydration and electrolyte
imbalance; cause is excess activity of the colon,
faulty absorption or infection
– constipation - acute due to obstruction or
diverticular inflammation (diverticulitis).
Chronic includes spastic constipation caused by
overuse of laxatives or enemas; flaccid
constipation usually caused by inactivity
Intestinal obstruction
•
Definition = an interference with the normal flow
of intestinal contents through the intestinal tract
–
May be acute or chronic, partial or complete
•
•
•
Chronic obstruction usually involves colon as a result of a tumor
Most obstructions involve SI
Complete is serious and requires early diagnosis and emergency
surgery to save life
Intestinal obstruction
•
2 types of obstructions
–
–
Non-mechanical – peristalsis is inhibited by toxic or
traumatic alteration in motility
Mechanical – caused by extrinsic pressure
•
•
Simple mechanical obstruction – only one point of obstruction
Closed-loop obstruction – at least 2 points of obstruction (can
lead to infarction due to strangulation)
Intestinal obstruction
•
Etiology
–
Non-mechanical
•
•
•
–
Common after abdominal surgery
Can be caused by peritonitis
Accompanies many traumatic conditions (rib fracture, concussion
of spinal cord or fracture of spine)
Mechanical
•
•
•
•
•
About 50% of all are in adults and result from adhesions following
previous surgeries
Malignant tumors, diverticulitis and vulvulus are the most
common causes in middle aged and older people
Inguinal or femoral hernia common causes of SI obstruction
Intussusception is the most common cause in infants and small
children
Foreign objects and congenital abnormalities also common causes
in infants and children
Intestinal obstruction
•
Pathophysiology – events similar regardless of
cause
–
–
Wall is distended by fluid and gas
Distension reduces movement of water and ions from
lumen to blood
•
•
–
–
–
~8 Liters secreted into GI tract each day
Vomiting and intestinal secretion result in fluid and electrolyte
loss
Shock due to reduced ECF volume
Continued distension results in viscous cycle of
decreased fluid absorption and increased secretion
Local effects include ischemia and increased
permeability due to necrosis resulting in absorption of
bacterial toxins into peritoneal cavity and systemic
circulation
Intestinal obstruction
•
Signs and symptoms
– Cardinal symptoms
•
•
•
•
Abdominal distension
Pain
Vomiting
Absolute constipation
– Abdominal radiograph essential for diagnosis
Intestinal obstruction
•
Treatment
–
–
–
–
–
Correct fluid and electrolyte imbalance
Relieve distention and vomiting by intubation and
decompression
Control peritonitis and shock
Remove obstruction
Small bowel obstruction more serious and rapid than
colonic
•
•
Mortality for non strangulation 5-8% if surgical intervention
is soon enough
Delay or development of strangulation or other
complications raises mortality to 35-45%
Disorders of the GI tract
• Intestinal Disorders, continued
– Colon cancer - one of the most common types in
the US - usually adenocarcinomas that arise from
the mucosal lining. Occurrence is equal in the
sexes, however, rectal cancer is greater in men
than women. Early detection is afforded with
fecal occult blood testing and sigmoidoscopy
Disorders of the GI tract
• Liver Disorders
– Hepatitis - inflammation of the liver by drugs, alcohol or
infection
• A - transmitted in fecal matter; rarely fatal; infection affords lifelong immunity; Vaccine available
• B - transmitted by direct exchange of blood or body fluids; Vaccine
available
• C - primarily transmitted by direct exchange of blood; sexual
transmission can occur, but limited
• D - transmitted by direct exchange of blood, only in concert with
HepB infection
• E - transmitted by fecal contamination of water
Disorders of the GI tract
• Liver Disorders, continued
– Cirrhosis - chronic disease in which active liver
cells are replaced by inactive connective tissue;
most common cause is alcoholism compounded
with malnutrition. In later stages there is
hampering of portal circulation causing congestion
in the peritoneal cavity - ascites
– Cancer - the liver is a common site for metastases
Disorders of the GI tract
• Liver Disorders, continued
– Jaundice - yellow coloring of the skin and eyes;
cause is damage to the liver making it unable to
conjugate bilirubin or a blockage in the bile ducts
with bile pigment accumulation in the blood
Disorders of the GI tract
• Gallbladder
– Gall stones (cholelithiasis) - formed from
cholesterol and block the ducts; pain occurs when
the stones prevent the flow of bile and hamper
the digestive process
– Cholecystitis - Inflammation of the gall bladder
Disorders of the GI tract
• Pancreas
– Pancreatitis - inflammation of the pancreas caused
by blockage of the bile ducts causing the
pancreatic enzymes to back up into the gland
which causes destruction of the tissue; another
cause is infection of the pancreas.
Disorders of the GI tract
• Digestive Disorders
– Anorexia - chronic loss of appetite; causes can be
physical (heavy exercise) or mental (more likely to be
emotional and/or social rather than physiological
disruption in the brain). Anorexia nervosa affects
mostly young women
– Bulimia (binge-purge syndrome) - prevention of the
absorption of food because of induce vomiting or
large doses of laxatives
Overall lessons:
• The large intestine functions to store symbionts, absorb water,
vitamins, wastes, and toxins.
• The large intestine has no villi, but does have a folded epithelium.
• The cecum does most of the water resorption.
•The colon moves contents along by peristalsis.
• Defecation is mainly autonomic except for the final step.
• Many nutrients are absorbed via cotransport with ions.
• Na+ must be pumped out of cells actively.
• The brush border has enzymes which break down polysaccharides
& peptides into monomers before absorption.
• Water is absorbed by passive osmosis.
• Lipids are absorbed through membrane & exocytosed to lacteal.
Thank You
Muntah
(Vomitus)
Pancreas
Pengaturan
sekresi pancreas
Fungsi Hati
Hepar & Fesica
Vellea
Pengaturan
sekresi empedu
Usus Halus