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Dr. Yudi Herlambang
Prof dr Abdul Majid
Dr Nur Aiza
Department of Physiology
School of Medicine
University of Sumatera Utara




Non Nutrient


Primary Functions of Digestive System
Activity necessary:




Primary Functions of Digestive System
Activity necessary:

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
 muscular contraction.
•Endocrine (secretion of hormones that
regulate digestive process)
•Exocrine (secretion of water, enzymes,
acid, bicarbonate, into GI tract  enzyme &
other digestive juices.

.Digestio n 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 Absorptio n Transfer of monomer subunits across wall of small intestine into blood or lymph  transport modified nutrients.

chemicals. and stomach content (local stimuli) • Activity of plexuses can be modified .Regulation. Neural: • 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).

• 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 .

Hormonal. • Paracrine regulation – production of hormone-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 .


Mout h: .

submaxillary. sublingual) secrete saliva parotid gland parotid duct lubricates and softens sublingual gland submandibular gland food. aids in swallowing contains amylase = enzyme that begins breakdown of carbohydrates .Mouth: Teeth – – grind and tear food into smaller pieces increases surface area upon which digestive enzymes work Salivary glands (parotid.

continuous 2.SALIVARY GLANDS Sympathetic and parasympathetic responses are not antagonistic 1. Parasympathetic system has the dominant role . 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 .

cerebral cortex

salivary centre
in medulla

pressure receptors
and chemoreceptors
in the mouth


other inputs

autonomic nerves
salivary glands
 salivary secretion

To convey food
into the
Important role
in swallowing.

Hollow muscular tube
connecting pharynx and
Bounded by sphincters.
Lined w/ stratified
squamous epithelium.
Lower esophageal
(gastro esophageal)
sphincter ; transition
from low pressure
( intrathoracic )  high
pressure (intraabdominal).
Disorder o/t LES tone
 major cause




Stomach wall .

mucus. – Absorbs some water. in ileum . – HCl converts pepsinogen into pepsin. alkohol.Secretion/Digestion • Stomach: – Temporary stores ingested food. mixes food with gastric juice. glucose. B12  allows abs.  sphincters prevent backward flow of materials into esophagus and regulate release of stomach contents into small intestine – Churn. – Sterilization of stomach contents by acid – Pepsin digests proteins into peptide fragments. – Mechanical and chemical breakdown of ingested material – Produces. – Binds vit. HCl and pepsinogen.

 Additional secretions:  Histamine (ECL cell)  Somatostatin HCl Gastrin Histamine Pepsinogen Mucous cell. B12 mucus. secrete : - Gastric lipase. . Stomach:  lower region of stomach (antrum) secretes the hormone “gastrin”.HCl . Pepsinogen HCl Pepsin Parietal (oxyntic) cells.Intrinsic factor  binds Pyloric gland  Alkaline vit. Chief cells. secrete : . . secrete mucous  protects mucosa (epithel) from acid & pepsin.

histamine and acetylcholine increase numbers of enzyme in plasma membrane. Gastrin Pepsinogen .+ + H K ATP-ase • Somatostatin inhibits acid secretion. K-ATPase pump. • Gastrin.Control of Acid Secretion • Secretion is dependent upon activity of H.

Gastric phase. 3. Cephalic phase. 2. 1. .Control of Acid Secretion May be considered as three separate phases. Intestinal phase.

CEPHALIC PHASE Vagus nerve Sight. smell or thought of food Parasympathetic activation of gastric motility & gastric juice secretion .1.

Gastrin FOOD GO Gastrin stimulates secretion from both chief & . GASTRIC PHASE Food arrival causes muscular reflexes & gastrin secretion by G cells.2.

INTESTINAL PHASE Arrival of food in duodenum triggers release of hormones that inhibit gastric motility & secretions.e.3. Secretin & Cholecystokinin (CCK) Circulation • Intestinal phase – signals come from intestine and have inhibitory effect i. and increase in osmolality stimulate nerve reflex that inhibits gastric motility and secretion – presence of fat in duodenum stimulates secretion of inhibitory hormones (enterogastrones) . slow the rate of gastric secretion – stretch of duodenum.

Hormones Released During the Intestinal Phase When acidic chyme arrives. hormones are released by the duodenum. Cholecystokinin (CCK) • stimulates production / release of pancreatic enzymes • stimulates bile release from gallbladder • inhibits gastric secretion and motility of stomach . 1. Secretin • stimulates pancreas to secrete bicarbonate ions that neutralise stomach acid • inhibits gastric secretion and motility of stomach 2.

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 • Also functions to absorb Divisions (@ 12 feet long total length) 3 segments (12 ft long. and electrolytes . 22 ft in cadaver) duodenum = upper portion (@ 1 foot long) closest to stomach jejunum = middle section nutrients. fluids.

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 .

Intestine Digestive Activity • Secretin • Cholecyctokinin (CCK) • Enterokinase • Pancreatic enzymes – Lipase. Trypsinogen. Peptidases.Hormones Important in Sm. Trypsin . Amylase.

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 juice .

calcium. fats. sugar. vitamins Ileum: vitamin B12 and bile salts – Most bile salts are absorbed and recirculated to the liver – important in maintaining bile pool . vitamins Jejunum: fat. amino acid (largely complete by mid jejunum). fatty acids and amino acids – Principle sites of absorption • Duodenum: iron. sugars.Physiology • Absorption – Nutrients broken down into simple sugars. • • amino acids. vitamins.

breaks CHO starch to maltose.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 . maltriose. and small branched structures • Lipase .Pancreatic Enzymes • Amylase .

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’ .

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 . not just a digestive function • regulates carbohydrate metabolism through glycogen storage and release • regulates many aspects of lipid metabolism.essential for digestion and absorption of fats – Function . cholesterol synthesis and release of ketones • detoxifies blood • urea and bile synthesis . eg.overall is to filter and process nutrient-rich blood.

destroys aged or abnormal blood cells and produces clotting factors – converts protein metabolites to urea for elimination by kidneys – immune function (Kupffer cells) – functions as blood reservoir in regulation of blood volume .Liver (continued) • Non-digestive functions – circulatory functions.

and stored until secretion into the small intestine • Gall bladder contraction forces bile into small intestine – Cholecystokinin = hormone released by ‘I’ cells of small intestine • stimulates release of digestive enzymes from pancreas and bile from gall bladder .Gall Bladder • Located on underside of liver • Bile produced in liver is carried to gall bladder. concentrated.

bile salts. breaks large fat globules into smaller fat droplets.Bile • Product of the liver cells – bile contains bile pigment. cholesterol. provides greater surface area on which lipase can act . form micelles = lipid aggregates with non-polar parts in central region and polar regions toward water • Essential for absorption of fat from the digestive tract – Emulsifies fat. and inorganic ions • bile pigment = bilirubin = breakdown product of hemoglobin • bile salts = derivatives of cholesterol that are combined with taurine or glycine. phospholipids.

not excreted main bile pigment is bilirubin. derived from RBC heme bile is synthesized in the liver and stored in the gallbladder release is stimulated by cholecystokinin and vagus nerve . • • • • • Approximately 1 liter per day is produced bile salts are cholesterol derivatives and function to emulsify fats bile salts are recycled.Bile Synthesis • This is the main digestive function of the liver.

Intestinal Contractions and Motility • 2 major types of contractions occur in the small intestine: – Peristalsis: • Slow movement. • Contraction of circular smooth muscle.14 . 18. – Segmentation: • Major contractile activity of the small intestine. • Pressure at the pyloric end of small intestine is greater than at the distal end. Insert fig. – Mix chyme.

Brush border enzymes reassembly .

Large  Intestine  .

Anatomy and Physiology • 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 .

Anatomy and Physiology – – – Secretes mucus (no enzymes) Bacteria produce vitamin K and several B’s Flatus (NH3. 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 • Colon and rectal cancer . CO2. H2S. H2. H2. CH4) • CO2 produced when fatty acids and HCl are • • • – neutralized by bicarbonate Bacterial fermentation of carbohydrates produces CO2.

• 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 .

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 .

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 Lumen ACTIVITY Bacterial activity RESULT Breaks down undigested carbohydrates.

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 .

common in smokers and may be a precursor to cancer .characterized by thickened white patches on the mucous membranes of the mouth .infection of the gum.Disorders of the GI tract • Mouth and throat – gingivitis .a kind of gingivitis caused by a spirochete – Leukoplakia . can lead to periodonititis involving the supporting bone of the teeth – Vincent’s disease .

diffuse esophageal spasm .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.

• 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 .Symptoms of esophageal disorders – cont.

or cancer . elevated LES pressure and failure of LES to relax completely • Foods and liquids accumulate in lower esophagus Exact etiology unknown • 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.Disorders of esophageal motility • Achalasia – – – Definition = uncommon hypomotility disorder characterized by weak and uncoordinated peristalsis or aperistalsis within the body of the esophagus.

– 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 • Achalasia .cont.

nonpropulsive contractions in response to swallowing – Cause unknown – more common in patients > 50 • Fairly common – Usually asymptomatic • Sometimes dysphagia and odynophagia that are aggravated by cold foods. • Diffuse esophageal spasm – Definition = uncoordinated. nitroglycerine • Esophageal dilation is symptoms persistent and distressing . sedatives. large boluses and nervous tension Sometimes chest pain that may be confused with angina – • Treatment • Avoid cold foods and large meals • Antacids.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 .Disorders of esophageal motility – cont.

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). severe follows ingestion of strong alkalis or acids . herpes virus Acute.

The same lesions are also seen at the upper right in the . Tan-yellow plaques are seen in the lower esophagus.This is Candida esophagitis. along with mucosal hyperemia.

contrasted with the normal pale white esophageal mucosa at the far left.The lower esophagus here shows sharply demarcated ulcerations that have a brown-red base. 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 .

• 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 .Esophagitis – cont.

caused by an interruption of forward movement of nutrition.a weakness in the diaphragm at the point where the esophagus connects allowing the stomach or other abdominal organs protrude upwards – nausea and vomiting .Disorders of the GI tract • Stomach – Hiatal hernia . 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 .

hot tea and smoking may predispose – May lead to gastric ulcers or carcinoma .Gastritis . pepsin and intrisic factor production – Caused mainly by H. pylori • More often in elderly • Alcohol.cont. • Chronic atrophic gastritis – Progressive atrophy of glandular epithelium with loss of parietal and chief cells • Decreased HCl.

The rods are seen here with a methylene blue stain.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. .

pylori organisms break down mucosal glycoproteins and damage epithelial cells. leading to inflammation--a chronic gastritis that is asymptomatic in most cases. pylori reduces these complications . These are Helicobacter pylori organisms. which may also play a role in development of gastric carcinoma. pylori infection increases with age. particularly duodenal ulceration. The incidence of H. Antibiotic treatment of H.This of gastric mucosa reveals the presence of many short. Peptic ulcer disease. with half of American adults infected by age 50. whose home is the gastric mucus. curved rod-like organisms overlying the mucosa. pylori infection. H. is strongly associated with H.

Gastritis . – 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 .cont.


PENDAHULUA  Penyebab gastritis N dan tukak peptik adalah multifaktor  Patofisiologi dasar adalah gangguan keseimbangan antara faktor-faktor agresif dan faktor-faktor defensif  Sebagian penderita yang telah diobati dan sembuh ternyata kambuh lagi  Kualitas penyembuhan luka diduga berperan penting dalam terjadinya kekambuhan penyakit ini .

Epithelial defense mechanism III. Other ulcerogenic Multiple causes of PUD NSAIDs Gastric acid Defense H. HP IV. Pylori Inflammation Stress . NSAID V.Pathophysiology of Peptic Ulceration I. Gastric acid secretion homeostatatis and gastroduodenal motility II.


all gastric ulcers should be biopsied to rule out a malignancy.A 1 cm acute gastric ulcer is shown here in the upper fundus. It is probably benign. The ulcer is shallow and sharply demarcated. . However. with surrounding hyperemia.

Seen here is a penetrating acute ulceration in the duodenum just beyond the pylorus. .The strongest association with Helicobacter pylori is with duodenal peptic ulceration--over 85% of duodenal ulcers. An acute duodenal ulcer is seen in two views on upper endoscopy in the lower panels.

Peptic ulcer disease .higher for patients over 50 .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% .

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 .

cystic fibrosis Hepatobiliary disease • Bile tract obstruction. hepatitis Disease of small intestine • Nontropical sprue. enteritis. cancer. cirrhosis. calcium carbonate .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. giardiasis Hereditary disorders • Lactase deficiency Drug-induced malabsorption • Neomycin.

continued – pyloric stenosis .more common in males than females. requires surgery to repair . causes persistent vomiting because of the stricture in the pyloric sphincter.Disorders of the GI tract • Stomach.

Disorders of the GI tract • Intestinal disorders – diarrhea .acute due to obstruction or diverticular inflammation (diverticulitis). faulty absorption or infection – constipation . danger is dehydration and electrolyte imbalance.abnormal frequent watery stools. Chronic includes spastic constipation caused by overuse of laxatives or enemas. cause is excess activity of the colon. 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

• Etiology

• Common after abdominal surgery
• Can be caused by peritonitis
• Accompanies many traumatic conditions (rib fracture,
concussion of spinal cord or fracture of spine)

• 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
Intussusception is the most common cause in infants
and small children
Foreign objects and congenital abnormalities also
common causes in infants and children

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

transmitted by direct exchange of blood. infection affords life-long immunity. sexual transmission can occur.inflammation of the liver by drugs.primarily transmitted by direct exchange of blood. Vaccine available • C . rarely fatal. only in concert with HepB infection • E .Disorders of the GI tract • Liver Disorders – Hepatitis .transmitted in fecal matter. Vaccine available • B .transmitted by fecal contamination of water . but limited • D .transmitted by direct exchange of blood or body fluids. alcohol or infection • A .

In later stages there is hampering of portal circulation causing congestion in the peritoneal cavity ascites – Cancer .chronic disease in which active liver cells are replaced by inactive connective tissue.the liver is a common site for metastases .Disorders of the GI tract • Liver Disorders. continued – Cirrhosis . most common cause is alcoholism compounded with malnutrition.

Disorders of the GI tract • Liver Disorders. 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 .yellow coloring of the skin and eyes. continued – Jaundice .

pain occurs when the stones prevent the flow of bile and hamper the digestive process – Cholecystitis .Inflammation of the gall bladder .formed from cholesterol and block the ducts.Disorders of the GI tract • Gallbladder – Gall stones (cholelithiasis) .

.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 • Pancreas – Pancreatitis .

chronic loss of appetite.Disorders of the GI tract • Digestive Disorders – Anorexia .prevention of the absorption of food because of induce vomiting or large doses of laxatives . Anorexia nervosa affects mostly young women – Bulimia (binge-purge syndrome) . causes can be physical (heavy exercise) or mental (more likely to be emotional and/or social rather than physiological disruption in the brain).

Thank You .

Pencernaan di rongga mulut .

Pengaturan salivasi .

Struktur oesophagus .

Proses menelan .

Struktur & Fungsi Lambung .

Sekresi & Gerakan Lambung .

Gerakan Lambung .

Muntah (Vomitus) .

Pancreas .

Pengaturan sekresi pancreas .

Fungsi Hati .

Hepar & Fesica Vellea .

Pengaturan sekresi empedu .

Usus Halus .







Mechanisms of Defense of the GIT the external & An interface between internal environments An external nutrients imported into internal bloodstream Must be defended from pathogens. . and corrosive products. irritants.


Physiology of Digestion Dr. Yudi Herlambang Department of Physiology School of Medicine University of Sumatera Utara .