GI Path: Small and Large Intestine Flashcards
Describe the Small Intestine
-Extends from pyloric sphincter to ileocecal valve/sphincter - inferior to the stomach/liver
- 3 sections: duodenum –> jejunum –> ileum
-Contains villi and microvilli
-Glands in crypts of Lieberkuhn (secretes enzymes for digestion)
-Lacteals
What is the function of the small intestine?
-Pyloric sphincter –> junction with stomach
-Ileocecal valve –> junction with large intestine
-Duodenum = receives chyme, pancreatic juice, bile neutralizes stomach acid
Pyloric Stenosis
Hyperplastic muscle at birth preventing food passage from stomach to duodenum
What is the pathogenesis of Pyloric Stenosis? The oral/clinical signs?
Pathogenesis:
-Developmental thickening of pylorus muscle –> prevents movement
Oral/Clinical:
-Projectile vomiting
-Failure to thrive (weight loss)
-Persistent hunger
Meckel Diverticulum
Most common birth defect of digestive tract –> developmental outpouching of all 3 layers of the ileum wall
What is the pathogenesis of Meckel Diverticulum? The oral/clinical signs?
Pathogenesis:
-Failure of vitelline duct to involute
Oral/Clinical:
“rule of 2’s”
- 2% of population affected
- 2 inches long
-Located w/in 2 ft of ileocecal valve
-Presents during first 2 yrs w/ bleeding
Volvulus
Twisting of bowel along its mesentery causing obstruction
What is the pathogenesis of Volvulus? The most common locations? The oral/clinical signs?
Pathogenesis:
-Loop of bowel gets twisted –> disruption of blood supply due to compromised venous return –> hemorrhagic infarction occurs = obstruction
Common Locations:
-Sigmoid colon –> elderly
-Cecum –> young adults
Oral/Clinical:
-Abdominal distention
-Pain
-Nausea/vomiting
Hernia
Weakened wall in the abdomen
*causes 40% of obstructions
What are the complications of a Hernia? The 3 types? The oral/clinical sings?
Complications:
1) obstruction
2) strangulation
3) infarction
3 Types:
1) Inguinal –> males 7:1
2) Femoral –> females
3) Umbilical
Oral/Clinical:
-Bulge or lump
-Pain or discomfort
Adhesions
Scar tissue formation –> can lead to partial obstruction
What is the pathogenesis of Adhesions? The oral/clinical signs?
Pathogenesis:
-Fibrous tissue forms from previous surgery
Oral/Clinical:
-Abdominal/back pain
-Constipation
Intussusception
Telescoping of proximal segment of bowel forward into distal segment
*most common cause of intestinal obstruction in children under 3 yrs
What is the pathogenesis of Intussusception? What it is associated with? What are the oral/clinical signs?
Pathogenesis:
-Segment of bowel pulled forward by peristalsis –> obstruction and disruption of blood supply = infarction
Associated w/:
1) Lymphoid hyperplasia (children)
2) Tumors (adults)
Oral/Clinical:
-Children
-Pain
-Diarrhea/bloody mucous stool
-Nausea/vomiting
*treatment is emergency surgery
Mesenteric Arterial Occlusion
Occlusion of the arterial vascular supply of the intestinal system
*segmental infarct –> usually of superior mesenteric artery
What is the pathogenesis of Mesenteric Arterial Occlusion? The oral/clinical signs?
Pathogenesis:
1) Atherosclerosis –> especially in DM
2) Thrombosis –> A.fib; birth control pills after 40
3) Embolism –> I.E.
4) Tumors
5) Trauma
Oral/Clinical:
-Sudden severe pain
-Peritonitis/shock
- 90% fatal w/in 48hrs
Mesenteric Venous Occlusion
Occlusion due to thrombosis of one or more major veins draining the intestinal system
What is the pathogenesis of Mesenteric Venous Occlusion? The oral/clinical signs?
Pathogenesis:
1) Peritonitis
2) Volvulus
3) Embolism –> I.E.
4) Portal HTN
5) Tumors
Oral/Clinical:
-bloating/vomiting/pain
-bloody stool/diarrhea
-fever
Crohn Disease
Chronic relapsing granulomatous disease resulting in segmental bowel thickening, luminal obstruction, and malabsorption
What are the most common sites of Crohn Disease?
Distal Ileum, Proximal Colon and Rectum
What is the pathogenesis of Crohn Disease?
1) Surface ulceration with loss of villi –> replaced with edematous cobblestone mucosa
2) Transmural inflammation with GRANULOMAS and knife-like FISSURES extending deep into bowel wall (possible perforation)
3) Thickening + fibrosis + stricture in segments of bowel wall –> separated by segments of normal bowel = “SKIP LESIONS”
What are the causes of Crohn Disease?
1) Genetic susceptibility
2) Immune response (increased T-cell response)
3) Worse in smokers
What are the clinical signs of Crohn Disease? Oral signs?
Clinical:
-LRQ (lower R quadrant) colicky pain/bloody diarrhea
-Anorexia/weight loss/nausea-vomiting/fever
-Rectal fissures/abscesses/fistulas - 90%
-White, female - 20-30yrs
-Chronic diarrhea –> bloody if rectal involvement
Oral:
-Angular cheilitis
-Mucosal oral ulcers
-Orofacial granulomatosis
*risk for carcinoma if colon involvement
What are the complications of Crohn Disease?
1) Obstruction from stricture
2) Perforation of fissures
3) Peritonitis
4) Adhesions
5) Hospitalization
What are the treatments for Crohn Disease?
-Corticosteroids
-Feeding tube/ I.V.
*Surgery is often needed but reserved for last resort
Celiac Disease
Immune-mediated disease of small intestine causing severe, generalized malabsorption
What is the pathogenesis of Celiac Disease? The oral/clinical signs?
Pathogenesis:
-Gliadin induces T-cell response = destruction of villi of small intestine –> villi become atrophic = severe malabsorption
Oral/Clinical:
-Children = failure to thrive
-Abdominal distension/diarrhea
-ORAL ULCERS
-Herpiform dermatitis
*may present latently in adults/treatment = remove gluten from diet
What is Celiac Disease associated wtih?
1) Specific HLA profile
2) Risk of adenocarcinoma
3) Risk of T-cell lymphoma
Carcinoma of Ampulla
Most common site of small intestinal malignancy in the ampulla of Vater
What is the pathogenesis of Carcinoma of Ampulla? What is it associated with? The oral/clinical signs?
Pathogenesis:
-Adenocarcinoma
Associated with:
1) Genetic factors
2) FAP (familial adenomatous polyposis)
Oral/Clinical:
-Obstructive jaundice - 80%
-Abdominal pain
-Fatigue/weight loss
*Good prognosis due to early diagnosis
Where is the Large Intestine located?
Extends from the ileocecal valve to the external anal sphincter surrounds small intestine
What are the 4 sections of the Large Intestine?
1) Colon = cecum + appendix –> ascending colon –> transverse colon –> descending colon –>
2) Sigmoid colon –>
3) Rectum –>
4) Anal canal + external anal sphincter
What is the function of the large intestine?
-Absorbs water and salts
-Eliminates indigestible food as feces
- 2 sphincters control opening/closing:
*ileocecal valve
*external anal sphincter
Hirschsprung Disease = Congenital Megacolon
Developmental defect in relaxation and peristalsis of rectum and distal sigmoid colon = obstruction
*associated with Down’s syndrome
What is the pathogenesis of Hirschsprung Disease = Congenital Megacolon? The oral/clinical signs?
Pathogenesis:
-Congenital failure of ganglion cells to descend –> causes massive dilation of bowel proximal to obstruction = megacolon
Oral/Clinical:
-Newborns/children
-Failure to pass meconium
-Megacolon develops
*Tx is resection of bowel due to risk of colon rupture
Acquired Megacolon
Persistent dilation and lengthening of the colon in the absence of obstruction with loss of peristalsis
What is the pathogenesis of Acquired Megacolon? the oral/clinical signs?
Pathogenesis:
1) Infection
2) Disease
3) Medications
4) Congenital
Oral/Clinical:
-Constipation
-Bloating/abdominal pain
-Fecal impaction/fecalomas
Diverticular Disease
Pouch-like protrusions of mucosa and submucosa that herniate through the walls of colon - usually sigmoid colon
*Diverticulosis = multiple diverticula (pouches) in the colon
*Diverticulitis = inflammation of diverticula
What is the pathogenesis of Diverticular Disease? What is it associated with?
Pathogenesis:
-Constipation = muscle hypertrophy = increased pressure in colon –> herniation of mucosa/submucosa –> fecal material trapped in pouch = infection and possible perforation and peritonitis
Associated with:
-Chronic constipation/straining
-Family history
-Low fiber diet
-Smoking/alcohol/NSAIDs
What are the oral/clinical signs of Diverticular Disease? The complications associated with it?
Oral/Clinical:
- 40+yrs
-Diverticulosis –> asymptomatic
-Diverticulitis –> acute LLQ pain, fever, and rectal bleeding
Complications:
1) Bowel obstruction
2) Abscess formation
3) Rupture = peritonitis
*Tx is to mitigate symptoms and monitor
Immune-mediated inflammatory bowel conditions –> includes:
1) Ulcerative colitis
2) Crohn Disease
Ulcerative Colitis
Chronic relapsing ulcerative-inflammatory disease of colon resulting in bouts of explosive bloody diarrhea
(“kissing cousin” to Crohn Disease)
What are the most common sites for Ulcerative Colitis?
Rectum (always) –> extends proximally
*only involves large intestine
What is the pathogenesis for Ulcerative Colitis?
Always begins in rectum –> may extend proximally but contained within colon –> neutrophilic absesses form in mucosal crypts and coalesce –> mucosa and submucosa constantly slough and regenerate –> form granulation tissue masses = pseudopolyps
What are some notes to consider about Ulcerative Colitis?
1) Muscle/serosa NOT affected = not full thickness
2) Bowel wall NOT thickened
3) Involvement is confluent - NO “skip lesions”
4) NO granulomas
What are the causes of Ulcerative Colitis?
1) Genetic susceptibility
2) Auto-immune disease (hyper-response to irritants)
3) Less symptomatic in smokers
What are the clinical signs of Ulcerative Colitis? The oral signs?
Clinical:
-LLQ colicky pain - possible megacolon
-Crypt abscesses
-White females - 30s
-Attacks of bloody-mucoid diarrhea
-Arthritis-rashes-sclerosing choleangitis
Oral:
-Aphthous-like ulcers
-Pyostomatitis vegetans
*Risk for carcinoma
Pseudomembranous Colitis
Acute necrotizing ulceration of colon mucosa
*causes explosive diarrhea and electrolyte loss
What is the pathogenesis of Pseudomembranous Colitis? What is it associated with? The oral/clinical signs?
Pathogenesis:
-Clostridium difficile overgrows as opportunistic infection due to clindamycin or spore ingestion –> C. diff produces endotoxin = cell death –> WBCs + fibrin + necrotic cells form membrane-like structure = “pseudomembrane”
Associated with:
1) Antibiotics (especially clindamycin)
2) Recent hospitalization or exposure = contagious
Oral/Clinical:
-Explosive watery-mucous-bloody diarrhea
-Electrolyte loss/fever/malaise
Appendicitis
Lumen obstruction of appendix leading to inflammation
What is the pathogenesis of Appendicitis? The oral/clinical signs?
Pathogenesis:
-Intraluminal content stasis –> increased lumen pressure –> thrombosis –> ischemia/necrosis –> increased bacteria = secondary infection
Oral/Clinical:
- 10-30yrs –> males
-LRQ pain - begins periumbilical
-Fever/nausea/vomiting
What are the obstruction causes of appendicitis? The complications?
Obstruction causes:
1) Viral infection
2) Foreign body
3) Low fiber diet
Complications:
- peritonitis - death (2%)
Adenomatous Polyps
Neoplastic proliferation of colon mucosal glands
*benign but premalignant
*malignant transformation
What is the pathogenesis of Adenomatous Polyps? What is it associated with? The oral/clinical signs?
Pathogenesis:
-Accelerated division of epithelial cells –> epithelial dysplasia –> polyp formation
Associated with:
1) older age
2) genetic
3) IBDs
4) colon cancers –> 90%
Oral/Clinical:
-Asymptomatic
-Bleeding if large
Adenocarcinoma - Colorectal Carcinoma
Common malignancy of large intestine/rectum usually arising from adenomatous polyps
What is the pathogenesis of Adenocarcinoma - Colorectal Carcinoma? What is it associated with? The oral/clinical signs?
Pathogenesis:
1) adenomatous polyp –> APC
2) inherited syndrome –> DNA
Associated with:
1) heredity -FAP
2) IBDs
3) lifestyle
Oral/Clinical:
-African American males - 50yrs+
-Asymptomatic
-Diarrhea/constipation/rectal bleeding-occult
*60% 5yr survival
List the Polyposis Syndromes
1) Familial Adenomatous Polyposis - FAP
*most common
*autosomal dominant
2) Gardner Syndrome
*autosomal dominant
3) Peutz-Jeghers Syndrome
*autosomal dominant
Familial Adenomatous Polyps - FAP
-Most common polyposis syndrome - autosomal dominant
- 1,000s of adenomatous polyps
-Carcinomas develop in 100% of patients by age 40
What are the oral/clinical signs of Familial Adenomatous Polyps - FAP
-Asymptomatic
-Family history
Gardner Syndrome
-Autosomal dominant –> 33% new gene mutations
- 1000’s of adenomatou spolyps
-Carcinomas develop in 100% of patients by age 30
What are the oral/clinical signs of Gardner Syndrome?
1) GI polyps
2) Osteomas of jaws
3) Supernumerary teeth
4) Skin tumors
Peutz-Jeghers Syndrome
-Autosomal dominant
-Benign hamartomatous polyps throughout small intestine, colon, and stomach (hamartoatous polyps = reddish polyps/mucin-filled glands/less than 3mm)
-Increased incidence of cancers
What are the oral/clinical signs of Peutz-Jeghers Syndrome?
1) Benign harmartomatous polyps
2) Multi melanotic macules
3) Palmar/plantal melanotic macules
4) ORAL melanotic macules –> LIPS/buccal mucosa
