Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MS2 GI > 10/14- Large Intestine, Pathology > Flashcards

10/14- Large Intestine, Pathology Flashcards

1
Q

T/F: There are villi and crypts in the colon

A

False

  • Colon has crypts but no villi
  • Crypts look like racked test tubes and reach muscularis mucosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is seen here?

A

Cross section of previous pic

  • Crypts are equally spaced with mild lymphoplasmacytic infiltrate and capillaries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe Entamoeba histolytica

  • Transmission
  • Prevalence
  • Characteristics of agent
  • Reproduction
  • Location
  • Disease
A
  • Amebiasis
  • Fecal-oral transmission
  • Esp developing countries (500M)
  • E. histolytica cysts has a chitin wall and four nuclei
  • Resistant to gastric acid: pass through the stomach
  • Cysts colonize the epithelial surface of the colon and release trophozoites
  • Most frequently in cecum and ascending colon

Results in:

  • Dysentery
  • Liver abscess
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does Entamoeba histolytica cause dysentery?

A
  • Amebae attach to the colonic epithelium… apoptosis
  • Invade crypts and burrow into lamina propria
  • Neutrophils -> tissue damage
  • Flask-shaped ulcer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How to identify Entamoeba histolytica histologially?

A

May be difficult; amebae are similar to macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does Entamoeba histolytica cause liver abscess?

A
  • Parasites may penetrate splanchnic vessels
  • Embolize to liver -> abscesses (40% of patients with amebic dysentery)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is seen here?

A

Scanning EM of intestinal amebiasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is seen here?

A

Intestinal specimen from pt with acute amebic colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is seen here?

A

Entamoeba histolytica cause liver abscess?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the clinical presentation of Entamoeba histolytica?

A
  • Abdominal pain, bloody diarrhea and weight loss
  • Occasionally, acute necrotizing colitis and megacolon
  • Significant mortality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How to treat Entamoeba histolytica?

A

(Obligate fermenters of glucose)

The most effective treatment: metronidazole

  • Inhibits enzyme pyruvate oxidoreductase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is Pseudomembranous colitis?

What commonly causes it?

A

Antibiotic-associated colitis or antibiotic-associated diarrhea

  • Diarrhea during or after a course of antibiotic therapy
  • Usually caused by Clostridium difficile
  • Salmonella, C. perfringens type A
  • Staphylococcus aureus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the pathogenesis of Pseudomembranous colitis

A
  • Disruption of the normal colonic flora by antibiotics allows C. difficile overgrowth
  • Most commonly: third-generation cephalosporins
  • Predisposing factor: immunosuppression
  • Toxins:
  • Ribosylation of small GTPases, such as Rho
  • Disruption of the epithelial cytoskeleton, tight junction barrier loss, cytokine release and apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are risk factors for Pseudomembranous colitis?

A
  • Advanced age
  • Hospitalization
  • Antibiotic treatment

Up to 30% of hospitalized adults are colonized with C. difficile (tenfold greater than the general population)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is seen here?

A

Psuedomembranes (C. difficile) in Pseudomembranous colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is seen here?

A

Pseudomembranous colitis

  • “Volcano eruption” of neutrophils and dead cells is common
  • Increased chronic inflammatory cells in lamina propria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is seen here?

A

Pseudomembranous colitis

  • Higher magnification of volcano eruption of neutrophils and dead cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the clinical presentation of Pseudomembranous colitis?

How is it diagnosed?

A
  • Fever, leukocytosis
  • Abdominal pain, cramps,
  • Hypoalbuminemia
  • Watery diarrhea and dehydration

+/- fecal leukocytes and occult blood

Diagnosis: C. difficile toxin and characteristic histopathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Treatment for Pseudomembranous colitis (C. difficile)?

A
  • Metronidazole
  • Vancomycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is Inflammatory bowel disease?

What does it include? (Important!)

A

Chronic condition due to inappropriate mucosal immune activation

Two disorders: Crohn disease and ulcerative colitis

- Ulcerative colitis: a severe ulcerating inflammatory disease limited to colon and rectum involving mucosa and submucosa

- Crohn disease: regional enteritis, involves any area of the GI tract and typically transmural

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Pictoral difference between Crohn’s disease and ulcerative colitis? (Important!)

A

Crohn’s:

  • Skip lesions (not continuous)
  • Transumural inflammation,ulcerations, fissures

Ulcerative colitis:

  • Continuous colonic involvement beginning in the rectum
  • Pseudopolyps and ulcers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe the epidemiology of IBD

A
  • More in females
  • Common in teens/early 20s
  • Most common in Caucasians in Western industrialized nations
  • 3-5x more in eastern European (Ashkenazi) Jews
  • Geographic distribution is highly variable
  • Most common in N America, N Europe, and Australia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Pathogenesis of IBD (picture)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe the pathogenesis of IBD

A

In genetically susceptible host, release of TNF and other immune-mediated signals epithelia

  • > increase tight junction permeability
  • > further increases in the flux of luminal material
  • Self-amplifying cycle to initiate

A variety of factors are associated with disease for unknown reasons

  • Appendicitis: reduced risk of developing UC
  • Tobacco modifies IBD epidemiology: increase risk of Crohn while reduce risk of UC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the morphology of Crohn’s disease:

  • Location
  • Continous/not
  • Common features
A

Affects all the GI tract

  • Most common in ileum, ileocecal valve, and cecum
  • 40% limited to the small intestine
  • 30% involvement of small intestine and colon
  • Multiple, separate, sharply delineated areas of disease; skip lesions are characteristic
  • Stricture common
26
Q

What is seen here?

A

Skip lesions in Crohn’s

  • Normal mucosa separated by inflamed mucosa
27
Q

What is seen microscopically in Crohn’s disease?

A
  • Cryptitis and crypt abscess with crypt destruction
  • Ulcer with abrupt transition between ulcerated and adjacent normal mucosa
  • Distortion of architecture due to repeated crypt destruction and regeneration
  • Epithelial metaplasia
  • Architectural and metaplastic changes may persist even in inactive disease
  • Noncaseating granuloma: hallmark of Crohn (35% of cases)
  • Absence of granuloma does not rule out Crohn
28
Q

What is seen here?

A

Colon with distortion of architecture (Crohn’s disease):

  • Crypts not equally spaced
29
Q

What is seen here?

A

Crohn’s disease

  • Increased chronic inflammatory cells in lamina propria
  • Granulomas
30
Q

What is seen here?

A

Crohn’s disease:

  • Cryptitis: neutrophils in the crypt epithelial cells
  • Granuloma in lamina propria: epithelioid macrophages surrounded by lymphocyte
31
Q

What is seen here?

A

Crohn’s disease:

  • Cryptitis: neutrophils int he crypt epithelial cells
  • Increased chronic inflammatory cells in lamina propria
  • Crypts abscess: neutrophils inside the crypt
32
Q

Describe ulcerative colitis

  • Location
  • Extra-intestinal manifestations
  • Prognosis
A
  • Limited to colon and rectum

Common extra-intestinal manifestations of ulcerative colitis overlap with those of Crohn disease

  • Migratory polyarthritis
  • Sacroiliitis
  • Ankylosing spondylitis
  • Uveitis
  • Skin lesions
  • Pericholangitis
  • Primary sclerosing cholangitis (2.5% to 7.5%)

Prognosis depends on severity of active disease and disease duration

33
Q

What is seen here?

A

Ulcerative colitis

  • Riable edematous mucosa
  • Pancolitis and its response to treatment.

A: only scattered fragments of mucosa are left,

C-D: over time mucosa is being regenerated

34
Q

Describe the morphology of ulcerative colitis

  • Location
  • Skip lesions?
  • Extent of disease
  • Gross features
  • Complications
A
  • Always involve rectum; then proximal extension
  • No skip lesions
  • Pancolitis: disease of the entire colon
  • Small intestine normal, although mild mucosal inflammation of the distal ileum, backwash ileitis, may be present in severe cases of pancolitis

Grossly: colonic mucosa red and granular or with extensive, broad-based ulcers

  • Abrupt transition between diseased and uninvolved colon
  • Ulcers along the long axis of colon
  • Pseudopolyp: isolated islands of regenerating mucosa
  • Mucosal atrophy in chronic disease
  • No mural thickening or strictures

Complications:

  • Colonic dilation and toxic megacolon: risk of perforation
35
Q

What is seen here?

A

Ulcerative colitis

36
Q

Describe the histology of Ulcerative colitis

A

Similar to Crohn: inflammatory infiltrates, crypt abscesses, architectural crypt distortion, and epithelial metaplasia

  • Inflammation diffuse, limited to mucosa and superficial submucosa
  • Severe case: extensive mucosal destruction with ulcers that extend more deeply into the submucosa
  • Involvement of muscularis propria: rare

Signs of healed disease:

  • Submucosal fibrosis
  • Mucosal atrophy
  • Distorted mucosal architecture to almost normal in prolonged remission

No granuloma

37
Q

What is seen here?

A

Ulcerative colitis

  • Increased chronic inflammatory cells in lamina propria
38
Q

What is seen here?

A

Ulcerative colitis

  • Cryptitis: neutrophils in the crypt epithelial cells
39
Q

What are the clinical features of Ulcerative colitis?

Treatment?

A

Relapsing disorder:

  • Episodes of bloody diarrhea with stringy, mucoid material
  • Lower abdominal pain, and cramps
  • Temporarily relieved by defecation
  • Duration of symptoms days to months

Initial attack can present as medical or surgical emergency

  • > 50% patients have mild disease, all with one relapse in 10 year
  • 30% require colectomy in the first 3 years after presentation

Colectomy cures intestinal disease, but not extra-intestinal manifestations

40
Q

T/F: Colitis is associated with a risk of malignancy

A

True- depends on duration and extent of disease

  • (2% after 10 years, 8.5% after 20 years, and 17.8% after 30 years of disease)
41
Q

What should be considered in the management of pts with ulcerative colitis?

A

Early detection of malignancy: surveillance 8 years after disease initiation

  • Major exception: patients with primary sclerosing cholangitis; enrollment in surveillance at the time of diagnosis
  • Regular and extensive mucosal biopsy is expensive
42
Q

Describe diverticular disease

  • Genetic or acquired
  • Prevalence
  • Contributing factors
  • Basic mechanism
A
  • Acquired pseudo-diverticular outpouchings of the colonic mucosa and submucosa
  • Rare under 30 yo; 50% are 60+ yo in Western population
  • Multiple = “diverticulosis”
  • Dietary differences: less common in Japan
  • Increased intraluminal pressure due to increased peristaltic contractions, enhanced by low fiber diet -> decrease stool bulk, especially in sigmoid colon
43
Q

Pathophysiology of diverticular disease?

A

Low fiber diet

  • > Chronic constipation
  • > Increased intraluminal pressure

(Combined with possible connective tissue disorders)

  • > Muscular hypertrophy
  • > Herniation of mucosa through the muscular wall
44
Q

What is seen here?

A

Diverticulosis

45
Q

Describe the morphology of diverticular disease

  • Location
  • Shape
  • Histology
A
  • Most common in sigmoid colon
  • Small, flask-like outpouchings, 0.5 to 1 cm in diameter, along the taeniae coli

Histology:

  • Thin wall of a flattened or atrophic mucosa - Compressed submucosa,
  • Attenuated or absent muscularis propria

Obstruction -> inflammatory change: diverticulitis and peri-diverticulitis -> perforation -> pericolonic abscesses, sinus tracts, and peritonitis

46
Q

What is seen here?

A

Diverticular disease

47
Q

Clinical features of diverticular disease?

A
  • Most patients asymptomatic
  • Often an incidental finding
  • 20% have intermittent cramping, continuous lower abdominal discomfort, constipation, distention, and a sensation of never being able to completely empty the rectum
  • Rarely regress in early stage of development
  • More common: number increases and become large
  • Symptomatic improvement with high-fiber diet
  • When diverticulitis occurs, it most often resolves spontaneously and rare patients need surgery
48
Q

What are polyps?

A
  • Any localized projection above the surrounding colonic mucosa
  • Most common in colon
  • Most bengin
  • Intestinal polyps: Non-neoplastic or neoplastic
  • The most common neoplastic polyp: adenoma with potential to become malignant
49
Q

Describe neoplastic polyps

  • What types of tumors occur int he colon
  • What is the most common neoplastic polyp
A
  • Any neoplastic mass lesion in GI tract
  • Carcinoid tumors, stromal tumors, lymphomas, and even metastatic carcinoma
  • The most common neoplastic polyps: adenomas
  • Benign polyps… majority of colorectal adenocarcinomas
50
Q

Describe adenoma

  • Shape
  • Gender
A
  • Sessile or pedunculated
  • Equal genders
  • 50% of adults in Western world by age 50 - Surveillance colonoscopy by age 50
  • If family history: screen 10 years before the youngest age at which a relative was diagnosed
  • Less common in Asia; increasing frequency
  • ADENOMA = MILD DYSPLASIA
51
Q

Describe the morphology of adenoma

A
  • 0.3 to 10 cm in diameter
  • Histologic hallmark: nuclear hyperchromasia, elongation and stratification
  • Tubular, tubulovillous, or villous based on architecture
  • Tubular adenoma: small, pedunculated polyps with small rounded, or tubular glands
  • Villous adenoma: larger and sessile with slender villi
  • Tubulovillous adenoma: mixture of tubular and villous
  • Invasion more in villous adenoma
52
Q

What is seen here?

A

Normal colonic mucosa (pedunculated tubular adenoma); the rest of crypts are darker

53
Q

What is seen here?

A

Villous adenoma

54
Q

Describe adenocarcinoma of the colon:

  • Epidemiology
A

1 malignancy of the GI tract

Epidemiology

  • 15% of all cancer-related deaths (2nd to lung cancer)
  • Incidence peak: 60-70 yrs of age, fewer than 20% before 50
  • Males > females
  • Most prevalent in US, Canada, Australia, New Zealand…
55
Q

Describe the pathogenesis/molecular events for development of cancer in the colon?

A
  • Genetic and epigenetic abnormalities
  • Two distinct genetic pathways:
  • APC/β-catenin pathway, associated with WNT and the classic adenoma-carcinoma sequence
  • Microsatellite instability pathway, associated with defects in DNA mismatch repair
  • Stepwise accumulation of multiple mutations
  • Epigenetic events, the most common one methylation-induced gene silencing, may enhance progression
56
Q

Adenoma-carcinoma sequence?

A
57
Q

Describe the morphology of tumors in the proximal vs. distal colon

A
  • Tumors in proximal colon often polypoid, rarely cause obstruction
  • Carcinomas in distal colon: annular with “napkin-ring” constrictions and luminal obstruction
  • Both: grow into bowel wall: palpable firm mass

Right- and left-sided cancer have similar microscopic features

  • Invasion: a strong stromal desmoplastic response
  • Poorly differentiated tumor: few glands
  • Some mucin production: poor prognosis
58
Q

What is seen here?

A

Glands with necrotic material inside

59
Q

What is the clinical presentation of colon cancer

A
  • Endoscopic screening for adenomas
  • Cecal and other right-sided colon cancers: fatigue and weakness due to iron deficiency anemia
  • Iron deficiency anemia in an older man or postmenopausal woman is GI cancer until proven otherwise
  • Left-sided tumors: occult bleeding, changes in bowel habits, or cramping/discomfort left lower quadrant
60
Q

What is the prognosis of colon carcinoma?

A
  • Poorly differentiated and mucinous tumors: poor prognosis
  • Two most important prognostic factors: depth of invasion and lymph node metastases
  • Patients with small numbers of metastases do well for years following resection of distant tumor nodules
  • Clinical and molecular heterogeneity of colorectal carcinomas
  • Metastases: regional lymph nodes, lungs and bones
  • The most common site of metastases: liver

MS2 GI (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions