Post on 22-Sep-2014
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.