Diagrammatic view of Digestive System

ANATOMY OF DIGESTIVE SYSTEM

Components of Digestive system: 1. Mouth 2. Teeth 3. Tongue 4. Saliva 5. Pharynx 6. Esophagus 7. Stomach 8. Accessory organs (pancreas, gall bladder and spleen) 9. Liver 10. Duodenum 11. Small Intestine 12. Large Intestine

INGESTION
Mouth
mechanical digestion
teeth
breaking up food

chemical digestion
saliva
amylase enzyme digests starch mucin slippery protein (mucus) protects soft lining of digestive system lubricates food for easier swallowing buffers neutralizes acid to prevent tooth decay anti-bacterial chemicals kill bacteria that enter mouth with food

INGESTION
mouth break up food digest starch kill germs moisten food

MOUTH
Chemical and mechanical digestion. Food is chewed (masticated) mechanically. A bolus (lump) is formed with saliva and the tongue.

Swallowing (& not choking)

Epiglottis
flap of cartilage closes trachea (windpipe) when swallowing food travels down esophagus

Peristalsis
involuntary muscle contractions to move food along

SWALLOWING
Complex reflex
Tongue forces food into pharynx Epiglottis and vocal cords close off trachea;

breathing temporarily ceases

Bolus moves into esophagus, then through esophageal sphincter into stomach

TEETH

TONGUE

SALIVA
Saliva is produced by salivary glands (Sublingual gland, Submandibular gland and Parotid gland) at back of mouth and under tongue Saliva includes Salivary amylase (enzyme) Bicarbonate (buffer) Mucins (bind food into bolus) Water

MAJOR SALIVARY GLAND

PHARYNX
The back of the throat.
Larynx- passage for air,

closes when we swallow. Is approximately 15cm long.

ESOPHAGUS
It is the tube that connects your mouth and your stomach Usually collapsed (closed) 3 constrictions Aortic arch Left primary bronchus Diaphragm Surrounded by SNS plexus Blood vessels Functions Secrete mucous Transport food

Peristalsis
series of involuntary wave-like

muscle contractions which move food along the digestive tract

ANATOMY OF STOMACH
3 muscle layers
Oblique Circular Longitudinal

Regions
Cardiac sphincter Fundus Antrum (pylorus) Pyloric sphincter

Vascular Inner surface thrown into folds Rugae

Contains enzymes that work best at pH 1-2

STOMACH
mouth break up food digest starch kill germs moisten food stomach kills germs break up food digest proteins store food

STOMACH SECREATIONS
Secreted into lumen (gastric fluid)
Hydrochloric acid (HCl- pH 1.5-2.5) Mucus (protective) Pepsinogen (inactive form of a protein-digesting enzyme

pepsin)
Stomach cells also secrete the hormone gastrin into the

bloodstream Food is further broken down into a thin liquid called chyme.

MIXING CHYME
A thick mixture of food and gastric fluid
High acidity kills many pathogens Mixed and moved by waves of stomach contractions

(peristalsis)

Accessory Organs
Pancreas
Spleen Gall Bladder

Accessory Organs

PANCREAS
An organ which secretes both digestive enzymes (exocrine) and

hormones (endocrine)

** Pancreatic juice digests all major nutrient types. Nearly all digestion occurs in the small intestine & all digestion is

completed in the SI. Digestive enzymes

digest proteins

trypsin, chymotrypsin amylase

digest starch

Buffers neutralizes acid from stomach

LIVER & GALL BLADDER

Detoxifies/removes Drugs Alcohol Stores Glycogen Vitamins (A, D, E, K) Fe and other minerals Cholesterol Activates vitamin D Fetal RBC production Phagocytosis Metabolizes absorbed food molecules Carbohydrates Proteins Lipids Dual blood supply: -Hepatic portal vein -Direct input from small intestine -Hepatic artery/vein -Direct links to heart

GALL BLADDER
Pouch structure located near the liver which concentrates

and stores bile

Bile duct a long tube that carries BILE. The top half of

the common bile duct is associated with the liver, while the bottom half of the common bile duct is associated with the pancreas, through which it passes on its way to the intestine. Bile emulsifies lipids (physically breaks apart FATS)

Bile is a bitter, greenish-yellow alkaline fluid, stored in the

gallbladder between meals and upon eating is discharged into the duodenum where it aids the process of digestion.

DUODENUM & RELATED ORGANS

DUODENUM
Receive juices from pancreas, liver and its own wall
* Secretion from the duodenum: They finish off the

last step of digestion. - Peptidases (or dipeptidases) break off the bond between dipeptides to free 2 amino acids - Disaccharidase (maltase, sucrase, lactase) break off disaccharides into 2 monosaccharides (mostly glucose) - Intestinal lipase breaks off diglycerides into monoglycerides and fatty acids. Nutrients are completely degraded into forms that can be absorbed by cell (step 2 of chemical digestion)

Most chemical digestion takes place here. Simple sugars and proteins are absorbed into the inner lining. Fatty acids and glycerol go to lymphatic system. Lined with villi, which increase surface area for absorption, one cell thick. Secretions of SI: Secretes digestive enzymes
Peptidases

SMALL INTESTINE

AminoDiTri-

Sucrases Maltase Lactase Saccharidases

DiTri-

Lipase Nucleases

SMALL INTESTINE
Function chemical digestion

major organ of digestion & absorption

absorption through lining over 6 meters! small intestine has huge surface area = 300m2 (~size of tennis court)

Structure 3 sections

duodenum = most digestion jejunum = absorption of nutrients & water ileum = absorption of nutrients & water

Jejunum-Ileum
Nutrients will be reabsorbed along the jejunum-ileum Brush border contains villi which increase the surface of

absorption The villi are structured for nutrient absorption

VILLI

LARGE INTESTINE
Extends from ileocecal valve to anus Regions
Cecum Appendix
Colon Ascending Transverse Descending Rectum Anal canal

LARGE INTESTINE

LARGE INTESTINE
Functions of LI:
Mechanical digestion

Haustral churning Peristalsis Reflexes

Gastroileal Gastrocolic

Chemical digestion Bacterial digestion

Ferment carbohydrates Protein/amino acid breakdown More water Vitamins

Absorbs

B K

Concentrate/eliminate wastes

APPENDIX (VESTIGIAL ORGAN)

RECTUM
Last section of colon (large intestines) eliminate feces

undigested materials

extracellular waste mainly cellulose from plants roughage or fiber masses of bacteria

FAECES FORMATION &DEFECATION

Chyme dehydrated to form feces Feces composition
Water Inorganic salts Epithelial cells Bacteria Byproducts of digestion

Defecation
Peristalsis pushes feces into rectum Rectal walls stretch

Control Parasympathetic Voluntary

Physiology of digestive system Which type of digestion is the following?

1. Chewing a saltine? MECHANICAL
2. Saliva breaking the saltine down into molecules of glucose? - CHEMICAL 3. Your tongue breaking pieces of a hamburger apart? MECHANICAL 4. Pepsin (an enzyme) in your stomach breaking the hamburger into amino acids? CHEMICAL

Gastrointestinal System (Physiology)

Overview Digestion of nutrients Absorption of nutrients and water Fate of nutrients in the liver Principles of GI regulation GI secretion and regulation GI motility and regulation

Overview
Food for body:
Carbohydrates, proteins and lipids are absorbed in a

form that can not be taken up by the cells food needs to be broken a small pieces (mechanical digestion) and broken down chemically (chemical digestion)

Steps in food digestion

Carbohydrates, proteins and lipids are absorbed in a

form that can not be taken up by the cells food needs to be broken a small pieces (mechanical digestion) and broken down chemically (chemical digestion) Chemical digestion refers to the degradation of: 1 2
1- Carbohydrates 2- Proteins 3- Lipids

---> disaccharides ---> peptides ---> diglycerides

---> monosaccharides ---> amino acids ---> monoglycerides and fatty acids

Gastrointestinal system

Overview Functional anatomy of the GI system Digestion and absorption of nutrients and water Fate of nutrients in the liver Principles of GI regulation GI secretion and regulation GI motility and regulation

ABSORPTION OF CARBOHYDRATES
Monosaccharides (mostly glucose) are absorbed The monomers are carried by transporter molecules across the epithelial cells and into the blood capillary present in the villus portal vein liver

ABSORPTION OF PROTEIN
Proteins are degraded into amino acids (a.a.)
A.a. are carried by transporter molecules across the

cells and into the blood capillaries portal circulation liver

ABSORPTION OF LIPID
Lipids (triglycerides) are degraded to monoglycerides and fatty-acids. They are absorbed into the cell by diffusion. The cell resynthesizes triglycerides. Because TG are not soluble in H2O, the TG are surrounded with proteins and packaged into chylomicrons The chylomicrons are emptied into lymphatic capillaries, the lacteal lymph circulation blood cells and liver

ABSORPTION OF MINERALS
Sodium: active absorption in jejunum-ileum. Chloride follow by

electromagnetic attraction.

Potassium: passive secretion or absorption, depending on lumenal

concentration if diarrhea, hypokalemia due to loss of K+ buffer

HCO3-: secreted by pancreas, neutralizes H+ from stomach. Used as a Calcium: need an active transport to cross the intestinal epithelium.

Absorption promoted by a derivative of Vit D

Iron: actively reabsorbed. Stored as ferritin Water: Two liters of fluids are taken as food or drink per day. In

addition, 7 liters are used to secrete digestive jiuces need to reabsorb most of H2O.

H2O reabsorbed throughout the small and large intestines. Colon is

especially designed to reabsorb H2O

Absorptive state

Post absorption stage

GASTROINTESTINAL SYSTEM

Overview Functional anatomy of the GI system Digestion and absorption of nutrients and water Fate of nutrients in the liver Principles of GI regulation GI secretion and regulation GI motility and regulation

FATE OF NUTRIENTS
Glucose:

- used as needed by liver cell - blood stocked on glucose - glycogen syntesized - TG synthesized if needed and sent to adipose tissue Amino acids: - used to restock the blood - used by the liver to synthesize its own proteins - used to synthesize blood proteins - if excess: a.a. are deaminated NH2 used to make urea and the rest used for energy or stored as TG

GASTROINTESTINAL SYSTEM

Overview Functional anatomy of the GI system Digestion and absorption of nutrients and water Fate of nutrients in the liver Principles of GI regulation GI secretion and regulation GI motility and regulation

GI organization
Need to regulate GI function to

changing states (after or before meals..) Sensors: 3 different receptors: - mechanoreceptors: monitor state of distention - chemoreceptors monitor concentrations of substances in the lumen - osmoreceptors monitor osmolarity of lumen contents Integrating centers: CNS and enteric NS Effectors: endocrine, exocrine cells, smooth muscles

Control Pathways
Both hormonal and neural Short pathways: involves automatic regulation within the

enteric system itself Long pathways: involves the CNS (somatic and autonomic) Three phases: cephalic, gastric and intestinal phases

Cephalic phase: salivary and gastric secretions

Salivary secretion stimulated by parasympathetic NS by odors, sight,

taste saliva fluid and rich in enzymes Stimulated by sympathetic NS thick secretion, rich in proteins Gastric secretion: increase acid and enzymes secretion in response to sight, smell and taste of food

Gastric phase
Stimuli: presence of

food in the stomach (both distention and nutrients) Stimulation of the parasympathetic NS and secretion of gastrin (hormone) Response: increased motility and juice secretion

Intestinal Phase
Arrival of nutrients in duodenum decreased gastric secretion and motility
Promotes secretion of cholecystokinin (CCK) and secretin

- CCK promotes: - increased pancreatic enzyme secretion - gallbladder contraction and sphincter of Oddi relaxation - secretin promotes: - bicarbonate ion secretion (pancreas) - bile secretion

Intestinal Phase

GASTROINTESTINAL SYSTEM
Overview
Digestion of nutrients Absorption of nutrients and water Principles of GI regulation GI secretion and regulation GI motility and regulation

Motility and its regulation

The wall has 2 layers

of smooth muscles with radial and longitudinal fibers. The fibers communicate through gap junctions The parasympathetic NS stimulates smooth muscle contraction

Motility and its regulation

Peristalsis: waves of contraction of longitudinal muscle fibers moving down the GI tract
Segmentation: in small intestine for mixing chyme Chewing and swallowing:

GASTRIC MOTILITY
Gastric motility increases with the presence of gastrin and decreased

under the influence of CCK, secretin and gastric inhibitory peptide (GIP)
Vomiting:
- emotional stress, severe pain, illnesses, toxins stimulate the vomiting center in the medulla oblongata sensation of nausea, increased HR, skin paleness is followed by food coming back up

MOTILITY INTESTINAL
Segmentation and peristalsis increased by distention of the wall Intestino-intestinal reflex: severe distention or injury inhibits motility in the region. Ileo-gastric reflex: distension of ileum inhibits gastric motility

Gastro-ileal reflex: presence of chyme in stomach increases motility in ileum

MOTILITY IN COLON
Haustration: like segmentation, for mixing Colono-colonic reflex: distension in 1 part of the colon induces relaxation in other parts Gastro-colic reflex: a meal in the stomach increases colonic motility Defecation: - triggered by distention of the rectal wall - signal sent to sacral parasympathetic and cortex - smooth muscle anal sphincter open - if the person decides to go to the bathroom open voluntary muscle sphincter

DISORDERS OF GASTROINTESTINAL SYSTEM

Oral cavity disorders

Dental Plaque
Accumulations of dextrans (biofilm)

May calcify

Dental Caries
Streptococcus mutans Lactic acid erodes dental enamel

Periodontal disease Tooth support structures

Gingivitis gum inflammation Periodontitis root of tooth also affected

Oral Cavity Viral disease

Mumps Paramyxovirus
URT and salivary glands are affected Resurgence recently due to complacency and failure to vaccinate Complications male sterility, meningitis, eye, ear infections, attack on other

exocrine/ endocrine glands

Gastrointestinal Bacterial Intoxications

Staphylococcal Enterotoxicosis (Staph. aureus)
High starch or cream content, high protein foods

Pies, picnic foods, poultry, dairy products Foods subjected to temperature abuse Cooked foods need to be covered/refrigerated to avoid bacterial growth and toxin production Toxin can survive 30 minutes of boiling Low mortality Diarrhea symptoms 1-8 hr after food consumption

Clostridium perfringens Enterotoxicosis

Casseroles

Anaerobic bacterium
Toxin produced during endospore formation Diarrhea 8-24 hr after food consumption

Self-limiting
*Also causes gas gangrene, see Nervous System

diseases

Gastrointestinal Bacterial Intoxications

Botulism (Clostridium botulinum) Consumed toxin can cause flaccid paralysis Life support needed to prevent suffocation Bacillus cereus Food poisoning associated with rice/ meat contamination Found in water and soil Pseudomonas cocovenenans Polynesian coconut contamination Food poisoning may be fatal

Bacterial Infections
Enteritis Inflammation of the intestine Physical damage

Invasion of cells by bacteria

Dysentery

Submucosal damage leads to blood and mucus in the stool

Gram negative bacteria may cause fever to accompany

symptoms

Bacterial Infections
Salmonellosis (S. enteritidis) Poultry and poultry products Salmonella enteritidus

2000 strains Notifiable disease Strains help to trace public health problems to their source

Diarrhea 8-24 hr after food consumption

Self limiting, low mortality in infants and elderly

Typhoid Fever
Salmonella typhi

Human reservoir only

Fever headache diarrhea Many organs invaded
Bact. in urine, blood, feces WBC count decreases

Less than 500 cases/yr in U.S.A. Fluoroquinolones, chloramphenicol

Good public health measures prevent transmission

Asiatic Cholera
Vibrio cholerae Developing nations

Rice water stool Death due to shock/fluid loss

Rehydration therapy may be

more effective than antibiotics

Bacterial Intestinal Infections

Vibriosis Vibrio parahemolyticus Seafood associated Marine bacteria, may also infect wounds Self limiting 2-5 days Travelers Diarrhea Escherichia coli is a common pathogen Water sources Dehydration is biggest danger Complications infectious IBS , lactose intolerance

Enterohemorrhagic E. coli
E. coli O157:H7

Shiga toxins cause intestinal hemorrhage, kidney

failure, blindness Children most sensitive Ground beef, uncooked produce 3000 cases/yr estimated, 30 deaths in U.S.A.

Campylobacter jejuni
Food/H2O borne, copious diarrhea Opportunistic Second only to Salmonella in incidence Animal intestines are source Fluid replacement most important

Bacterial Upper G.I. Disease

Peptic Ulcer/Chronic Gastritis Helicobacter pylori Neutralizes stomach acid by degrading urea 4 million sufferers in U.S.A. Treatment

Antibiotics Acid suppressors Stomach liners, e.g. Pepto Bismol

H. pylori Stomach Damage

Viral Gastrointestinal Disease

Viral Enteritis Rotavirus Common in children Enterovirus Norwalk virus

Protozoan GI Disease Giardiasis

Giardia lamblia Backpackers disease Dysentery from drinking unpurified water Endemic in mountain areas

Protozoan GI Disease Amebic Dysentery

Entameba histolytica Endemic in developing nations

Protozoan GI Disease Balantidiasis

Balantidium coli Rare, severe dysentery Caused by ciliate

Anorexia, Vomiting and nausea

Anorexia precedes the above Nausea- general unpleasant subjective feeling. Vomiting is forceful expulsion of irritant. Medulla

coordinates reflex.

Characteristics of Vomiting:Coffee grounded color-Blood, partial digestion of protein in blood. Yellowish Green: Contents from bile or duodenum Deep brown: Contents from lower intestine.

DISORDERS FOR GASTROINTESTINAL SYSTEM

Gastro-oesophageal reflux disease - GORD

(heartburn & dyspepsia)

Discomfort caused by the reflux of acidic chyme from

the stomach into the oesophagus which can become inflamed

Causes of GORD are various but commonly it is the

inappropriate relaxation of the gastro-oesophageal sphincter that allows chyme to enter the oesophagus.
The symptoms may be worsened by coughing, lifting

or by certain foods.

Drugs used for Gastro-oesophageal reflux disease - GORD

Antacids - these usually contain aluminium or

magnesium compounds that increase the pH of chyme, making it less acid and reducing its irritating effect on the oesophagus.
Alginates - form a raft that floats on top of the

stomach contents that reduces reflux and protects the oesophageal mucosa. They are usually combined with an antacid.
Most are available OTC such as Gaviscon (sodium

alginate, sodium bicarbonate, calcium carbonate)

Antacid side effects

Magnesium salts diarrhoea Aluminium salts constipation Most cause burping from release of CO2 gas Interactions may delay un-coating of other drugs by

stomach acid

Control of gastric secretions

parietal cells

H+/K+ATPase proton pump

H+

Cl-

lumen of stomach

H2 receptor antagonists
Examples; cimetidine, famotidine, nizatidine and

ranitidine.
These block H2 (histamine) receptors in the gastric

mucosa.

The release of hydrochloric acid (HCl) and pepsin is

under the control of acetyl choline, gastrin and histamine

H2 receptor antagonists block the H2 receptors from

the stimulatory effect of histamine and thus reduce gastric secretions

Diarrhea
Diarrhoea involves either an increase in fluid secretion into

the gut, a reduction of fluid absorption from the gut or an increase in motility Diarrhoea is the frequent passage of liquid faeces. It can range from minor discomfort to emergency requiring fluid and electrolyte replacement. Diarrhoea can be acute or chronic Acute causes
food poisoning gastroenteritis - infection from:

- bacteria - Campylobacter, Salmonella, E. coli - viruses - astrovirus, rotavirus anxiety drugs e.g. antibiotics

Diarrhea
Classification of diarrhea:

Large Volume Diarrhea:-Secretory or osmotic -Lead to watery stool (increase secretion into intestine) -Often related to infection or short transits time Small volume Diarrhea - It is inflammatory bowel disorder - It is stool with blood, mucus and pus. Steatorrhea -Fatty diarrhea -Frequent, bulk, greasy loose stool with foul odor. -Characteristics of malabsorption disorder.

 Blood

Frank Blood:- Red blood on the surface of the stool. May be due to lesion in rectum / anal cavity. Occult Blood: Small hidden amount in stool, not visible by eyes. Is due to bleeding ulcers in stomach and small intestine. Melena: dark colored is due to significant bleeding in digestive tract. Gas: Develops normally in digestive tract. Due to swallowing of air and digestion/bacterial action.

Chronic Diarrhoea
Chronic diarrhoea - causes include
irritable bowel syndrome (IBS) inflammation of the bowel - eg. ulcerative colitis chronic bowel infections hormonal changes e.g. diabetes foods intolerance - milk (lactose intolerance)

- wheat (coeliac disease)

Anti-diarrhoea drugs
First there is a need to identify and remedy the cause

of the problem, not just to relieve the symptoms. For example, in the case of bacterial infection, an antibiotic may be required plus any necessary rehydration.
Anti-diarrhoea drugs can either reduce motility eg. opiates

absorb excess fluid eg. kaolin

Anti-diarrhoea drugs
Antimotility agents are mainly based on opiates.

They increase muscle tone of the GIT which decreases the rate of propulsion through the system.

Codeine phosphate Co-phenotrope (diphenoxylate and atropine) Loperamide hydrochloride Morphine (as kaolin and morphine) constipation and drowsiness

Unwanted effects - nausea, vomiting, (ironically)

Adsorbents - kaolin increases the viscosity of gut

contents thus slowing their passage

Constipation
Difficult or infrequent defecation that can have many

causes including abdominal muscle weakness eg. from surgery pain eg. from haemorrhoids low fibre diet sedentary lifestyle depression antidepressants (anticholinergics block parasympathetic system) opiates dehydration

Treatment for constipation

Treatment is primarily directed at cause e.g. diet Bulk forming laxatives - increases faecal mass and

stimulates peristalsis eg. ispaghula husk, methylcellulose and sterculia

Osmotic laxatives - pulls water into gut and softens

stools and increases faecal mass eg. lactulose and macrogols (polyethylene glycols)
Stimulant laxatives - increases fluid secretion into gut

and stimulates peristalsis eg. bisacodyl & senna

Haemorrhoids (piles)
Haemorrhoids (piles) are enlarged and engorged

blood vessels in or around the anus. Often result of constipation, pregnancy or inactivity. Symptoms include pain on defecation, blood streaked stools, bloody discharge and itching.

Haemorrhoids (piles)
Many OTC preparations are available that contain

combinations of mild astringents such as zinc oxide and local anaesthetics such as lignocaine
Prescription only medicines contain corticosteroids

such as hydrocortisone as well as astringents and local anaesthetics

All may be combined into ointment or suppositories

Gastric Ulcers (gastritis)

Inflammation of stomach, intestine

Usually caused by an infection

Inflammation of gastric mucosa leads to vomiting Inflammation of intestine causes increased motility,

impaired absorption lead to diarrhea Nausea and abdominal cramps Microorganism transmitted by contaminated food, water, oral feceal route

Peptic ulcers
Proximal duodenum most common Also found in antrum of stomach or lower esophagus Usually appear as single, small, round cavities- reaches smooth margins

and even penetrates submucosal layer. Once acid or pepsin penetrate mucosal barrier tissues exposed to continuous damage. When acid diffuses into gastric wall may erodes deeply into musculature and eventually perforate wall. Erosion invades by wall, bleeding occurs it could be Persistant loss of small amount of blood Or massive hemorrhage Development begins due to break down of mucosal barrier Decreased resistance of mucosa or increase Hcl or pepsin secretion due to impaired mucosal defenses (gastric ulcer) and increase acid secretion (duodenal ulcer) Most have H. pylori present.

ULCERS PATHOLOGY
Mucosal barrier damaged by: - Inadequate blood supply - Excessive glucocorticoid secretion or medicines -

(prednisone) Ulcerogenic substances Atropy of gastric mucosa. Increases acid/pepsin secretion associated with Increased gastrin secretion Increased vagal stimulus or increased sensitivity to stimulus Increased acid-pepsin secretory cells in stomach Increased acid-pepsin secretion Interference with normal feedback mechanism Rapid gastric emptying

Ulcers-pathophysiology
Stress affects Healing is difficult

-Granulation tissue forms deep in cavity which break down -Longer healing time Complications are: Hemorrhage Perforation Obstruction

ULCER ETIOLOGY
Common , particulary in men Western countries have higher incidence Genetic factor only in case of duodenal Gastric common in older people

Ulcers signs and symptoms Epigastric burning/aching -2 to 3 hours after meals, at night -cyclic pain relieved by eating Heartburn, nausea and vomiting. Treatment Test are: Fibroscopic endoscopy, Barium X-ray and Biopsy Treatment: Combo of drugs- 2-3 antimicrobial drugs and medicines to decrease acid secreation.

Disorders of liver and pancreas

Gallstones: Formation of masses of solid material (calculi) that is formed in bile. The vary in size sometimes small stones and large can obstruct flow of pile. Initially form in bile ducts, gall bladder, cystic ducts. May consist primarily of cholesterol (white), bilirubin (black) or both. Tend to form when bile contains high concentration of component or when bile salts low. Stone grows in size as deposit increases. Presence of stones can cause irritation and inflammation of gallbladder wall Stones can obstruct bile flow in cystic or common bile duct which lead to spasms of pain. In adverse condition may lead to pancreatitis.

Etiology of gall stones

Cholesterol gallstones

-Common in females High cholesterol level in bile Obesity, oral contraceptives, estrogen supplements
Bile pigments stones - Common in individual with hemolytic anemia and

alcoholic cirrhosis. - Large stones may lead to rupture of gall bladder. - Only treatment is surgery to remove stones and gall bladder.

Pathology - Hernias
Diaphragmatic Hernia:-Part of stomach elevated,

protruded through hiatus of diaphragm into thoracic cavity. They are of two type:- Sliding and Rolling Sliding one is more common in which portion of stomach and gastro esophageal junction move up diaphragm. On standing herniated portion slides down in abdominal cavity. Rolling (paraesophageal hernia): Fundus moves up through enlarged or weak hiatus in diaphragm.

 Food lodges in pouch

Hiatal Hernia

-Inflammation of mucosa, reflex of food unto esophagus, dysphagia (difficulty swallowing) Often incompetent gastro esophageal sphincter. Contributing factors -shortening of esophagus -weakness of diaphragm -increase abdominal pressure (pregnancy) Signs -Heartburn -Frequent Belching Discomfort when lying supine Dysphagia common due to inflammation of esophagus or mass food in pouch compresses esophagus.

Hepatitis
Inflammation of liver May results from local infection (viral), infection

elsewhere or from chemo/drug toxicity. Mild inflammation and necrosis -obstruction of blood and bile flow in liver Decrease liver cell function Damage to liver cells -because of function of liver - But good because functional reserve and excellent regeneration.

Viral Hepatitis
Infection from group of viruses that specifically target

hepatocytes -HAV, HBV, HCV, HDV, HEV Liver cells damaged in 2 ways: -direct action of virus (HCV) -Cell mediated immune response (HBV) Cell injury results in: -Inflammation and necrosis -Swollen hepatocytes and liver |-With severe inflammation biliary stasis

Viral Hepatitis
Degree of inflammation and damage varies -Many cases mild and not identified -Some show few manifestations but not jaundice -Other massive necrosis and liver failure -Depending on severity Hepatic cells may regenerates or fibrous tissue forms which blocks channels fro blood and bile further damage. Chronic inflammation - B, C and D - Persistent inflammation and necrosis of liver - -eventually causes permanent liver damage

HAV
Contagious period (fecal shedding) -Begins several weeks before onset of symptoms -1st antibodies IgM-HAV appear -2nd IgG-HAV they remains for years and provide further protection.

Viral Hepatitis (HBV- Serum Hepatitis)

Double stranded DNA virus 3 antigens -2 core antigens (HBcAG, HBcAg) -1 surface antigen (HBsAg) These antigens stimulates antibody productin in body.

HBV
Carrier state common Relative incubation period is 2 months More difficult to tract source of infection It cant be detected but can be transmitted by blood or sexual transmission. There are vaccine for long term protections.

HCV (NANB Hepatitis)

Single strand RNA Transmission common by blood transfusion. Increases the risk of hepatocellular carcinoma

HDV (Delta Virus Hepatitis)

Incomplete RNA virus Requires the presence of HBsAg to replicate and produce active infection, increase the severity of HBV. Transmission is by blood and increase administration of IV drugs.

HEV
Single stranded RNA virus Spread by oral fecal route Similar to HAV Common in Asia and Africa

Signs and symptoms Asymptomatic, mild and fatal 3 Stages -Precicteric (prodomal) Icteric (Jaundice) -Postietric (recovery)

Treatment of Viral Hepatitis

No method to destroy virus Gamma globulin helpful when given early Supportive measures (rest, diet high in protein, carbohydrates and vitamins) Chronic B and C treated with -Interferon alpha -lamivudin -gradual destruction of liver will lead to cirrhosis, hepatocellular cancer.

Colorectal Cancer
Malignant neoplasms from adenomatous polyps Polyps is mass that protrudes into the limen As increase in size increase the risk of dysplasia and malignant changes. Adenocarcinoma is distributed in R colon and L colon, distal sigmoid colon and rectum Occurs primarily in the age of 55, In western hemisphere Genetic factors Environmental factors like High fat, sugar, red meat produce carcinogenic substances Decrease fiber and increase risk Prolong contact of mucosa with carcinogen

Colorectal Cancer Signs and Symptoms

Initial depends on location and characteristic of feces at that location. -Circumferential lesion in recto-sigmoid Fecal mass solid Causes partial obstruction with dilation of proximal sigmoid Vague cramping, small, flat pellets, feeling of incomplete emptying. -Right colon Feces liquid, no obstruction General systemic signs Unexplained changes in bowel habits Blood in feces. Treatment: Surgical removal of involved area, radiation, chemotherapy.