Precancerous colonic polyp are one of the most common lesions reported in intestinal biopsy. Diagnosis becomes more important as the early diagnosis immensely helps in patients management.

2.  Colorectal carcinoma(CRC) , one of the most
common cancer worldwide.
 Virtually all CRCs originate from a benign polyp
, which makes this cancer potentially
preventable by appropriate screening
colonoscopy programs in patients at increased
risk.

3.  The nature of precursor polyp is an essential
classifier of CRC because each tumor is
thought to develop from an unique benign polyp
with its own set of morphologic and molecular
characteristics.

4.  The two most common polyps identified as
precursors of CRCs-
 Adenomatous polyps and ,
 Serrated polyps.

5.  INFLAMMATORY POLYPS
 HAMARTOMATOUS POLYPS
 EPITHELIAL POLYPS
 MALIGNANT EPITHELIAL POLYPS
 POLYPOID ENDOCRINE TUMORS

6.  METASTASIS TO COLON
 LYMPHOID POLYPS
 MESENCHYMAL POLYPS
 MISCELLANEOUS POLYPOID LESIONS

7.  Junenile polyps and polyposis
 Peutz jeghers syndrome
 Cowden syndrome
 Cronkhite-canada syndrome

9. Grossly, these polyps grossly appear
rounded, smooth, and unilobular with
an erythematous cap of eroded tissue.
Their cut surface reveals multiple
dilated, mucin-filled crypts, leading to
the term mucus retention polyp. These
polyp share many features with
inflammatory polyp

12. 1. Serrated polyps
2. Conventional Adenomas
3. Adenomatous Polyposis Syndrome
4. Adenomas and adenoma – like DALMS in
Inflammatory Bowel Disease

13.  Most common type of polyps in colon.
 May progress to malignancy.
 May grow to large sizes, show abnormal
proliferation and maturation (right side), and
may be sessile.

14.  Decrease in the rate of cell death, leading to,
 Prolonged cell life
 Increase in the no. of epithelial cells
 Serrated phenotypic growth pattern

15.  Higher susceptibility to DNA methylation
(Unknown reasons)
 Transcriptional silencing of promoters of tumor
suppressor genes (MLH1, BRAF, MGMT)
 Progression to dysplastic serrated polyps and
ultimately adenocarcinomas

18.  Small, sessile, smooth bumps, flatten on insufflation
of air

19. 1. Microvesicular hyperplastic polyp
2. Goblet cell hyperplastic polyp
3. Mucin poor hyperplastic polyps,
(based on morphologic growth pattern and lack
of proliferative/maturation abnormalities)

20.  Simple tubular
architecture – no
branching, budding
or crypt dilatation

21. Luminal serrated
surface (irregular
sawtooth
appearance)

22.  Columnar cells with
apical vesicular
mucin, eosinophilic
like absorptive cells
and goblet cells

23.  Large proliferative
zone displaying-
 Mucin depletion
 Nuclear features-
Hyperchromatism ,
Elongation, and
Crowding

24.  Lesser degree of
luminal serrations
 Elongated crypts rich in
goblet cells, but without
microvesicular mucin

25.  Least common
 Prominent serrations
along the entire length of
the crypt
 Micropapillary
architecture

26.  Prominent
serrations
throughout the
crypt
 Mucin cells at the
base of crypt

27.  Branching at the base
of crypt (flask shaped)
 Irregular distribution of
mature and dystrophic
goblet cells and
mucinous cells

28.  Greater degree of
nuclear stratification
and atypia

30.  Sessile serrated polyps with dysplasia
 Serrated adenomas (traditional polyp)
 Conventional adenomas with serrated
architecture

31.  As a result of dysplastic change within a
sessile serrated polyp.
 Resembles a conventional adenoma,
composed of elongated cigar shaped
hyperchromatic nuclei with stratification and
with architectural serration.

32.  Sessile serrated
polyp with
prominent
serrations
 Conventional
adenoma-type
with low-grade
dysplasia

33.  Dysplasia arising
in a sessile
serrated polyp
imparting a
traditional serrated
adenoma
appearance

34.  Hyperplastic
epithelium
 Dysplastic
epithelium with
stratified nuclei
and hyper-
eosinophilic
cytoplasm

35.  Sessile serrated polyps with dysplasia
 Serrated adenomas
 Conventional adenomas with serrated
architecture

36.  Exclusively in the left colon – sigmoid,
rectum
 60-65 yrs
 Pedunculated
 Develop via alternate pathway

37.  Cells with
eosinophilic
cytoplasm
 Nuclear atypia with
confluent
stratification

38.  Confluent
nuclear
stratification
 Mucin depletion
 Variable no. of
goblet cells

39.  Large and
filiform in shape
 Dilated
lymphatics in
lamina propria

40.  Occasionally serrated adenomas may show
 Adenoma – like foci
 High grade dysplasia characterized by
increased cytological atypia, marked nuclear
stratification and back to back epithelial growth
pattern

43.  Sessile serrated polyps with dysplasia
 Serrated adenomas
 Conventional adenomas with serrated
architecture

44.  Rarely adenomas with serrated architecture
 Evidence of a of
carcinogenesis – chromosomal instability
pathway and serrated molecular pathway
(acquisition of KRAS mutation )
“fusion” molecular pathway

45.  Cigar shaped nuclei
with clumped
chromatin
 Prominent nuclear
stratification
 Mucin depletion

46.  Due to overlapping features or processing
artifacts.
 Cytologic evidence of dysplasia to place the
lesion into either “nondysplastic” or “dysplastic”
serrated polyp category.

47. DYSPLASTIC SERRATED
POLYPS
CONVENTIONAL
ADENOMA (CA)
CA WITH SERRATED
ARCHITECTURE
Discrete areas of
hyperplastic change along
with areas of adenoma–type
low grade dysplasia
Dystrophic goblet cells
Hyperchromatic nuclei
Cigar shaped with open
chromatin
Prominent nuclear
stratification
Crypt showing nuclear
features of adenoma along
with serration

48. 1. Serrated polyps
2. Conventional Adenomas
3. Adenomatous Polyposis Syndrome
4. Adenomas and adenoma – like DALMS in
Inflammatory Bowel Disease

49.  Almost always aymptomatic
 Overt or occult rectal bleeding
 Risk increases with age, at age >50y, 12%
have adenomas, of which 25% are
considered high risk lesion.

50.  Sessile
 Pedunculated
 Occasionally, multilobulated and/or filiform

51.  Categorized architecturally as :--
1) Tubular (if >75%)
2) Villous (if >75%)
3) Tubullovillous (25-75%)

54.  Low grade
 High grade

55. 1) Non complex
crypts
2) Psuedostratified or
partially stratified
nuclei reach only
the lower half of
cytoplasm
3) Minimal nuclear
pleomorphism/loss
of polarity
4) Brisk mitosis but
minimal atypical
mitosis
5) Arranged more in
parallel
configuration

56.  Marked degree of
nuclear
hyperchromaticity,
pseudostratification,
and loss of polarity
from the base to the
surface of the
mucosa.
 Intraluminal
cribriforming of the
glands is seen
without a definite
breach of the
basement membrane.

57. More complex intraluminal cribriforming and large gland formation with the
appearance of expanding-type infiltration into the lamina propria without
desmoplasia. In intramucosal carcinoma, the nuclei become more rounded,
rather than cigar shaped, and often contain an open chromatin pattern rather
than a coarse chromatin pattern.

60. Well circumscribed
lobule of misplaced
glands in the
submucosa of a polyp
stalk

61. The misplaced crypts
are slightly separated
from one another and
marked congestion and
hemosiderin deposition
are seen around the
edges of the misplaced
epithelium.

62. Smooth-edged pool of mucin,
lined by low-grade dysplastic
epithelium on the periphery,
The pool of mucin does not
contain floating atypical cells
or glands

63. Lack of lamina propria
surrounding the invasive
glands; no evidence of
hemorrhage or hemosiderin
deposition is seen.
Irregular and jagged in
contour and infiltrate in a
nonlobular fashion

65. 1. Serrated polyps
2. Conventional Adenomas
3. Adenomatous Polyposis Syndrome
4. Adenomas and adenoma – like DALMS in
Inflammatory Bowel Disease

66. 1) Familial adenomatous polyposis
2) Gardner`s syndrome
3) Turcot`s syndrome
4) Attenuated familial adenomatous polyposis
5) MYH associated polyposis

68. 1. Serrated polyps
2. Conventional Adenomas
3. Adenomatous Polyposis Syndrome
4. Adenomas and adenoma – like DALMS in
Inflammatory Bowel Disease

69.  clinically important to make a distinction because sporadic
adenomas are generally treated by polypectomy and
continued surveillance, whereas (adenoma-like) polypoid
dysplastic lesions associated with an underlying IBD have
generally been regarded as an indication for colectomy in
medically fit patients

71. 1) Mutations in DNA mismatch repair genes,
leading to a DNA microsatellite instability (MSI)
phenotype (15-20% cases)
2) Mutations in APC and other genes that
activate Wnt pathway, characterized by
chromosomal instability (CIN) phenotype (75-
85%)
3) Global genome hypermethylation, resulting in
switch off of tumor suppressor genes, indicated
as CpG island methylator phenotype (CIMP).