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Gastrointestinal RT > Small Bowel and Colorectal Pathology > Flashcards

Small Bowel and Colorectal Pathology Flashcards

1
Q

what is diverticulae disease?

A

little outpouchings of the colon caused by the strain of chronic constipation

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2
Q

compare an obstruction in proximal small bowel to distal small bowel- in terms of vomiting and distention?

A

proximal small bowel: vomiting, no distention

distal small bowl: no vomiting, gross distension

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3
Q

what type of pain does a patient feel with small bowel obstruction usually?

A

central colicky pain

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4
Q

what are the 3 main causes of small bowel obstruction?

A

adhesions
hernia
cancer
(+other causes eg crohn’s stricture, bezoar)

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5
Q

how do you treat a small bowel obstruction if there is no strangulation involved?
(excluding hernia)

A

IV fluids + nasogastric suctoin (‘drip and suck’)

operate if no resolution within 24-48 hours

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6
Q

how do you treat a small bowel obstruction if there is strangulation involved?

A

resuscitate
antibiotics
early surgery

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7
Q

what are the 3 main signs a small bowel obstruction has become stangulated?

A

constant pain
signs of sepsis
shock

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8
Q

what is gall stone ileus?

A

a rare cause of small bowel obstruction:

large gallstones migrate through fistulas into the small bowel and become lodged causing an obstruction

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9
Q

where is the commonest site for Crohns disease lesions?

A

terminal ileum

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10
Q

what is is called when Crohn’s disease affects the large bowel?

A

crohn’s colitis

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11
Q

how do you diagnose suspected Crohn’s disease?

A

barium enema

gastroscopy/colonoscopy

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12
Q

which is more associated with perianal disease- UC or crohns?

A

crohns disease

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13
Q

what is the basis of medical therapy for Crohn’s disease?

A

steroids and immunosuppression

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14
Q

why might a patient undertake surgery for Crohn’s disease?

A

for mechanical complications

usually small bowel resection

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15
Q

what is the pain patients usually present with small bowel ischaemia/infarction?

A

severe, poorly localised pain

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16
Q

what is the treatment for small bowel ischaemia and infarction?

A

surgery to revascularise intestine and resection of gangrenous intestine

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17
Q

what is meckers diverticulum?

A

a congenital diverticulum formed from a remnant of the vitelline duct

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18
Q

what is ileus of the small bowl?

A

the small bowel has stopped working but there is no mechanical obstruction

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19
Q

when do patients tend to feel the pain from chronic ischaemia of the SMA?

A

post-prandially

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20
Q

why is colonic infarction unlikely?

A

marginal artery of drummond provides an anastomoses

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21
Q

where does meckels diverticulum occur?

A

usually 2 feet from ileocaecal valve

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22
Q

when does meckels diverticulum usually present?

although remember most are asymptomatic

A

before 2 years of age

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23
Q

what type of diet is diverticular disease related to?

A

low fibre diet

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24
Q

what are the 5 main complications of diverticular disease?

A 
inflammation
rupture
abscess
fistula
massive bleeding
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25
Q

what are the 6 factors that can cause ischaemia of the large bowel?

A 
CVS disease
Atrial Fibrillation
Embolus
Atherosclerosis of mesenteric vessels
Shock
Vasculitis
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26
Q

what are the 3 main complications of ischaemic colitis?

A

massive bleeding
rupture
stricture

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27
Q

what is causes pseudomembranous colitis?

A

C. dif

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28
Q

what is a factor for getting clostridium difficile?

A

broad spectrum antibiotics

ciprofloxacin, ceftriaxone, clindamycin, co-amoxiclav especiially

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29
Q

what does pseudomembranous colitis cause?

A

massive diarrhoea and bleeding

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30
Q

what is collagenous colitis?

A

a patchy, inflammatory condition of the bowl where the basement membrane becomes thickened

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31
Q

what are the main symptoms of IBS?

A 
abdominal pain
bloating
change in bowel habit (diarrhoea, consti[ation, mixed)
urgency
nocturia
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32
Q

what is the F:M ratio of IBS?

A

2 : 1

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33
Q

what are the main pathophysiological features of IBS?

A

disturbed GI motility

visceral hypersensitiviry

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34
Q

what type of GI distrurbance occurs in IBS?

A

high-amplitude propagating contractions

exaggerated gastro-colic reflex

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35
Q

what are the 2 mechanisms of visceral hypersensitivity in IBS patients?

A

peripheral sensations:
up-regulation of sensitivity of nociceptor terminals
central sensations:
increased sensitivity of spinal neurones

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36
Q

what are nociceptor terminals responsible for?

A

sensation of pain

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37
Q

what might cause up-regulation of sensitivity of nociceptor terminals?

A

inflammatory mediators

eg gastroenteritis trigger

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38
Q

what is the Rome III criteria for IBS?

A

recurrent abdo pain/discomfort for at least 3 days per months for 3 months
+2 out of:
-improvement of pain with defecation
-onset associated with change in stool frequency
-onset associated with change in stool form

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39
Q

what is nocturia- and why does IBS cause it?

A

poor sleep
IBS sufferers don’t actually get up to go to the toilet at night they just can’t sleep because they are worried about their stomach

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40
Q

what 5 conditions have associations with IBS?

A 
fibromyalgia
chronic fatigue syndrome
temporomandibular joint dysfunction
chronic elvic pain
psychiatric problems
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41
Q

when a patient presents with possible IBS what are the alarm features that it is something more sinister?

A 
age >50
short duration of symptoms
woken from sleep to run to toilet
rectal bleeding
weight loss
anaemia
FH of colorectal cancer
recent antibiotics
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42
Q

what does waking up from sleep to run to the toilet suggest? (rather than IBS)

A

IBD

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43
Q

why in some rare cases may IBS give you weight loss or anaemia?

A

the diet they are on is too strict

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44
Q

what investigations must you carry out for a patient with suspected IBS?

A 
FBC
ESR
CRP
antibody testing for anti-TTG
(lower GI tests if >50 or strong FH of colorectal cancer)
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45
Q

what is the diet treatment of IBS?

A

regular meal times

reduce or increase fibre

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46
Q

what is the drug treatment of IBS?

A

stop opiate analgesia
anti-diarrhoeals
anti-spasmodics
anti-depressants

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47
Q

why must yous top opiates in a patient with IBS?

A

because even though opiates have anti-diarrhoea effects they have a long term effect on bowel function: opiate/narcotic bowel syndrome

  • worsening pain
  • reliance on opiates
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48
Q

why are anti-depressants used in IBS?

A

reduces visceral hypersensitivity

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49
Q

compare doses of anti-depressants used for IBS to doses used for depression?

A

much lower doses for IBS

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50
Q

what anti-depressant is used most commonly in IS?

A

amitriptyline

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51
Q

what forms the outpouchings within the colon in diverticular disease?

A

mucosal herniation through muscle coat

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52
Q

where within the colon is diverticular disease most common?

A

sigmoid colon

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53
Q

what are the 3 main clinical features of diverticulitis?

A

left iliac fossa pain/tenderness
septic
altered bowel habit

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54
Q

what investigations can you use to diagnose diverticulitis?

A

barium enema

sigmoidoscopy

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55
Q

what is the treatment for diverticulitis?

A

IV fluids
bowel rest
IV antibiotics

surgery if no improvement or complications

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56
Q

what are the 5 main complications of diverticular disease?

A 
pericolic abscess
perforation
haemorrhage
fistula
stricture
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57
Q

where are the 2 surgical operations used for diverticular disease?

A

hartmanns procedure

primary resection/anastomosis

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58
Q

what is hartmanns procedure?

A

surgical resection of the recto sigmoid colon and formation of an end colostomy

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59
Q

what are the 4 main causes of acute/chronic colitis?

A

infective colitis
ulcerative colitis
crohns colitis
ischaemic colitis

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60
Q

what are the 6 main symptoms of acute/chronic colitis?

A 
diarrhoea (possibly bloody)
abdominal cramps
dehydration
sepsis
weight loss
anaemia
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61
Q

how do you diagnosis acute/chronic colitis?

A

AxR
sigmoidoscopy + biopsy
stool cultures
barium enema

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62
Q

what artery is blocked for ischaemic colitis to take place?

A

inferior mesenteric artery

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63
Q

where is the most common site for angiodysplasia?

A

right side of colon

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64
Q

what are the treatment options of colonic angiodysplasia?

A

embolisation
endoscopic ablation
surgical resection

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65
Q

what are volvulus’s usually caused by?

A

chronic constipation

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66
Q

what is the mechanisms of a volvulus?

A

bowel twists on mesentery -may cause it to become gangrenous

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67
Q

how do you treat a sigmoid vovulus?

A

flatus tube

surgical resection

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68
Q

what are polyps?

A

protrusions above the epithelial surface

-hyperplastic growth

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69
Q

what are adenomas of the colon?

A

benign tumours- dysplastic growth

ie non invasive, don’t metastasise

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70
Q

what is the risk with adenomas?

A

precursors of colorectal adenocarcinomas

71
Q

why must all adenomas be removed?

A

because they are premalignant

72
Q

how are adenomas removed?

A

endoscopically or surgically

73
Q

what are the dukes stagings of colorectal carcinoma?

A

dukes A: confined by muscularis propria
dukes B: through muscularis propria
dukes C: metastatic to lymph nodes
dukes D: distant mets

74
Q

what are the 3 main symptoms with left sided colorectal carcinomas? (75%)

A

rectal bleeding
altered bowel habit
obstruction

75
Q

what are the 2 main symptoms with right sided colorectal carcinomas? (25%)

A

anaemia

weight loss

76
Q

where is the usual lymphatic spread from a colorectal carcinomas?

A

mesenteric nodes

77
Q

where is the usual haematogenous spread from colorectal carcinomas?

A

liver

78
Q

what are 2 important inherited colorectal cancer syndromes?

A

heriditary non polyposis coli (HNPCC)

familial adenomatous polyposis (FAP)

79
Q

which inherited colorectal cancer syndrome has the on average greatest number of polyps?

A

familial adenomatous polyposis (FAP)

80
Q

compare the onset of heriditary non polyposis coli and familial adenomatous polyposis?

A

HNPCC: late onset
FAP: early onset

81
Q

what type of inheritance are inherited coloretal cancer syndromes?

A

autosomal dominant

82
Q

what is the defect within heriditary non polyposis coli?

A

defect in DNA mismatch repair

83
Q

what is the defect within familial adenomatous polyposis?

A

defect in tumous supression

84
Q

compare the locations of heridatry non polyposis coli to familial adenomatous polyposis?

A

HNPCC: right sided tumours
FAP: thorugh colon

85
Q

compare the inflammatory responses of heriditary non polyposis coli and familial adenomatous polyposis?

A

HNPCC: crohns like inflammatory response
FAP: no specific inflammatory response

86
Q

compare the histological classes of cancers between heriditary non polyposis coli adn familial adenomatous polyposis?

A

HNPCC: mucinous tumours
FAP: adenocarcinomas

87
Q

what other cancers is heriditary non polyposis coli associated with?

A

gastric carcinoma

endometrial carcinoma

88
Q

what other cancer is familial adenomatous polyposis associated with?

A

desmoid tumours and thyroid carcinomas

89
Q

what are the most common benign colorectal neoplasia?

A

adenoma

90
Q

what are the most common malignant colorectal neoplasia?

A

adenocarcinoma

91
Q

what do all adeno-carcinomas start as?

A

adenomas

92
Q

what are proto oncogenes?

A

promote cell growth and division

93
Q

what are oncogens?

A

mutated proto oncogenes that cause excessive cell growth and division

94
Q

what are tumour suppressor genes?

A

suppress cell growht and division

95
Q

what happens when tumour suppressor genes mutate?

A

they allow uncontrollable cell growth and divison

96
Q

when a proto oncogene mutates into a oncogene what happens- loss of function of gain of function?

A

gain of function

97
Q

when a tumour suppressor gene mutates what happens- loss of function or gain of function?

A

loss of function

98
Q

what are the 3 macroscopic appearances of colorectal cancers?

A

polypoidal
ulcerative
annular

99
Q

what are the 2 main classes of adenomas of the colon?

A

tubular

villous

100
Q

which type of adenoma of the colon is more likely to form an adenocarcinoma?

A

villous adenomas

101
Q

what is T1 of TNM staging?

A

cancer has invaded submucosa only

ie dukes A

102
Q

what is T2 of TNM staging?

A

cancer has invade into muscle layer

ie dukes stage A

103
Q

what is T3 of TNM staging?

A

cancer has invade through the muscle layer

ie dukes stage B if no mets)

104
Q

what is T4 of TNM staging?

A

cancer has invaded into adjacent structures

ie dukes stage B if no mets

105
Q

what is N0 of TNM staging?

A

no lymph node involved

106
Q

what is N1 of TNM staging?

A

less than or equal to 3 nodes involved

107
Q

what is N2 of TNM staging?

A

more than 3 lymph nodes involved

108
Q

what is M0 of TNM staging?

A

no distant mets

109
Q

what is M1 of TNM staging?

A

distant mets

110
Q

what are the 3 protective lifestyle factors from colorectal cancer?

A

vegetables
fibre
exercise

111
Q

what are the 4 causative lifestyle factors of colorectal cancer?

A

red and processed meat
smoking
alcohol
obesity

112
Q

how does exercise protect from colorectal cancer?

A

exercise activated AMPkinase (which is also up regulated by tumour suppressore proteins) which increases glucose uptake by muscle and decreases cell turnover

113
Q

what is the only treatment for familial adenomatous polyposis?

A

resection of the colon

114
Q

what are the 3 most important predisposing conditions of colorectal cancer?

A

adenomatous polyps
UC
crohns

(background of chronic inflammation)

115
Q

if a patient over 50 presents with iron-deficiency anaemia what should your number one thought be?

A

colorectal cancer

116
Q

how do you diagnose a colorectal carcinoma?

A

barium enema
CT colography
sigmoidoscopy
colonoscopy (gold standard)

117
Q

what is the screening test for colorectal carcinoma?

A

faecal occult blood testing

FOBT

118
Q

in what type of patients is FOBT useful?

A

asymptomatic patients NOT symptomatic

119
Q

what investigations do you use to stage colorectal carcinoma?

A 
primary rectal cancer:
-CT or MRI
look for liver mets:
-US or CT
look for lung mets:
-CXR or CT
120
Q

what are the 3 main emergency presentations of colorectal cancer?

A

obstruction
bleeding
perforation

121
Q

what does obstruction present as?

A

distension
constipation
pain
(vomiting)

122
Q

what are the 3 treatment options of obstruction?

A

colostomy alone
resection and colostomy
stenting

123
Q

what are the 3 treatment options of colorectal cancer?

A

surgery
radiotherapy
chemotherapy

124
Q

why do you use radiotherapy for rectal cancer?

A

adjuvant (pre/post op)

palliative

125
Q

what is the fucntion of radiotherapy as an adjuvant in addition to surgery for a rectal cancer?

A

pre-op: shrinks cancer to make it more operable

post op: reduces local recurrence after rectal excision

126
Q

when palliative radiotherapy for colorectal cancer used?

A

for inoperable primary rectal cancer or recurrent rectal cancer

127
Q

what specific chemotherapy agent is used as an adjuvant for stage C colorectal cancer?

A

5-FU

5-fluorouracil

128
Q

what is ileus?

A

paralysis of intestinal motility

129
Q

what is ileus caused by?

A 
handling of the bowel
peritonitis
retroperitoneal injury
immobilisation
hypokalaemia
drugs
130
Q

what is the presentation of ileus?

A

vomiting
abdominal distension
dehydration
silent abdomen

131
Q

what causes throbbing pain?

A

inflammation

132
Q

what causes colicky pain?

A

obstruction

133
Q

what type of blood is vomitted in ‘coffee ground’ vomit?

A

digested blood

134
Q

how do haemorrhoids present?

A

painless bleeding
fresh blood, not mixed with stool
perianal itchiness
no change in bowel habit

135
Q

what degree piles shows obvious haemorrhoids?

A

3rd degree piles

136
Q

what are the management options of symptomatic haemorrhoids?

A 
sclerosation therapy
rubber band ligation
open haemorrhoidectomy
stapled haemorrhoidectomy
haemorrhoidal artery ligation operation (HALO)
137
Q

what imaging technique is used to help visualise the haemorrhoids for haemorrhoidal artery ligation operation?

A

doppler ultrasound

138
Q

compare a partial rectal prolapse to a complete rectal prolapse?

A

partial- involves mucosa only

complete- involves all layers of the wall

139
Q

how do rectal prolapses present?

A

protruding mass from anus- more prominent during defecation

bleeding and passing mucus per rectum is common

140
Q

on PR exam of a rectal prolapse what do you find?

A

protruding mass

poor anal tone

141
Q

what is an anal fissure?

A

a tear in the anal margin due to passage of a constipated stool

142
Q

what is the treatment of a complete rectal prolapse?

A

rectoplexy or resection

143
Q

what is the management of an incomplete rectal prolapse?

A

in children: dietary advice (increase fibre) and treatment of constipation
adults: haemorrhoidectomy

144
Q

how do anal fissures present?

A

acute onset of severe anal pain usually following an episode of constipation
(pain lasts 30 mins after defecating)
bright rectal bleeding

145
Q

what are the treatment options for anal fissures?

A 
dietary advice
stool softners
pharmacological sphyncterotomy
lateral sphyncterotomy
botox injection
146
Q

what are the 2 types of ischaemia of the small bowel?

A

mesenteric arterial occlusion

non occlusive perfusion insufficiency

147
Q

what are the 2 main reasons for mesenteric arterial occlusion?

A

mesenteric artery atherosclerosis

thromboembolism from heart (eg A fib)

148
Q

what are the 4 main reasons for non occlusive perfusion insufficiency of the blood supply to the small bowel?

A

shock
strangulation
drugs
hyperviscosity

149
Q

which layer of the bowel wall is most sensitive to effects of hypoxia?

A

mucosa

150
Q

in non occlusive ischaemia when does most of the tissue damage actually occur?

A

after reperfusion

151
Q

what is the outcome of a mucosal infarct of the small bowel?

A

regeneration with mucosal integrity restored

152
Q

what is the outcome of a mural infarct of the small bowel?

A

repair and regeneration leaving a fibrous stricture

153
Q

what is the outcome of a transmural infarction of the small bowel?

A

gangrene

154
Q

which is more common- primary or secondary tumours of the small bowel?

A

seconday tumours

155
Q

what are the 3 main types of primary tumours?

A

lymphomas
carcinoid tumours
carcinomas

156
Q

where is the most commonest site for a carcinoid tumour of the small bowel?

A

appendix

157
Q

what is coeliacs disease?

A

an abnormal reaction to gluten which damages enterocytes and reduces absorptive capacity

158
Q

what immune cell is the main mediator of coeliacs disease?

A

intra-epithelial lymphocytes

159
Q

what happens to the villi in coeliacs disease?

A

destroyed, flat duodenal surface forms

160
Q

what are the main metabolic effects of coeliacs disease?

A
  • malabsorption of sugars, fats, amino acis, water and electrolytes
  • reduced intestinal hormone production
161
Q

what does reduced intestinal hormone production in coeliacs disease lead to?

A

gallstones

due to stasis of bile because of reduced CCK

162
Q

what are the 5 effects of malabsorption within coeliacs disease?

A 
loss of weight
anaemia (macrocytic and microcytic)
abdominal bloating
failure to thrive
vitamin deficiencies
163
Q

what is intussusception?

A

when a segment of bowel wall becomes telescoped into the segment distal to it

164
Q

what is the first line investigation for suspected perforation?

A

erect chest x-ray

165
Q

what is the first line investigation for suspected appendicitis?

A

ultrasound

166
Q

what is the first line investigation for diverticulitis?

A

CT

167
Q

what is the investigation you should chose to do if there appears to be a bowel cause of abdominal distension?

A

abdominal x ray

168
Q

what is the investigation you should choose to do if there appears to be a fluid cause of abdominal distension?

A

ultrasound

169
Q

what is the main investigation procedure of haematemesis?

A

endoscopy

170
Q

what is the main investigation procedure for dysphagia?

A

endoscopy or barium swallow

171
Q

what is the radiological investigation for change in bowel habit?

A

barium enema or CT virtual colography

172
Q

what is the investigation for change in bowel habit if there appears to be an inflammatory bowel disease underlying cause?

A

endoscopy

colonoscopy

173
Q

what is the first line investigation for patient presentation with jaundice?

A

ultrasound

Gastrointestinal RT (15 decks)

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