Week 6 lower Gi tract Flashcards

(91 cards)

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
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