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General Pathology > GI Path: Small and Large Intestine > Flashcards

GI Path: Small and Large Intestine Flashcards

1
Q

Describe the Small Intestine

A

-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

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2
Q

What is the function of the small intestine?

A

-Pyloric sphincter –> junction with stomach
-Ileocecal valve –> junction with large intestine
-Duodenum = receives chyme, pancreatic juice, bile neutralizes stomach acid

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3
Q

Pyloric Stenosis

A

Hyperplastic muscle at birth preventing food passage from stomach to duodenum

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4
Q

What is the pathogenesis of Pyloric Stenosis? The oral/clinical signs?

A

Pathogenesis:
-Developmental thickening of pylorus muscle –> prevents movement

Oral/Clinical:
-Projectile vomiting
-Failure to thrive (weight loss)
-Persistent hunger

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5
Q

Meckel Diverticulum

A

Most common birth defect of digestive tract –> developmental outpouching of all 3 layers of the ileum wall

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6
Q

What is the pathogenesis of Meckel Diverticulum? The oral/clinical signs?

A

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

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7
Q

Volvulus

A

Twisting of bowel along its mesentery causing obstruction

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8
Q

What is the pathogenesis of Volvulus? The most common locations? The oral/clinical signs?

A

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

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9
Q

Hernia

A

Weakened wall in the abdomen
*causes 40% of obstructions

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10
Q

What are the complications of a Hernia? The 3 types? The oral/clinical sings?

A

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

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11
Q

Adhesions

A

Scar tissue formation –> can lead to partial obstruction

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12
Q

What is the pathogenesis of Adhesions? The oral/clinical signs?

A

Pathogenesis:
-Fibrous tissue forms from previous surgery

Oral/Clinical:
-Abdominal/back pain
-Constipation

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13
Q

Intussusception

A

Telescoping of proximal segment of bowel forward into distal segment
*most common cause of intestinal obstruction in children under 3 yrs

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14
Q

What is the pathogenesis of Intussusception? What it is associated with? What are the oral/clinical signs?

A

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

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15
Q

Mesenteric Arterial Occlusion

A

Occlusion of the arterial vascular supply of the intestinal system
*segmental infarct –> usually of superior mesenteric artery

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16
Q

What is the pathogenesis of Mesenteric Arterial Occlusion? The oral/clinical signs?

A

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

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17
Q

Mesenteric Venous Occlusion

A

Occlusion due to thrombosis of one or more major veins draining the intestinal system

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18
Q

What is the pathogenesis of Mesenteric Venous Occlusion? The oral/clinical signs?

A

Pathogenesis:
1) Peritonitis
2) Volvulus
3) Embolism –> I.E.
4) Portal HTN
5) Tumors

Oral/Clinical:
-bloating/vomiting/pain
-bloody stool/diarrhea
-fever

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19
Q

Crohn Disease

A

Chronic relapsing granulomatous disease resulting in segmental bowel thickening, luminal obstruction, and malabsorption

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20
Q

What are the most common sites of Crohn Disease?

A

Distal Ileum, Proximal Colon and Rectum

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21
Q

What is the pathogenesis of Crohn Disease?

A

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”

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22
Q

What are the causes of Crohn Disease?

A

1) Genetic susceptibility
2) Immune response (increased T-cell response)
3) Worse in smokers

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23
Q

What are the clinical signs of Crohn Disease? Oral signs?

A

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

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24
Q

What are the complications of Crohn Disease?

A

1) Obstruction from stricture
2) Perforation of fissures
3) Peritonitis
4) Adhesions
5) Hospitalization

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25
Q

What are the treatments for Crohn Disease?

A

-Corticosteroids
-Feeding tube/ I.V.
*Surgery is often needed but reserved for last resort

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26
Q

Celiac Disease

A

Immune-mediated disease of small intestine causing severe, generalized malabsorption

27
Q

What is the pathogenesis of Celiac Disease? The oral/clinical signs?

A

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

28
Q

What is Celiac Disease associated wtih?

A

1) Specific HLA profile
2) Risk of adenocarcinoma
3) Risk of T-cell lymphoma

29
Q

Carcinoma of Ampulla

A

Most common site of small intestinal malignancy in the ampulla of Vater

30
Q

What is the pathogenesis of Carcinoma of Ampulla? What is it associated with? The oral/clinical signs?

A

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

31
Q

Where is the Large Intestine located?

A

Extends from the ileocecal valve to the external anal sphincter surrounds small intestine

32
Q

What are the 4 sections of the Large Intestine?

A

1) Colon = cecum + appendix –> ascending colon –> transverse colon –> descending colon –>
2) Sigmoid colon –>
3) Rectum –>
4) Anal canal + external anal sphincter

33
Q

What is the function of the large intestine?

A

-Absorbs water and salts
-Eliminates indigestible food as feces
- 2 sphincters control opening/closing:
*ileocecal valve
*external anal sphincter

34
Q

Hirschsprung Disease = Congenital Megacolon

A

Developmental defect in relaxation and peristalsis of rectum and distal sigmoid colon = obstruction
*associated with Down’s syndrome

35
Q

What is the pathogenesis of Hirschsprung Disease = Congenital Megacolon? The oral/clinical signs?

A

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

36
Q

Acquired Megacolon

A

Persistent dilation and lengthening of the colon in the absence of obstruction with loss of peristalsis

37
Q

What is the pathogenesis of Acquired Megacolon? the oral/clinical signs?

A

Pathogenesis:
1) Infection
2) Disease
3) Medications
4) Congenital

Oral/Clinical:
-Constipation
-Bloating/abdominal pain
-Fecal impaction/fecalomas

38
Q

Diverticular Disease

A

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

39
Q

What is the pathogenesis of Diverticular Disease? What is it associated with?

A

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

40
Q

What are the oral/clinical signs of Diverticular Disease? The complications associated with it?

A

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

41
Q

Immune-mediated inflammatory bowel conditions –> includes:

A

1) Ulcerative colitis
2) Crohn Disease

42
Q

Ulcerative Colitis

A

Chronic relapsing ulcerative-inflammatory disease of colon resulting in bouts of explosive bloody diarrhea

(“kissing cousin” to Crohn Disease)

43
Q

What are the most common sites for Ulcerative Colitis?

A

Rectum (always) –> extends proximally
*only involves large intestine

44
Q

What is the pathogenesis for Ulcerative Colitis?

A

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

45
Q

What are some notes to consider about Ulcerative Colitis?

A

1) Muscle/serosa NOT affected = not full thickness
2) Bowel wall NOT thickened
3) Involvement is confluent - NO “skip lesions”
4) NO granulomas

46
Q

What are the causes of Ulcerative Colitis?

A

1) Genetic susceptibility
2) Auto-immune disease (hyper-response to irritants)
3) Less symptomatic in smokers

47
Q

What are the clinical signs of Ulcerative Colitis? The oral signs?

A

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

48
Q

Pseudomembranous Colitis

A

Acute necrotizing ulceration of colon mucosa
*causes explosive diarrhea and electrolyte loss

49
Q

What is the pathogenesis of Pseudomembranous Colitis? What is it associated with? The oral/clinical signs?

A

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

50
Q

Appendicitis

A

Lumen obstruction of appendix leading to inflammation

51
Q

What is the pathogenesis of Appendicitis? The oral/clinical signs?

A

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

52
Q

What are the obstruction causes of appendicitis? The complications?

A

Obstruction causes:
1) Viral infection
2) Foreign body
3) Low fiber diet

Complications:
- peritonitis - death (2%)

53
Q

Adenomatous Polyps

A

Neoplastic proliferation of colon mucosal glands
*benign but premalignant
*malignant transformation

54
Q

What is the pathogenesis of Adenomatous Polyps? What is it associated with? The oral/clinical signs?

A

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

55
Q

Adenocarcinoma - Colorectal Carcinoma

A

Common malignancy of large intestine/rectum usually arising from adenomatous polyps

56
Q

What is the pathogenesis of Adenocarcinoma - Colorectal Carcinoma? What is it associated with? The oral/clinical signs?

A

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

57
Q

List the Polyposis Syndromes

A

1) Familial Adenomatous Polyposis - FAP
*most common
*autosomal dominant

2) Gardner Syndrome
*autosomal dominant

3) Peutz-Jeghers Syndrome
*autosomal dominant

58
Q

Familial Adenomatous Polyps - FAP

A

-Most common polyposis syndrome - autosomal dominant
- 1,000s of adenomatous polyps
-Carcinomas develop in 100% of patients by age 40

59
Q

What are the oral/clinical signs of Familial Adenomatous Polyps - FAP

A

-Asymptomatic
-Family history

60
Q

Gardner Syndrome

A

-Autosomal dominant –> 33% new gene mutations
- 1000’s of adenomatou spolyps
-Carcinomas develop in 100% of patients by age 30

61
Q

What are the oral/clinical signs of Gardner Syndrome?

A

1) GI polyps
2) Osteomas of jaws
3) Supernumerary teeth
4) Skin tumors

62
Q

Peutz-Jeghers Syndrome

A

-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

63
Q

What are the oral/clinical signs of Peutz-Jeghers Syndrome?

A

1) Benign harmartomatous polyps
2) Multi melanotic macules
3) Palmar/plantal melanotic macules
4) ORAL melanotic macules –> LIPS/buccal mucosa

General Pathology (32 decks)

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