Patho GI Tract

• Mouth/ oral cavity
• Esophagus
• Stomach
• Duodenum
• Liver?
• Pancreas?

• SI
• Gall bladder
• Large intestine
• Anus

• Mucosa
• Submucosa
• Serosa

• Inner most layer
• epithelium includes mucus producing cells

• - it is the middle layer
• - connective tissue
• - blood vessels
• - nerves
• - lymphatic
• - secretory glands
• - circular and longitudinal muscle layers

• outer layer
• visceral peritoneum
• fluid (sera)

• - initial phase of mechanical breakdown of food
• - mastication by teeth
• - initial chemical digestion- salivary amlase
• - formation of bolus
• Swallowing - tounge and pharynx
• Esophagus- closed except for when swallowing, skeletal mm at superior end which gradually replaced by smooth mm

• - deglutition
• - tounge and pharynx

CN V- trigeminal

CN IX- glossopharyngeal

CN X- Vagus

CN XII- Hypoglossal

• - cleft lift and cleft palate
• - Aphthous Ulcers
• - Inections- opportunistic flora
• - Dental caries- infection
• - Peridontal disease
• - Inflammatory Dysfunction- hyperferatosis, Sialadenitis, infectious parotitis

• - disorder of the oral cavity
• - arise 2-3 months of gestation
• - feeding problems
• - high risk of aspirating fluid
• - speech development impaired

• - An inflmmatory lesions
• - Oral cavity disorder
• - physical injury
• - chemical injury
• - infection- streptococcus sanguis
• - immunological
• - allergy
• - dietary
• - painful, heat, redness, swelling
• - ulceration- intact or ruptured mucosa (cranker)

• Opportunstic flora
• Herpes
• Dental caries

• - streptococcus sanguies
• - candida albicans (candidasis- fungal)
• - immunocompromised

• - herpes simplex virus 1 (HSV-1)
• - clse contact transmission
• - viruse in sensory ganglion may remain dormant
• - activated by stress, trauma, other infetion
• - formation of blister, ulcers, clear fluid release- virus. Lesions heal spontaneously in 7-10 days
• May spread to eyes- conjunctivitis

• - infection
• - initiating microorganism- streptococcus mutans- lactobacillus follows in large numbers
• - bacteria break down sugars- increase LA
• - LA dissolves mineral in tooth enamel- tooth erosion and cavity formation- caries

• - intake of sugars and acids
• - fissures in tooth surface
• - dry mouth
• - laque formation
• - periodontal disease

• - infection and damage to the gingiva, periodontal ligament and bone- poor oral hygiene, systemic factors
• - Gingivitis- local or systemic problem- inflammation of the gingiva- red, soft, swollen, bleeds easily
• - Periodontitis- activity of the destructive microbe, aggravated by smoking, cancer, diabetes, inflammation in tissues/ bone around the tooth

• - leukoplakia
• - whitish plaque or epidermal thickening of mucosa
• - occurs on buccal mucosa, palate, lower lip
• -chronic irriation- epithelial may develop into squamous cell carcinoma

• Inflammation og the salivary glands
• can be infectious and non infectious
• most common- parotid gland

• - inflammatory dysfunction of the oral cavity
• - viral infection- mups

• -upper esophagus- striated mm
• -lower " " - smooth muscle
• Longitudinal and circular layers for peristalsis

• Obstruction
• - stenosis- chromic inflammation, fibrosis, esophagitis
• - tumor- internal or external
• - diverticular formation- outpouching, herniation
• - developmental defects- atresia (narrowing of opening to trachea), fistula (hole betweento organs or surfacesthat isnt to bethere)
• Neurological defects- infection, stroke, achalasia (disorder of esophagus- problems swallowing)
• Muscle impairment- ie diaphragm dystrophy-hiatal hernia

• Hiatus hernia
• Gastroerophageal reflux (GORD)

• - part of the stomach protrudes through the diaphragm into the thoracic cavity
• - sliding hernia- more common type, portion of the stomach and gastroesophageal junction slide up above the diaphragm
• - rolling or paraesophageal hernia- part of the fundus of the stomach moves up through an enlarged or weak hiatus in the diaphragm and may become trapped. Food lodges in pouch- inflammation of mucosa, reflux of food up esophagus- obstruction, dyspahgia, blood vessels trapped- ulceration, esophagitis
• 

- periodic reflux/ flow of gastric contents into distal esophagus- pain, inflammation- errosion of mucosa- ulceration, fibrosisand stricture

• Precipitated by:
• - hiatal hernia
• - lower esophageal sphincter incompetence
• - delayed gastric emptying
• - carreince, fatty/ spicy foods, alcohol, smoking and certain drugs

• - gastritis- acute and chronic
• - gastroenteritis
• - gastric and peptic (duodenal) ulcers
• - dumping syndrome
• - pyloric stenosis

• - inflamation
• - acute (self limiting)
• - gastric mucosa inflammation- ulcerated and bleeding (transient or progressive)

• Precipitating events:
• - infection by microorganisms
• - allergies to food
• - spicy or irritating foods
• - excessive alcohol intake
• - ingestion of ulcerogenic drugs eg aspirin
• - ingestion of corrosive or toxic substances
• - radiation or chemotherapy

• Chronic inflammation of the stomach mucosa
• Atrophy of the mucosa and loss of secretory glands
• decrease parietal cells- achlorhydria and decrease intrinsic factory- loss of vit B12 absorption

• - anorexia, nausea, epigastric discomfort, vomiting, cramps, pain and hematemesis (vomiting blood)
• - infection- headache, fever, diarrhea
• - prolonged vomiting- dehydration, electrolyte loss and metabolic acidosis
• - chronic- peptic ulcers and gastric carcinoma (stomach cancer)

• - inflammation of stomach and intestinal mucosa
• stomach- vomiting
• intesting- diarrhea

• Usually due to infection
• - enterotoxins
• - inflammation
• - ulceration
• - neurotoxins
• - allergic reactions to food or drugs

• - stomach and duodenum
• -penetrates submucosa

• - inadequate blood supply
• - increase in glucocorticoid secretion (involed in COH absorption)
• - ulcerogenic substances
• - chromic gastritis (inflammation of the lining of the stomach)

• - acid or pepsin penetrates the mucosalbarrier
• - tissue damage into muscularis
• - inflammation around the area
• - blood vessel involvement (perforation)- bleeding or hemorrhage
• - increase in acid and pepsin secretions
• - rapid gastric emptying

• - decrease mucosal resistance
• - increase in HCL
• - increase in pepsin secretions
• - helicobacter pylori (bacteria in stomach)
• 

• - increase gastric secretions
• - increase vagal stimulation (secretion and peristalsis)
• - increase number of acid- pepsin secretory cells
• - stimulates acid- pepsin secretions- alcohol, caffeine,certain foods
• - rapid gastric emptying

• - stomach syndrome
• - loss of control of gastric emptying
• - due to gastrectomy (removal of pyloric sphincter)
• - dumping of food into intestine
• 

• - stomach disorder
• - narrowing and obstruction of pyloric sphincter
• - developmental or acquired

• Developing
• - projectile vomiting immediately after feeding
• - firm mass at pylorus
• - decrease wieght
• - increase dehydration
• - persistnet hunger
• Acquired
• - persistent feeling of fullness
• - increased incidence of vomiting

• Celiac disease
• Chronic inflammatory Bowel disease
• Chroh's disease
• Appendicitis
• Diverticular disease
• Colorectal Cancer (CRC)
• Interstinal Obstruction
• Peritonitis

• - lower GI tract
• - malabsorption syndrome
• - primarily a childhood disorder- may occur in adults- middle age
• - defects in intestinal enzymes- might be linked to a genetic factor
• - prevents further digestion of gliadin-breakdown product of gluten- grains
• - immunological response- toxic effect on intestinal villi- atrophy of villi results in a decrease in enzyme production and SA
• - malabsorption and malnutrition- steatorrhea, mm wasting, low weight gain

• - Crohns disease- SI
• -ulcerative colitis- rectu, and proximally in colon
• 

• - inflammation - ulcer- coalesce- fissues/ abscesses/fistulas- fibrosis- stricture and obstructuion
• - involves all layers- granulomas are indicative
• - increase insetinal motility- decrease in digestion and absorption

• - a lwer GI tract disease
• - inflammation of mucosa and submucosa
• - changein goblet cell activity
• - edematous tissue and ulcerations develop- decrease in absorption of fluid and eletrolytes
• - increased risk of colorectal carsinoma

• - lower GI tract disease
• - inflammation and infection of the appendix

• - obstruction of appendiceal lumen - gallstone, foreigb material, twisting, spasm
• - increase fluid build up in appendix
• - microorganisms proliferate- inflammation of wall, purulent exudate, swelling, congestion and pressure within the appendix- ischemia and necrosis- increases permeability
• - bacteria and toxins escape through the wall - infection or peritonitis around the appendix- spread aling the peritoneal membrances
• -increased necrosis and gangrene in the wall- increase pressure
• - appendix ruptures or perforates- release of contents into peritoneal cavity- generalised peritonitis.
• 

• - lower GI tract disease
• - development of diverticular (pouching)
• - diverticulum- outpuching (herniation) of themucosa through the mm layer of the colon- sigmoid colon
• - diverticulosis
• * asymptomatic diverticular disease
• * imflammation of the diverticular

• - diverticula form at gaps between mm layers- weak wall
• - when pressure increases wall bulges outwards
• - stasis of feces in diverticula- inflammation and infection (diverticulitis)
• - intestinal obstruction
• - perforation/ peritoitis. abcess formation = cramping, tenderness, nausea, vomiting

• - develops from adenomatous polyps- dysplasia of polyp and malignant changes- CRC
• - distributed throughout the colon and rectum

• - genetic
• - diet
• - ulcerative colitis

• Which leads to
• - alter bowel function
• - obstruction
• - pain
• - bowel perforation

• - lower GI tract disease
• - lack of movement of intestinal contents through the intestines- more common in SI
• - Acute or progressive

• adhesions
• hernias
• tumors
• twist (volvulus)
• intussuception

• spinal cord injury
• paralytic ileus due to toxins
• abdominal surgery- ischemia
• inflammation or infection
• mesenteric thrombosis

• - gases and fluids proximal to blockage, distending the intestine
• - strong contractions of proximal intestine
• - pressure increases in lumen- increases secretions into intestine, compression of veins in wal, intestinal wall become edematous= prevention of absorption
• - inestinal distention- persistent vomiting- additional lossof fluid and electrolytes- hypovolemia
• - inetinal wall becomes ischmic and necrotic- decrease arterial blood supply due to the pressure- gangrene ensues, decrease innervation and cessation of peristalsis
• - bacteria leak into the peritoneal cavity or blood- peritonitis or septicemia

• - anorexia, nausea and vomitins- ways of eliminating noxious substances- emetic reflex
• - can lead to dehydration, acidosis, malnutrition
• - risk of aspiration- supine, unconsciou, drug/ alcohol
• - diarrhea
• - constipation
• - fluid and electrolyte imbalance
• - pain
• - malnutrition
•