Diagrammatic view of Digestive System

ANATOMY OF DIGESTIVE SYSTEMComponents of Digestive system:1.Mouth2.Teeth3.Tongue4.Saliva5.Pharynx6.Esophagus7.Stomach8.Accessory organs (pancreas, gall bladder and spleen)9.Liver10.Duodenum11.Small Intestine12.Large Intestine

INGESTIONMouth

mechanical digestionteeth

breaking up foodchemical digestion

salivaamylase

enzyme digests starchmucin

slippery protein (mucus)protects soft lining of digestive systemlubricates food for easier swallowing

buffers neutralizes acid to prevent tooth decay

anti-bacterial chemicals kill bacteria that enter mouth with food

INGESTIONmouthbreak up fooddigest starchkill germsmoisten 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 pharynxEpiglottis and vocal cords close off

trachea; breathing temporarily ceasesBolus moves into esophagus, then through

esophageal sphincter into stomach

TEETH

TONGUE

SALIVASaliva is produced by salivary glands (Sublingual gland, Submandibular gland and Parotid gland) at back of mouth and under tongueSaliva includes

Salivary amylase (enzyme)Bicarbonate (buffer)Mucins (bind food into bolus)Water

MAJOR SALIVARY GLAND

PHARYNXThe back of the throat.Larynx- passage for air, closes when we swallow.Is approximately 15cm long.

ESOPHAGUSIt is the tube that connects your mouth and your stomachUsually collapsed (closed)3 constrictions

Aortic archLeft primary bronchusDiaphragm

Surrounded bySNS plexusBlood vessels

FunctionsSecrete mucousTransport food

Peristalsisseries of involuntary wave-like muscle contractions which move food along the digestive tract

ANATOMY OF STOMACH3 muscle layers

ObliqueCircularLongitudinal

RegionsCardiac sphincterFundusAntrum (pylorus)Pyloric sphincter

VascularInner surface thrown into folds – Rugae

Contains enzymes that work best at pH 1-2

STOMACHmouthbreak up fooddigest starchkill germsmoisten food

stomachkills germs break up fooddigest proteinsstore food

STOMACH SECREATIONSSecreted 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 CHYMEA thick mixture of food and gastric fluid

High acidity kills many pathogens

Mixed and moved by waves of stomach

contractions (peristalsis)

Accessory Organs

PancreasSpleenGall Bladder

Accessory Organs

PANCREASAn 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, chymotrypsindigest starch

amylaseBuffers

neutralizes acid from stomach

LIVER & GALL BLADDERDetoxifies/removes

DrugsAlcohol

StoresGlycogenVitamins (A, D, E, K)Fe and other mineralsCholesterol

Activates vitamin DFetal RBC productionPhagocytosisMetabolizes absorbed food molecules

CarbohydratesProteinsLipids

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)

SMALL INTESTINEMost 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 Amino- Di- Tri-

Sucrases Maltase Lactase Saccharidases

Di- Tri-

Lipase Nucleases

SMALL INTESTINEFunction

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-IleumNutrients will be reabsorbed along the jejunum-

ileumBrush border contains villi which increase the

surface of absorptionThe villi are structured for nutrient absorption

VILLI

LARGE INTESTINEExtends from ileocecal valve to anusRegions

Cecum – AppendixColon

Ascending Transverse Descending

RectumAnal canal

LARGE INTESTINE

LARGE INTESTINEFunctions of LI:

Mechanical digestion Haustral churning Peristalsis Reflexes

Gastroileal Gastrocolic

Chemical digestion – Bacterial digestion Ferment carbohydrates Protein/amino acid breakdown

Absorbs• More water• Vitamins

– B– K

Concentrate/eliminate wastes

APPENDIX (VESTIGIAL ORGAN)

RECTUMLast section of colon (large intestines)

eliminate fecesundigested materials

extracellular wastemainly cellulose from plantsroughage or fiber

masses of bacteria

FAECES FORMATION &DEFECATIONChyme dehydrated to form fecesFeces composition

WaterInorganic saltsEpithelial cellsBacteriaByproducts of digestion

DefecationPeristalsis pushes feces into rectumRectal walls stretch

ControlParasympatheticVoluntary

Physiology of digestive systemWhich 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

OverviewFood 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 digestionCarbohydrates, 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 ---> disaccharides ---> monosaccharides

2- Proteins ---> peptides ---> amino acids

3- Lipids ---> diglycerides ---> monoglycerides and fatty acids

Gastrointestinal systemOverviewFunctional anatomy of the GI systemDigestion and absorption of nutrients and

waterFate of nutrients in the liverPrinciples of GI regulationGI secretion and regulationGI motility and regulation

ABSORPTION OF CARBOHYDRATESMonosaccharides (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 PROTEINProteins 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 LIPIDLipids (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 MINERALSSodium: 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+

HCO3-: secreted by pancreas, neutralizes H+ from stomach. Used as a buffer

Calcium: need an active transport to cross the intestinal epithelium. Absorption promoted by a derivative of Vit D

Iron: actively reabsorbed. Stored as ferritinWater: 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 SYSTEMOverviewFunctional anatomy of the GI systemDigestion and absorption of nutrients and

waterFate of nutrients in the liverPrinciples of GI regulationGI secretion and regulationGI motility and regulation

FATE OF NUTRIENTSGlucose:

- 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 SYSTEMOverviewFunctional anatomy of the GI systemDigestion and absorption of nutrients and

waterFate of nutrients in the liverPrinciples of GI regulationGI secretion and regulationGI motility and regulation

GI organization

Control PathwaysBoth hormonal and neuralShort pathways: involves automatic regulation

within the enteric system itselfLong pathways: involves the CNS (somatic and

autonomic)Three phases: cephalic, gastric and intestinal

phases

Cephalic phase: salivary and gastric secretionsSalivary secretion stimulated by parasympathetic NS by

odors, sight, taste saliva fluid and rich in enzymesStimulated by sympathetic NS thick secretion, rich in

proteinsGastric secretion: increase acid and enzymes secretion in response to sight, smell and taste of food

Gastric phaseStimuli: 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 SYSTEMOverviewDigestion of nutrientsAbsorption of nutrients and waterPrinciples of GI regulationGI secretion and regulationGI motility and regulation

Motility and its regulationThe 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 MOTILITYGastric 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 INTESTINALSegmentation 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 COLONHaustration: like segmentation, for mixingColono-colonic reflex: distension in 1 part of

the colon induces relaxation in other partsGastro-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 disordersDental 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 productsFoods subjected to temperature abuse

Cooked foods need to be covered/refrigerated to avoid bacterial growth and toxin production

Toxin can survive 30 minutes of boilingLow mortalityDiarrhea symptoms 1-8 hr after food consumption

Clostridium perfringens Enterotoxicosis

CasserolesAnaerobic bacteriumToxin produced during endospore formationDiarrhea 8-24 hr after food consumptionSelf-limiting*Also causes gas gangrene, see Nervous

System diseases

Gastrointestinal Bacterial Intoxications

Botulism (Clostridium botulinum)Consumed toxin can cause flaccid paralysisLife support needed to prevent suffocation

Bacillus cereusFood poisoning associated with rice/ meat

contamination Found in water and soil

Pseudomonas cocovenenansPolynesian coconut contaminationFood poisoning may be fatal

Bacterial InfectionsEnteritis

Inflammation of the intestinePhysical damage

Invasion of cells by bacteria

Dysentery Submucosal damage leads to blood and mucus in

the stoolGram negative bacteria may cause fever to

accompany symptoms

Bacterial InfectionsSalmonellosis (S. enteritidis)

Poultry and poultry productsSalmonella enteritidus

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

sourceDiarrhea 8-24 hr after food consumptionSelf limiting, low mortality in infants and

elderly

Typhoid FeverSalmonella typhiHuman reservoir onlyFever headache diarrheaMany organs invaded

Bact. in urine, blood, fecesWBC count decreases

Less than 500 cases/yr in U.S.A.Fluoroquinolones, chloramphenicolGood public health measures prevent

transmission

Asiatic CholeraVibrio choleraeDeveloping nations

Rice water stool Death due to shock/fluid

lossRehydration therapy

may be more effective than antibiotics

Bacterial Intestinal InfectionsVibriosis

Vibrio parahemolyticusSeafood associatedMarine bacteria, may also infect woundsSelf limiting 2-5 days

Traveler’s DiarrheaEscherichia coli is a common pathogenWater sourcesDehydration is biggest dangerComplications – infectious IBS , lactose

intolerance

Enterohemorrhagic E. coliE. coli O157:H7Shiga toxins cause intestinal hemorrhage,

kidney failure, blindnessChildren most sensitiveGround beef, uncooked produce3000 cases/yr estimated, 30 deaths in U.S.A.

Campylobacter jejuniFood/H2O borne, copious diarrheaOpportunisticSecond only to Salmonella in incidence

Animal intestines are sourceFluid replacement most important

Bacterial Upper G.I. DiseasePeptic Ulcer/Chronic Gastritis

Helicobacter pyloriNeutralizes stomach acid by degrading urea4 million sufferers in U.S.A.Treatment

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

H. pylori Stomach Damage

Viral Gastrointestinal DiseaseViral Enteritis

RotavirusCommon in children

EnterovirusNorwalk virus

Protozoan GI Disease — GiardiasisGiardia lamblia

Backpackers diseaseDysentery from drinking unpurified waterEndemic in mountain areas

Protozoan GI Disease — Amebic DysenteryEntameba histolytica

Endemic in developing nations

Protozoan GI Disease — BalantidiasisBalantidium coli

Rare, severe dysenteryCaused by ciliate

Anorexia, Vomiting and nauseaAnorexia precedes the aboveNausea- 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

duodenumDeep 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 effectsMagnesium 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

H+ Cl-

lumen of stomach

parietal cells

H+/K+ATPase proton pump

H2 receptor antagonistsExamples; 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

DiarrheaDiarrhoea 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 chronicAcute causes –

• food poisoning• gastroenteritis - infection from: - bacteria - Campylobacter, Salmonella, E. coli- viruses - astrovirus, rotavirus• anxiety• drugs e.g. antibiotics

DiarrheaClassification of diarrhea:Large Volume Diarrhea:--Secretory or osmotic-Lead to watery stool (increase secretion into

intestine)-Often related to infection or short transits timeSmall 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.

BloodFrank 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 DiarrhoeaChronic 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 drugsFirst 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 drugsAntimotility 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)

Unwanted effects - nausea, vomiting, (ironically) constipation and drowsiness

Adsorbents - kaolin increases the viscosity of gut contents thus slowing their passage

ConstipationDifficult 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 constipationTreatment 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, intestineUsually caused by an infectionInflammation of gastric mucosa leads to

vomitingInflammation of intestine causes increased

motility, impaired absorption lead to diarrheaNausea and abdominal crampsMicroorganism transmitted by contaminated

food, water, oral feceal route

Peptic ulcersProximal duodenum most commonAlso found in antrum of stomach or lower esophagusUsually 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 PATHOLOGYMucosal 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-pathophysiologyStress affectsHealing is difficult-Granulation tissue forms deep in cavity which

break down-Longer healing timeComplications are:-HemorrhagePerforationObstruction

ULCER ETIOLOGYCommon , particulary in menWestern countries have higher incidenceGenetic factor only in case of duodenalGastric common in older people

Ulcers signs and symptomsEpigastric burning/aching-2 to 3 hours after meals, at night-cyclic pain relieved by eatingHeartburn, nausea and vomiting.TreatmentTest are: Fibroscopic endoscopy, Barium X-ray and BiopsyTreatment: Combo of drugs- 2-3 antimicrobial drugs and

medicines to decrease acid secreation.

Disorders of liver and pancreasGallstones: 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 wallStones 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 stonesCholesterol gallstones-Common in femalesHigh cholesterol level in bileObesity, 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 - HerniasDiaphragmatic Hernia:-Part of stomach

elevated, protruded through hiatus of diaphragm into thoracic cavity.

They are of two type:- Sliding and RollingSliding 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.

Hiatal HerniaFood lodges in pouch-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 BelchingDiscomfort when lying supineDysphagia common due to inflammation of esophagus

or mass food in pouch compresses esophagus.

HepatitisInflammation of liverMay results from local infection (viral),

infection elsewhere or from chemo/drug toxicity.

Mild inflammation and necrosis-obstruction of blood and bile flow in liverDecrease liver cell functionDamage to liver cells-because of function of liver- But good because functional reserve and

excellent regeneration.

Viral HepatitisInfection from group of viruses that specifically

target hepatocytes-HAV, HBV, HCV, HDV, HEVLiver 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 HepatitisDegree 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 severityHepatic 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

HAVContagious 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 virus3 antigens-2 core antigens (HBcAG, HBcAg)-1 surface antigen (HBsAg)These antigens stimulates antibody productin in body.

HBVCarrier state commonRelative incubation period is 2 monthsMore difficult to tract source of infectionIt can’t be detected but can be transmitted by blood or sexual transmission.There are vaccine for long term protections.

HCV (NANB Hepatitis)Single strand RNATransmission common by blood transfusion.Increases the risk of hepatocellular carcinoma

HDV (Delta Virus Hepatitis)Incomplete RNA virusRequires 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.

HEVSingle stranded RNA virusSpread by oral fecal routeSimilar to HAVCommon in Asia and Africa

Signs and symptomsAsymptomatic, mild and fatal3 Stages-Precicteric (prodomal)Icteric (Jaundice)-Postietric (recovery)

Treatment of Viral HepatitisNo method to destroy virusGamma globulin helpful when given earlySupportive 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 CancerMalignant neoplasms from adenomatous polypsPolyps is mass that protrudes into the limenAs 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 hemisphereGenetic factorsEnvironmental factors like High fat, sugar, red meat produce carcinogenic substancesDecrease fiber and increase riskProlong contact of mucosa with carcinogen

Colorectal Cancer Signs and SymptomsInitial depends on location and characteristic of feces at that location.-Circumferential lesion in recto-sigmoidFecal mass solidCauses partial obstruction with dilation of proximal sigmoidVague cramping, small, flat pellets, feeling of incomplete emptying.

-Right colonFeces liquid, no obstruction General systemic signsUnexplained changes in bowel habitsBlood in feces.Treatment: Surgical removal of involved area, radiation, chemotherapy.