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06. Gastrointestinal Pathology > 5. Small & large intestines > Flashcards

5. Small & large intestines Flashcards

1
Q

Diseases of the small & large intestines

A
  1. Congenital anomalies
    - Meckel diverticulum
    - Hirschsprung Disease (Congenital Aganglionic Megacolon)
  2. Intestinal obstruction
  3. Angiodysplasia
  4. Ischemic bowel disease
  5. Infectious enterocolitis
    - Intestinal ameobiasis
    - Intestinal tuberculosis
  6. Acute appendicitis
  7. Inflammatory bowel disease
    - Crohn disease
    - Ulcerative colitis
  8. Diverticular disease
  9. Polyps
    - Hyperplastic polyps
    - Hamartomatous polyps
    - Inflammatory polyps
    - Adenomatous polyps
  10. Neoplasms
    - Colorectal carcinoma
    - Neoplasms of the small intestines
    - Neoplasms of the anal canal
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2
Q

Meckel Diverticulum

A
  1. Blind outpouching of gastrointestinal tract that has all 4
    layers of the wall (a true diverticulum)
    - Due to failure of involution of the vitelline duct
    - Hence found in the ileum, on the anti-mesenteric aspect of the bowel
  2. Mucosal lining may be:
    - Intestinal mucosa
    - Ectopic pancreatic mucosa
    - Ectopic gastric mucosa (may cause peptic ulceration
    of adjacent normal intestinal mucosa, leading to occult bleeding & abdominal pain mimicking acute appendicitis & intestinal obstruction)
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3
Q

Pathogenesis of Hirschsprung Disease

A
  1. Premature arrest of normal migration of neural crest cells from caecum to rectum or premature death of ganglion cells
  2. As such, distal intestinal segments lack both submucosal (Meissner’s) plexus & myenteric (Auerbach’s) plexus – aganglionosis
  3. This results in a lack of coordinated peristaltic contractions, leading to a functional obstruction, resulting in a dilation of the intestinal segment proximal to the affected segment
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4
Q

Pathological effects & complications of Hirschsprung Disease

A
  1. Intestinal obstruction & dilation

2. Rupture of colonic wall

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5
Q

Causes of intestinal obstruction

A
  1. Mechanical obstruction
    - Hernias
    i. Can occur through the umbilicus, inguinal or femoral canals & at sites of surgical scars
    ii. Produces intestinal obstruction as well as vascular obstruction
  • Adhesions
    i. Formed due to peritoneal inflammation following surgery, infections etc
    ii. Can form closed loops through which other viscera can slide & get entrapped, producing an internal herniation
  • Volvulus
    i. Complete twisting of a loop of bowel about its mesenteric base of attachment
    ii. Occurs most commonly in the sigmoid colon
    iii. Produces intestinal obstruction as well as vascular obstruction (due to twisting of vessels running within the mesentery)
  • Intussusception
    i. Occurs when a segment of intestine constricted by a wave of peristalsis telescopes into the immediately distal segment
    ii. Occurs most commonly in young children
    iii. In older children or adults, an intraluminal mass (e.g. a tumour) serves as the point of traction that cause intussusceptions
  • Strictures, atresias
  • Imperforate anus
    i. Due to failure of involution of the cloacal membrane
  • Obstructive gallstones, fecalith, foreign bodies
  • Tumour
  1. Functional obstructions
    - Bowel infarction
  • Neurogenic paralytic ileus
    i. Post-GI surgical procedures
    ii. Metabolic acidosis (e.g. in diabetic ketoacidosis)
    iii. Hypothyroidism
    iv. Drug-induced (e.g. opiates)
    v. Spinal cord injury above T5 level
  • Loss of ganglion cells
    i. Hirschsprung disease
    ii. Chagas’ disease
    iii. Toxic megacolon in ulcerative colitis
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6
Q

Pathological Effects & Complications of intestinal obstruction

A
  1. Abdominal pain & distention
  2. Vomiting & constipation
  3. Bowel rupture/perforation
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7
Q

Definition of angiodysplasia

A

Malformed submucosal & mucosal blood vessels (ectatic nests of tortuous veins, venules & capillaries) most commonly found in the caecum & right colon; idiopathic in nature

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8
Q

Associations of angiodysplasia

A
  1. Congenital associations:
    - Aortic stenosis
    - Meckel diverticulum
  2. Mechanical associations:
    - Normal distension & contraction of gut may intermittently occlude submucosal veins, leading to focal dilation & tortuosity of proximal vessels
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9
Q

Pathological effects & complications of angiodysplasia

A

Rupture & bleeding

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10
Q

Causes of ischemic bowel disease

A
  1. Arterial thrombosis
    - Atherosclerosis
    - Vasculitis
    - Hypercoagulable states
  2. Arterial embolism
    - Cardiac vegetations (e.g. in infective endocarditis)
    - Aortic atheroembolism
  3. Venous thrombosis
    - Hypercoagulable states
    - Oral contraceptives
    - Sepsis
  4. Non-occlusive causes of ischemia
    - Congestive heart failure
    - Shock, dehydration
    - Vasoconstrictive drugs
  5. Miscellaneous
    - Radiation
    - Volvulus
    - Herniations
    - Adhesions
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11
Q

Pathogenesis of ischemic bowel disease

A
  1. Major variables in ischemic bowel disease:
    - Time frame (acute vs insidious occlusion)
    - Severity of vascular compromise
    - Vessels affected (whether it is the celiac, superior
    mesenteric or inferior mesenteric artery; whether it is
    a proximal large branch or distal small branch)
  2. 2 aspects of intestinal vascular anatomy affecting
    distribution of ischemic damage:
    - Intestinal capillaries run alongside glands, from crypt to surface, before making a hairpin turn at the surface to empty into post-capillary venules, hence surface epithelium most susceptible to ischemia
    - Watersheds – intestinal segments at the end of their respective arterial supplies – are most prone to ischemia due to low perfusion pressures; the 2 watersheds are the splenic flexure & rectosigmoidal region
  3. Resultant bowel infarction may take several forms:
    - Mucosal: no deeper than muscularis mucosae
    - Mural: mucosa + submucosa
    - Transmural: full-thickness of wall
    * **Note: acute/chronic hypoperfusion tends to give rise to mucosal or mural infarction, whereas acute vascular obstruction tends to give rise to transmural infarction
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12
Q

Pathological Effects & Complications of ischemic bowel disease

A
  1. Functional intestinal obstruction
    - Abdominal pain, distension, vomiting
  2. Bleeding
    - May present with bloody diarrhea
  3. Necrosis of gut wall smooth muscle
    - Diminished bowel sounds
  4. Perforation & peritonitis
  5. Gram-negative bacteraemia & endotoxic shock
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13
Q

Causes of Infectious Enterocolitis

A
  1. Bacteria
    - Escherichia coli, Salmonella, Shigella, Vibrio, Campylobacter, Yersinia, Clostridium, Tropheryma whippelii, Mycobacteria
  2. Viruses
    - Rotavirus, enteric adenovirus, HSV, CMV, EBV
  3. Fungi (typically in immunosuppressed)
    - Candida, Aspergillus, Mucor, Histoplasma
  4. Protozoa
    - Entamoeba histolytica, Giardia lamblia, Cryptosporidia
  5. Helminths
    - Ascaris lumbricoides, Trichuris trichuria
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14
Q

Causative organism of intestinal ameobiasis

A

Entamoeba histolytica

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15
Q

Pathogenesis of intestinal ameobiasis

A
  1. Faecal-oral transmission
  2. Ingested cysts release trophozoites which invade
    colonic epithelium (specifically in the caecum &
    ascending colon)
  3. Amoebic proteins aid invasion (proteinases, lectin,
    amoebapore)
  4. Results in diffuse colitis with flask-shaped ulcers
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16
Q

Morphology of intestinal ameobiasis

A
  1. Amoebomas
  2. Flask-shaped ulcers with shaggy edges, forming a napkin-like constrictive mass (due to lateral burrowing in the lamina propria after initial invasion by trophozoites)
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17
Q

Pathological effects & complications of intestinal ameobiasis

A
  1. Bloody diarrhea with mucous, intestinal pain, fever

2. Liver abscesses (via haematogenous portal spread)

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18
Q

Causative organism of intestinal tuberculosis

A

Mycobacterium tuberculosis

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19
Q

Pathogenesis of intestinal tuberculosis

A
  1. May be primary involvement or secondary involvement (e.g. in miliary TB)
  2. Typically occurs in the ileocaecal region
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20
Q

Morphology of intestinal tuberculosis

A
  1. Circumferential ulcers (parallels direction of lymphatic drainage towards mesentery)
  2. Mural thickening, strictures
  3. Regional lymphadenopathy
  4. Caseating granulomas
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21
Q

Causes of acute appendicitis

A

Obstruction of lumen by:

  • Faecolith
  • Foreign matter
  • Lymphoid hyperplasia
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22
Q

Pathogenesis of acute appendicitis

A
  1. Stasis of luminal contents allows for multiplication of luminal bacteria
  2. Invasion of mucosa & wall
  3. Acute inflammatory response
  4. Necrosis & ulceration ensues
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23
Q

Morphology of acute appendicitis

A
  1. Edema & turgidity
  2. Congestion & hemorrhage
  3. Fibrinopurulent exudate (neutrophilic infiltrate)
  4. Necrosis & ulceration
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24
Q

Pathological Effects & Complications of acute appendicitis

A
  1. Abdominal pain
    - Initially: referred pain to umbilical region
    - Later: localized pain in right iliac fossa (due to irritation of overlying parietal peritoneum)
    - ***Note: atypical positions of appendix can give rise to pain in atypical areas (retrocaecal appendix gives right flank pain, appendix in malrotated colon gives left upper quadrant pain)
  2. Nausea, vomiting, low-grade fever, mildly elevated peripheral white cell count
  3. Perforation
    - Generalized peritonitis
    - Pelvic abscesses
    - Subphrenic abscesses
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25
Q

Definition of inflammatory bowel disease

A

Refers to the 2 idiopathic inflammatory bowel conditions: Crohn disease & Ulcerative Colitis

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26
Q

Etiology & Pathogenesis of inflammatory bowel disease

A
  1. Genetic predispositions:
    - Familial aggregations, HLA studies
  2. Associated infectious agents:
    - Mycobacterium paratuberculosis
  3. Abnormal host immunoreactivity
    - Host immunity is stimulated & then fails to down-regulate itself
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27
Q

Location of Crohn disease

A

Terminal ileum +/- colon

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28
Q

Distribution of Crohn disease

A

Skip lesions

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29
Q

Nature of inflammation of Crohn disease

A

Chronic (non-caseating granulomatous in 35%)

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30
Q

Extent of inflammation of Crohn disease

A

Transmural, producing deep ulcers/fissures

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31
Q

Fibrosis in Crohn disease

A

Marked, strictures

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32
Q

Gut wall in Crohn disease

A

Thickened with narrowed lumen (produces string sign in barium xray)

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33
Q

Sinuses & fistulae in Crohn disease

A

Present

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34
Q

Complications of Crohn disease

A
  1. Nutritional deficiencies
  2. Malignancy risk
  3. Perforation & peritonitis
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35
Q

Location of Ulcerative colitis

A

Rectum & distal colon

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36
Q

Distribution of Ulcerative colitis

A

Diffused, non-sparing

37
Q

Nature of inflammation in Ulcerative colitis

A

Acute-on-chronic (non-granulomatous)

38
Q

Extent of inflammation in Ulcerative colitis

A

Limited to mucosa, producing pseudopolyps

39
Q

Fibrosis in Ulcerative colitis

A

Mild to none

40
Q

Gut wall in Ulcerative colitis

A

Thin

41
Q

Sinuses and fistulae in Ulcerative colitis

A

Absent

42
Q

Complications of Ulcerative colitis

A
  1. Nutritional deficiencies
  2. Malignancy risk
  3. Toxic megacolon
43
Q

Systemic manifestations of Crohn disease and Ulcerative colitis

A
  1. Skin: erythema nodosum
  2. Eyes: uveitis, conjunctivitis
  3. Liver: primary sclerosing cholangitis
  4. Joints: migratory polyarthritis, sacroilitis, ankylosing spondylitis
44
Q

Morphology of Crohn disease

A
  1. [Grossly]
    - Cobblestone appearance (as diseased tissue is depressed below the level of interspersed spared mucosa)
    - Deep ulcers & fissures
  2. [Histologically]
    - Transmural inflammation (chronic inflammatory cells in all layers of gut wall)
    - Non-caseating granulomas
    - Distortion of mucosal architecture
    - Crypt abscesses
45
Q

Morphology of Ulcerative colitis

A
  1. [Grossly]
    - Shallow ulcers
    - Psuedopolyps & mucosal bridges (regenerating islands of mucosa amidst shallow ulceration)
  2. [Histologically]
    - Inflammatory pseudopolyps
    - Inflammation limited to mucosal layer (chronic inflammatory cells in lamina propria)
    - Crypt abscesses
    - Mucosal atrophy with loss of folds (in chronic phase)
46
Q

Definition of Diverticular Disease

A

Acquired pseudodiverticular outpouchings of colonic mucosa & submucosa (not complete 4 layers, hence not true diverticula)

47
Q

Pathogenesis of Diverticular disease

A
  1. Raised intraluminal pressure forces mucosa & submucosa through areas of weakness in gut wall
    - Occurs in the colon as the muscularis propria layer is
    aggregated into 3 bands (teniae coli)
  2. Occurs most commonly in the sigmoid colon
48
Q

Pathological Effects & Complications of Diverticular disease

A
  1. Acute diverticulitis (due to obstruction of diverticula)
    - Pericolic abscesses
    - Pericolic fibrosis & adhesions
    - Colovesical fistula formation
    - Strictures & intestinal obstruction
    - Perforation & peritonitis
  2. Erosion of blood vessels
    - Bleeding
    - Iron-deficiency anemia
49
Q

Definition of polyps

A

Generic term referring to a mass of tissue that protrudes from a membranous surface, typically arising from lesions of the epithelium; gastrointestinal polyps can classified as follows: hyperplastic polyps, hamartomatous polyps, inflammatory polyp & adenomatous polyps

50
Q

Hyperplastic polyps

A

Formed due to decreased epithelial cell turnover &
delayed shedding of surface epithelial cells, hence leading to a ‘piling up’
1. No malignant potential
2. Must be differentiated from histologically-similar
sessile serrated adenomas

51
Q

Morphology of hyperplastic polyps

A
  1. Smooth nodular mucosal protrusion (usually in left colon)

2. Serrated surface architecture of glands due to overcrowding of normal goblet & absorptive cells

52
Q

2 conditions that present with hamartomatous Polyps

A
  1. Peutz-Jeghers Syndrome

2. Juvenile Polyps

53
Q

Peutz-Jeghers Syndrome

A
  1. Autosomal dominant genetic condition
  2. Typically in children 10-15 years old
  3. Multiple hamartomatous polyps (small intestines >
    colon > stomach) & melanotic mucocutaneous
    pigmentation (lips, oral mucosa, face)
  4. Grossly: pedunculated polyps with firm lobular
    contour
  5. Histologically: arborizing network of connective
    tissue & well-developed smooth muscle extending
    into polyp to surround normal glandular tissue
  6. No malignant potential, however, patients with this syndrome are at higher risk of developing other
    malignancies (pancreas, breast, ovary, lung, uterus)
54
Q

Juvenile Polyps

A
  1. May be sporadic or syndromic (AD)
  2. Typically in children <5 years old
  3. Hamartomatous polyps (mostly in rectum)
  4. Grossly: pedunculated polyps with smooth surface with cystic spaces in cross-section
  5. Histologically: cystically dilated glands containing mucin & inflammatory debris
  6. Risk of colonic adenocarcinoma
  7. Other complications: rectal bleeding, rectal prolapse
55
Q

Inflammatory Polyps

A

Formed as a result of regeneration & repair amidst inflammation & ulceration

56
Q

Adenomatous Polyps (Adenomas)

A

Arise as a result of epithelial proliferative dysplasia

  1. Ranges from low to high-grade dysplasia
  2. Strong evidence that adenomas are precursors for invasive adenocarcinomas
  3. Doubling time for size of an adenoma is 10 years
57
Q

Histologic architectural types of adenomatous polyps

A
  1. Tubular adenoma (narrow base, with stalk)
  2. Tubulovillous adenoma
  3. Villous adenoma (broad base)
58
Q

Factors affecting risk of malignancy of adenomas in adenomatous polyps

A
  1. Polyp size (bigger → higher risk)
  2. Number of polyps (more → higher risk)
  3. Histologic architecture (villous has higher risk)
  4. Severity of dysplasia (higher grade → higher risk)

Low risk in tubular adenomas < 1cm in diameter
High risk in villous adenomas > 4cm in diameter

59
Q

Epidemiology & associations of colorectal carcinoma

A
  1. Peak incidence is between ages 60 & 79
    - If found in a young patient, must suspect familial syndromes or pre-existing inflammatory bowel disease
  2. Familial syndromes
    - Familial adenomatous polyposis
    - Hereditary non-polyposis colorectal cancer
  3. Pre-existing colorectal pathologies
    - Crohn disease
    - Ulcerative colitis
  4. Obesity & inactivity
  5. Dietary factors:
    - Excessive caloric intake relative to requirements
    - Low content of unabsorbable vegetable fibre
    - High content of refined carbohydrates
    - Intake of red meat
    - Decreased intake of protective micronutrients
60
Q

Molecular pathogenesis in colorectal carcinoma

A
  1. Chromosomal Instability Pathway

2. Microsatellite Instability Pathway

61
Q

Chromosomal Instability Pathway in colorectal carcinoma

A
  1. APC (tumour suppressor) loss of function
  2. Allows increased Wnt/beta-catenin pathway signaling
    which drives cell cycle
  3. Increased proliferative activity results in
    accumulation of further mutations: K-RAS, SMAD2,
    SMAD4, p53, telomerase
62
Q

Microsatellite Instability Pathway in colorectal carcinoma

A
  1. MSH2, MSH6, MLH1 (DNA mismatch repair genes)
    loss of function
  2. Allows accumulation of mutations in microsatellites
    which are generally silent
  3. Accumulation of mutations in microsatellites located
    within coding/promoter regions of genes results in further mutations: TGF-beta RII, BAX, BRAF
63
Q

Associated familial syndrome in chromosomal instability

A

Familial polyposis coli

64
Q

% of colorectal cancers via chromosomal instability

A

85%

65
Q

Precursor lesion in chromosomal instability

A

Tubular/villous adenoma

66
Q

Colorectal cancer type in chromosomal instability

A

Typical adenocarcinoma

67
Q

Amount of DNA in chromosomal instability

A

Aneuploid & polyploid

68
Q

Typical location in chromosomal instability

A

Left-sided (descending colon)

69
Q

Degree of differentiation in chromosomal instability

A

Highly differentiated histologic features

70
Q

Presence of lymphocytic infiltration in chromosomal instability?

A

Little

71
Q

Is chromosomal instability mucinous?

A

Rarely mucinous

72
Q

Relative prognosis of chromosomal instability

A

Worse prognosis

73
Q

Associated familial syndrome in microsatellite instability

A

Hereditary non-polyposis colorectal cancer

74
Q

% of colorectal cancers in microsatellite instability

A

15%

75
Q

Precursor lesion in microsatellite instability

A

Sessile serrated adenoma

76
Q

Colorectal cancer type in microsatellite instability

A

Mucinous adenocarcinoma (may have signet-ring cells)

77
Q

Amount of DNA in microsatellite instability

A

Diploid

78
Q

Typical location in microsatellite instability

A

Right-sided (ascending colon)

79
Q

Degree of differentiation in microsatellite instability

A

Poorly differentiated histologic features

80
Q

Presence of lymphocytic infiltration in microsatellite instability

A

Marked

81
Q

Is microsatellite instability mucinous?

A

Often mucinous

82
Q

Relative prognosis of microsatellite instability

A

Better prognosis

83
Q

Types of colorectal cancer familial syndromes

A
  1. Familial Adenomatous Polyposis (FAP)

2. Hereditary Non-polyposis Colorectal Cancer (HNPCC)

84
Q

Familial Adenomatous Polyposis (FAP)

A
  1. Hereditary AD disorder (APC)
  2. Development of numerous colorectal adenomas as
    teenagers, with 100% of untreated cases developing
    colorectal adenocarcinoma often before 30 years old
  3. Standard treatment: prophylactic colectomy
  4. Associated adenomas of GIT: stomach, adjacent to
    ampulla of Vater
  5. Associated extraintestinal manifestations: congential
    hypertrophy of retinal pigment epithelium
  6. Associated neoplastic syndromes: Gardner syndrome (intestinal adenomas + osteomas + thyroid tumours etc), Turcot syndrome (intestinal adenomas + CNS tumours)
85
Q

Hereditary Non-polyposis Colorectal Cancer (HNPCC)

A
  1. Hereditary AD disorder (MSH2, MSH6, MLH)
  2. Predominantly right colonic involvement, with the development of sessile serrated adenomas
  3. Amsterdam criteria: 3 family members with cancer, 2 generations apart, 1 with early onset cancer (before age of 50)
86
Q

Morphology of colorectal cancinoma

A
  1. Right-sided (ascending colon) colorectal cancers tend to grow as polypoid, exophytic masses
    - Obstruction is uncommon
    - Often called to clinical attention due to iron deficiency anemia
  2. Left-sided (descending colon) colorectal cancers tend to grow as annular, encircling lesions that produce napkin-ring constrictions of the bowel
    - Can produce obstruction
    - Often presents as occult bleeding, changes in bowel
    happens & cramping left lower quadrant pain
87
Q

Clinical features of colorectal carcinoma

A
  1. Altered bowel habits
  2. Signs of chronic blood loss
    - Iron deficiency anemia (high index of suspicion especially in men & post-menopausal women)
    - Melena
  3. Metastases: most commonly to liver (portal drainage)
  4. Prognostic factors:
    - Staging (by TMN system or Dukes Staging) – most important prognostic factor
    - Presence of familial syndromes (worse prognosis)
    - Molecular pathway implicated (chromosomal instability has poorer prognosis than microsatellite instability)
    - Concomitant inflammatory bowel disease (if present, increases risk of recurrence)
    - Presence of K-RAS mutations (if present, less likely to respond to cetuximab treatment)
  5. Treatment
    - Cetuximab (EFGR inhibitor)
    - Surgical excision
    - Colectomy
88
Q

Neoplasms of the small intestines

A
  1. Relatively uncommon (3-6% of all GIT tumours)
  2. Benign tumours most commonly adenomas
  3. Malignant tumours (rare) most commonly adenocarcinomas & carcinoids
89
Q

Neoplasms of the anal canal

A
  1. Squamous cell carcinoma
    - Associated with chronic HPV infection
    - Some rare cases related to immunosuppresion (as in renal transplants & AIDS patients)
  2. Adenocarcinoma
    - Often as an extension of rectal adenocarcinoma

06. Gastrointestinal Pathology (5 decks)

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