Week 6 lower Gi tract Flashcards Preview

Year 2 clinical pathology > Week 6 lower Gi tract > Flashcards

Flashcards in Week 6 lower Gi tract Deck (91)
1

What are the two types of diverticula?

Acquired --> develop during post natal life

Congenital

2

What is a diverticula?

Diverticula are blind ending outpouching of the bowel

3

What is diverticulosis of the colon?

Protrusions of mucosa and submucosa through the bowel wall. Commonly sigmoid colon but can extend into the proximal colon and cecum.

4

Where in the bowel wall do diverticulosis usually develop?

Located between mesenteric and anti-mesenteric taenia coli

5

What part of the world is diverticulosis more common in and what type of area ?

Common in developed ( western ) world
Rare in Africa , Asia , S. America

Common in urban cf. rural areas

Changing prevalence in migrant populations

6

What age group do you see diverticulosis mainly in and does diet have a affect?

Under the age of 40 it is rare but after 40 it becomes more and more common.

Male and females are equal.

However diet plays a part as there is a relationship between fibre content of diet.

Therefore less common in vengetarians due to less fibre

7

What are the 3 main types of diverticulosis?

Sigmoid diverticulosis

Diverticulosis of the right colon

Giant diverticulum

8

What is the pathogensis of diverticulum?

There is increased intra lumen pressure casued by Irregular , uncoordinated peristalsis which occurs in the sigmoid colon. Also overlapping semicircular arcs of bowel wall which caused increased pressure in the colon due to the irregular peristalsis.
Causing a point of relative weakness in the bowel wall--> caused by Penetration by nutrient arteries between mesenteric and antimesenteric taenia coli.
Can also be due to age related changes in the connective tissue

9

How does diverticulosis develop?

Thickening of muscularis propria ( earliest change – “prediverticular disease” )
Elastosis of taeniae coli ( leading to shortening of colon due to contraction of the taenia coli

Redundant mucosal folds and ridges  due to the shortening

Sacculation and diverticula

10

What is the usual clinical features of diverticular disease?

Asymptomatic ( 90 – 99 % )

Cramping abdominal pain

Alternating constipation and diarrhoea

Not to many problem

11

What percentage of people get chronic or acut complications of diverticular disease?

10-30%

12

What are the acute complications of diverticulosis?

You get diverticulitis which leads to peridiverticular abscess.
Perforation due to infection of the peritoneal cavity.

Finally can get haemorrhage if the surrounding artery or veins are ulcerated.

13

What is diverticulitis?

It is inflammation in the diverticula due to ulceration of diverticula lining and invasion of bacteria into the surrounding tissue.

14

What are the chronic complications of diverticulosis?

Intestinal obstruction ( strictures : 5 – 10 % )

Fistula ( urinary bladder, vagina )

Polypoid prolapsing mucosal folds

Diverticular colitis ( segmental and granulomatous ) --> inflammation in the lining of the bowel --> diarrhoea and rectum bleeding

15

What is colitis?

Inflammation of the colon usually causing mucosal inflammation but occasionally transmural or predominantly submucosal/muscular

16

What type of colitis causes inflammation in the transmural?

Crohns disease

17

What type of colitis causes inflammation in the submucosal/mscular?

Eosinophilic colitis

18

What can colitis be divided into?

Into acute or chronic

19

What are the different examples of acute colitis?

Acute infective colitis
Antibiotic associated colitis
Drug induced colitis
Acute ischaemic colitis ( transient or gangrenous )
Acute radiation colitis
Neutropenic colitis
Phlegmonous colitis

20

What are the different classification of chronic colitis?

Chronic idiopathic inflammatory bowel disease
Microscopic colitis ( collagenous & lymphocytic )
Ischaemic colitis
Diverticular colitis
Chronic infective colitis eg. amoebic colitis & TB
Diversion colitis
Eosinophilic colitis
Chronic radiation colitis

21

What are the main 2 types of idiopathic inflammatory bowel diseaese?

ULCERATIVE COLITIS
CROHN’S DISEASE

INDETERMINATE COLITIS ( 10 – 15 % )

22

What is more common UC or CD?

UC is more common and the incidence is highest in Scandinavia, UK, Northern Europe, USA

23

What is the peak age incidence of both UC and CD?

Between the age of 20-40 years of age

24

Is CD or UC more common in males or females?

CD is more common in females
For UC it is equally common in males andd females

25

Is smoking a risk factor for both UC and CD

For crohns it is a risk factor but it seems to decrease chance of getting UC.

26

Other than smoking what other factor can potentially increae your risk of IBD?

Oral contraceptive

27

Is there any familial clustering in IBD?

Yes there is if you have a family member who has UC or CD then the chances of you have either increases dramatically.

28

What is the clinical presentation of UC?

Diarrhoe with urgency/tenesmus
Constipation
Rectal bleeding
Abdominal plain
Anorexia
Weight loss
Anemia due to the excessive loss from rectal bleeding

29

What are the complications of UC?

Toxic meacolon and perforation
Haemorhage
Stricture --> rare in UC--> if you see it in UC then sign of cancer
Carcinoma

30

How is toxic megacolon and perforation caused in UC? How do you treat it?

Toxic megacolon is caused by UC having a remitting and relaxing course - occasionally get a very severe flare up that badly damages the colon wall, particularly affecting the transverse colon,
Get a severely inflamed and dilated transverse colon, gas can build up, leading to perforation. 40% die when this happens.

Treated with high dose steroids --> If it does not work then need to have the bowel removed before perforation

31

where does UC typical begin and where does it spread?

Typically starts in the rectum and goes to variable part of the colon --> continous

32

What are the two histological findings for UC?

Crypt abscess and crypt distortion

33

What are the clinical features of crohns disease?

Chronic relapsing disease  like Uc
Affects all levels of GIT from mouth to anus
Diarrhoea ( may be bloody )
Colicky abdominal pain
Palpable abdominal mass
Weight loss / failure to thrive
Anorexia
Fever
Oral ulcers
Peri – anal disease
anaemia

34

What is the action of peri-anal disease caused by CD?

Ulcers, strictures, fistula of the anus into the skin/vagina

35

What parts of the GI tract affected by CD and UC and how does it spread?

CD is patchy and can affect the whole GI tube --> mouth to anus

UC --> affects colon, appendix and terminal ilium but is a continous diseae

36

What is the most common distruction of crohns disease?

Ileocolic distribution.

Affects the end of the small intestines and the start of the large intestines

37

What is the defining histological feature of CD? How common is this?

Is the formation of granuloma's.
Not seen in UC.

However only 60% of patients with CD have granulomas

38

What are the complications of crohns disease?

Toxic megacolon
Perforation
Fistula
Stricture common unlike in UC.
Haemorrhage
Carcinoma --> both in large and smal bowel
Short bowel syndrome

39

What is short bowel syndrome?

Caused by repeated resection due to surgery treatment of trying to get rid of the disease. The small bowel becomes so small no longer effective

40

What is the pathology of UC and CD in terms of whether or not the rectum and terminal ileum is involved?

The rectum is always invovled in UC and 10% of the times terminal ileum involved

The rectum 50% times involved in CD and 30% of the times terminal ileum is involved.

41

What is the macroscopic appearance of UC and CD?

UC has Granular red mucosa with flat ,undermining ulcers

CD has cobblestone appearance with apthoid and fissuring ulcers

42

Do you see fistulaes and anal lesions in UC and CD?

There is no spontaneous fistulae in UC but there is a 25% chance of anal lesions

There is a greater than 10% chance of fistulae and 75% chance of anal lesion

43

What is the affect of Uc and CD on serosa?

No affect in UC but in CD you get serositis?

44

What type of inflammation is UC and CD?

Uc is mainly mucosal inflammation
While CD is mainly transmural inflammation

45

What are the affects of CD and UC are on crypts?

In UC there crypt absesses is common and the distrortion is severe

In CD the crypt abscesses is less and not as severe

46

Is there any presence of granuloma and inflammatory polyps in UC and CD?

In UC there is no granuloma and inflammatory polyps is common.

In CD 60% of cases there is granulomas--> inflammatory polyps are less common.

47

What affect does inflammatory bowel disease have on the liver?

Fatty change
Granulomas
Primary sclerosing cholangitis
Bile duct carcinoma

48

What is Primary sclerosing Cholangitis?

It is a chronic liver disease in which the bile ducts inside and outside the liver progressively decrease in size due to inflammation and scarring

49

What extra skeletal problems can you get with IBD?

Polyarthritis
Sacro-ileitis
Ankylosing spondylitis

50

What is sacro-ileitis?

Inflammation of the sacroiliac joints of the hip.

51

What is anyklosing spondylitis?

It is a form of spinal arthritis

52

What are the Muco-cutaneous extra intestinal manifestations of IBD?

Oral apthoid ulcers

Pyoderma gangrenosum--> skin condition causes painful ulcers

Erythema nodosum--> inflammation of the fat cells under the skin.

53

What are the Ocular intestinal manifestations of IBD?

Iritis/uveitis
Episcleritis
Retinitis

54

What are the renal intestinal manifestations of IBD?

Kidney and bladder stones

55

What are the haematological intestinal manifestations of IBD?

Anaemia

Leucocytosis --> increase number of white cells in the blood

Thrombocytosis --> production of too many platelets

Thrombo-embolic disease --> DVT

56

What affet can IBD have on systemic system?

Get manifestations of Amyloid and VAsculitis

57

What is the effect of UC on the development of colorectal cancer?

The longer you have UC the greater the chances of developing cancer. Become a problem after having UC for 10yrs

58

What are the risk factors of developing colorectal cancer in UC patients?

Early age of onset

Duration of disease > 8-10 years

Total or extensive colitis

Primary Sclerosing Cholangitis

Family History of CRC

Severity and continuous inflammation ( pseudopolyps )

Presence of dysplasia

59

What are the 4 steps in the development of colorectal cancer in UC?

Inflammed mucosa--> low grade dysplasia --> high grade dysplasia --> colorectal cancer

60

When is colitis surveillance provided and what is it?

Provided after have UC for 10 yrs.
The Surgeon will colonoscopy a bowel and systemic biopsy --> to try and pick up early stages of cancer

61

What are colorectal poylps?

A mucosal protusion of the lining of the bowel. Can be solitary or multiple, small or large. It is due to mucosal or submucosal pathology or a lesion deeper in the bowel wall.

62

What are the different groups of Colorectal polyps?

Neoplastic
Hamartomatous
Inflammatory or reactive

63

What are the two different group types can neoplastic Colorectal polyps divide into?

Bening or Malignant

Epithelial neoplasm or Mesenchymal Neoplasm

64

What are the different types of Non-Neoplastic polyps in the colo-rectum? (6)

Hyperplastic polyps --> V. common in large bowel

Hamartomatous polyps

Polyps related to mucosal prolapse

Inflammatory fibroid polyp

Benign lymphoid polyp

Post-inflammatory polyps


65

What are the two different types of Hamartomatous polyps?

Peutz-jeghers polyps
Juvenile polyps

66

What is the profile of common Hyperplastic poly?

1-5mm in size
Often multiple
Located in the rectum and sigmoid colon

Distal HP have no malignant potential

67

When can Hyperplastic polyp have a malignant potential?

Some large right sided ones may give rise to microsatellite unstable carcinoma --> account for 10-15% of all colorectal cancers.

68

What is the profile of Juvenile Polyp?

Often spherical and pedunculated

10 – 30 mm

Commonest type of polyp in children

Typically occur in rectum & distal colon

Sporadic polyps have no malignant potentia

69

What types of cancer is Juvenile polyp associated with?

Juvenile polyposis associated with increased risk of colorectal and gastric cancer

70

What is the cause of Peutz-Jeghers syndrome and what is its clinical presentation?

Autosomal dominant condition ( mutation in STK11 gene on chromosome 19 ).


Present clinically in teens or 20s with abdominal pain ( intussusception ), gastro-intestinal bleeding & anaemia

Muco-cutaneous pigmentation

Multiple gastro-intestinal tract polyps

71

What is the most common place Peutz-Jeghers syndrome mainly effect?

Small Bowel

72

Where else can Peutz-Jeghers syndrome effect?

Colon
Rectum
Stomach

Less common
Gallbladder
Urinary bladder
Nasopharynx

73

What are adenomas?

Benign epithelial tumours

74

What is adenomas precursor to, what age do you see them and where in the body does it effect?

Precursor of colorectal cancer (at least 80%)

Present 25% - 35% population > 50 years

Evenly distributed around colon BUT larger in recto-sigmoid and caecum

75

What are the marcoscopic appearance of adenomas?

pedunculated , sessile or “flat”

76

What are the different histological types of adenomas?

Villous, Tubulo-Villous or Tubular

77

What are all the benign neoplastic polyps?

Adenoma
Lipoma
Leiomyoma
Haemangioma
neurofibroma

78

What are all the malignant neoplastic polyps?

Carcinoma
Carcinoid
Leiomyosarcoma
GIST
Lymphoma
Metastatic tumour

79

How can you predict the malignant change of adenoma?

flat” adenomas

Size ( most malignant polyps > 10 mm )

Villous & Tubulo-Villous

Severe ( high grade ) dysplasia

HNPCC associated adenomas

80

What is the main cause of colerectal cancer?

Sporadic cause --> 75%

81

What two conditions cause colorectal cancer

Familial adenomatous polyposis
Hereditary nonpolyposis colorectal cancer

82

What are the risk factors for colorectal cancer

Diet
Dietary fibre, fat, red meat, folate, calcium

Obesity / Physical Activity
Alcohol
NSAIDs
HRT and oral contraceptives
Schistosomiasis
Pelvic radiation
Ulcerative colitis and Crohns disease

83

What is FAP and what is the cause?

Autosomal dominat disease caused by the mutation in the APC tumour suppressor gene.

It causes multiple benign adenomatous polyps in the colon and there is 100% lifetime risk of large bowel cancer

84

What is HNPCC and what is the cause?

It is a autosomal dominant disease with a 50-70% lifetime risk of large bowel cancer.

Due to mutation in the DNA mismatch repair genes.

85

Does FAP or HNPCC acount for more cases of colorectal cancer?

HNPCC

86

What other cancers does HNPCC increase the risk of?

Increased risk of endometrial, ovarian, gastric, small bowel, urinary tract and biliary tract cancer

87

What are are the 6 types of colorectal cancer? Which is the most common?

Adenocarcinoma --> most common
Adenosquamous carcinoma
Squamous cell carcinoma
Neuroendocrine carcinoma & MANEC
Undifferentiated carcinoma
Medullary carcinoma

88

How does coloreactal cancer spread?

Direct invasion of adjacent tissues

Lymphatic metastasis ( lymph nodes )

Haematogenous metastasis ( liver & lung )

Transcoelomic ( peritoneal ) metastasis

Iatrogenic spread

89

What are the two staging mechanisms of colorectal cancer?

Dukes
TNM

90

What is the N stage in TNM staging of colorectal cancer?

N0 no nodes involved

N1 1 – 3 nodes involved

N2 4 or more nodes involved

91

What is the duke staging of colorectal cancer?

Stage A : adenocarcinoma confined to the bowel wall with no lymph node metastasis

Stage B : adenocarcinoma invading through the bowel wall with no lymph node metastasis

Stage C : adenocarcinoma with regional lymph node metastasis regardless of depth of invasion

Stage D : distant metastasis presen