Week 6 lower Gi tract Flashcards

1
Q

What are the two types of diverticula?

A

Acquired –> develop during post natal life

Congenital

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2
Q

What is a diverticula?

A

Diverticula are blind ending outpouching of the bowel

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3
Q

What is diverticulosis of the colon?

A

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

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4
Q

Where in the bowel wall do diverticulosis usually develop?

A

Located between mesenteric and anti-mesenteric taenia coli

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5
Q

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

A

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

Common in urban cf. rural areas

Changing prevalence in migrant populations

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6
Q

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

A

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

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7
Q

What are the 3 main types of diverticulosis?

A

Sigmoid diverticulosis

Diverticulosis of the right colon

Giant diverticulum

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8
Q

What is the pathogensis of diverticulum?

A

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

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9
Q

How does diverticulosis develop?

A

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

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10
Q

What is the usual clinical features of diverticular disease?

A

Asymptomatic ( 90 – 99 % )

Cramping abdominal pain

Alternating constipation and diarrhoea

Not to many problem

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11
Q

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

A

10-30%

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12
Q

What are the acute complications of diverticulosis?

A

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.

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13
Q

What is diverticulitis?

A

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

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14
Q

What are the chronic complications of diverticulosis?

A

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

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15
Q

What is colitis?

A

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

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16
Q

What type of colitis causes inflammation in the transmural?

A

Crohns disease

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17
Q

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

A

Eosinophilic colitis

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18
Q

What can colitis be divided into?

A

Into acute or chronic

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19
Q

What are the different examples of acute colitis?

A
Acute infective colitis 
Antibiotic associated colitis 
Drug induced colitis
Acute ischaemic colitis ( transient or gangrenous )
Acute radiation colitis
Neutropenic colitis
Phlegmonous colitis
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20
Q

What are the different classification of chronic colitis?

A

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

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21
Q

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

A

ULCERATIVE COLITIS
CROHN’S DISEASE

INDETERMINATE COLITIS ( 10 – 15 % )

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22
Q

What is more common UC or CD?

A

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

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23
Q

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

A

Between the age of 20-40 years of age

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24
Q

Is CD or UC more common in males or females?

A

CD is more common in females

For UC it is equally common in males andd females

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25
Q

Is smoking a risk factor for both UC and CD

A

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

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26
Q

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

A

Oral contraceptive

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27
Q

Is there any familial clustering in IBD?

A

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

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28
Q

What is the clinical presentation of UC?

A
Diarrhoe with urgency/tenesmus
Constipation
Rectal bleeding
Abdominal plain
Anorexia
Weight loss
Anemia due to the excessive loss from rectal bleeding
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29
Q

What are the complications of UC?

A

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

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30
Q

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

A

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

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31
Q

where does UC typical begin and where does it spread?

A

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

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32
Q

What are the two histological findings for UC?

A

Crypt abscess and crypt distortion

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33
Q

What are the clinical features of crohns disease?

A
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
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34
Q

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

A

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

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35
Q

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

A

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

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36
Q

What is the most common distruction of crohns disease?

A

Ileocolic distribution.

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

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37
Q

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

A

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

However only 60% of patients with CD have granulomas

38
Q

What are the complications of crohns disease?

A
Toxic megacolon
Perforation
Fistula
Stricture common unlike in UC.
Haemorrhage
Carcinoma --> both in large and smal bowel
Short bowel syndrome
39
Q

What is short bowel syndrome?

A

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
Q

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

A

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
Q

What is the macroscopic appearance of UC and CD?

A

UC has Granular red mucosa with flat ,undermining ulcers

CD has cobblestone appearance with apthoid and fissuring ulcers

42
Q

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

A

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
Q

What is the affect of Uc and CD on serosa?

A

No affect in UC but in CD you get serositis?

44
Q

What type of inflammation is UC and CD?

A

Uc is mainly mucosal inflammation

While CD is mainly transmural inflammation

45
Q

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

A

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

In CD the crypt abscesses is less and not as severe

46
Q

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

A

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
Q

What affect does inflammatory bowel disease have on the liver?

A

Fatty change
Granulomas
Primary sclerosing cholangitis
Bile duct carcinoma

48
Q

What is Primary sclerosing Cholangitis?

A

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
Q

What extra skeletal problems can you get with IBD?

A

Polyarthritis
Sacro-ileitis
Ankylosing spondylitis

50
Q

What is sacro-ileitis?

A

Inflammation of the sacroiliac joints of the hip.

51
Q

What is anyklosing spondylitis?

A

It is a form of spinal arthritis

52
Q

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

A

Oral apthoid ulcers

Pyoderma gangrenosum–> skin condition causes painful ulcers

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

53
Q

What are the Ocular intestinal manifestations of IBD?

A

Iritis/uveitis
Episcleritis
Retinitis

54
Q

What are the renal intestinal manifestations of IBD?

A

Kidney and bladder stones

55
Q

What are the haematological intestinal manifestations of IBD?

A

Anaemia

Leucocytosis –> increase number of white cells in the blood

Thrombocytosis –> production of too many platelets

Thrombo-embolic disease –> DVT

56
Q

What affet can IBD have on systemic system?

A

Get manifestations of Amyloid and VAsculitis

57
Q

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

A

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

58
Q

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

A

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
Q

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

A

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

60
Q

When is colitis surveillance provided and what is it?

A

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
Q

What are colorectal poylps?

A

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
Q

What are the different groups of Colorectal polyps?

A

Neoplastic
Hamartomatous
Inflammatory or reactive

63
Q

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

A

Bening or Malignant

Epithelial neoplasm or Mesenchymal Neoplasm

64
Q

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

A

Hyperplastic polyps –> V. common in large bowel

Hamartomatous polyps

Polyps related to mucosal prolapse

Inflammatory fibroid polyp

Benign lymphoid polyp

Post-inflammatory polyps

65
Q

What are the two different types of Hamartomatous polyps?

A

Peutz-jeghers polyps

Juvenile polyps

66
Q

What is the profile of common Hyperplastic poly?

A

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

Distal HP have no malignant potential

67
Q

When can Hyperplastic polyp have a malignant potential?

A

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

68
Q

What is the profile of Juvenile Polyp?

A

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
Q

What types of cancer is Juvenile polyp associated with?

A

Juvenile polyposis associated with increased risk of colorectal and gastric cancer

70
Q

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

A

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
Q

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

A

Small Bowel

72
Q

Where else can Peutz-Jeghers syndrome effect?

A

Colon
Rectum
Stomach

Less common
Gallbladder
Urinary bladder
Nasopharynx

73
Q

What are adenomas?

A

Benign epithelial tumours

74
Q

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

A

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
Q

What are the marcoscopic appearance of adenomas?

A

pedunculated , sessile or “flat”

76
Q

What are the different histological types of adenomas?

A

Villous, Tubulo-Villous or Tubular

77
Q

What are all the benign neoplastic polyps?

A
Adenoma 
Lipoma
Leiomyoma
Haemangioma
neurofibroma
78
Q

What are all the malignant neoplastic polyps?

A
Carcinoma
Carcinoid
Leiomyosarcoma
GIST
Lymphoma
Metastatic tumour
79
Q

How can you predict the malignant change of adenoma?

A

flat” adenomas

Size ( most malignant polyps > 10 mm )

Villous & Tubulo-Villous

Severe ( high grade ) dysplasia

HNPCC associated adenomas

80
Q

What is the main cause of colerectal cancer?

A

Sporadic cause –> 75%

81
Q

What two conditions cause colorectal cancer

A

Familial adenomatous polyposis

Hereditary nonpolyposis colorectal cancer

82
Q

What are the risk factors for colorectal cancer

A

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
Q

What is FAP and what is the cause?

A

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
Q

What is HNPCC and what is the cause?

A

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
Q

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

A

HNPCC

86
Q

What other cancers does HNPCC increase the risk of?

A

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

87
Q

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

A
Adenocarcinoma --> most common          
Adenosquamous carcinoma
Squamous cell carcinoma
Neuroendocrine carcinoma & MANEC       
Undifferentiated carcinoma
Medullary carcinoma
88
Q

How does coloreactal cancer spread?

A

Direct invasion of adjacent tissues

Lymphatic metastasis ( lymph nodes )

Haematogenous metastasis ( liver & lung )

Transcoelomic ( peritoneal ) metastasis

Iatrogenic spread

89
Q

What are the two staging mechanisms of colorectal cancer?

A

Dukes

TNM

90
Q

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

A

N0 no nodes involved

N1 1 – 3 nodes involved

N2 4 or more nodes involved

91
Q

What is the duke staging of colorectal cancer?

A

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