GI Flashcards

1
Q

What are the two types of oesophageal cancers and list each of their risk factors?

A

squamous cell carcinoma = affects proximal 1/3
RF: smoking **, alcohol, HPV

adenocarcinoma most common = affects distal 2/3
RF: GORD**, barretts oesophagus

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2
Q

How does oesophageal cancer present?

A

DYSPHAGIA ** - solids first and progress to liquids

weight loss
nausea and vomiting
odynophagia (painful swallowing)
hoarseness + cough (invasion of recurrent laryngeal nerve)
aspiration
malaena
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3
Q

if a patient presents with dysphagia, how are they managed?

A
  1. referral to GI team within 2 weeks
  2. upper GI endoscopy and biopsy

CT scan for staging and PET scan for mets

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4
Q

how is oesophageal cancer managed?

A
  1. MDT involvement e.g. surgeon, dietician, nurse specialist, SALT
  2. surgical resection (Ivor lewis type oesophagectomy)
  3. plus chemotherapy
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5
Q

List possible risk factors of gastric cancer?

A
helicobacter pylori**
smoking**
diet (salt, nitrates, spicy, pickled)
alcohol**
EBV 
males
pernicious anaemia
duodenal ulcer**
blood group A 
gastric adenomatous polyps
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6
Q

Describe the pathology of gastric cancers?

A

adenocarcinomas - usually in cardia of stomach

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7
Q

What cells can be seen in gastric cancer?

A

signet ring cells

increase no. of signet ring cells = worse prognosis

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8
Q

how does gastric cancer present?

A

dyspepsia
weight loss, anorexia
nausea and vomiting
early satiety

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9
Q

Which investigations are done to diagnose and stage gastric cancer?

A

to diagnose = upper GI endoscopy and biopsy
to stage = CT scan or endoscopic USS
to look for mets = PET SCAN

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10
Q

How is gastric cancer managed?

A

surgery
- subtotal gastrectomy if >5-10 cm from OG junction
- total gastrectomy if <5cm from OG junction
- endoscopic mucosal resection if early cancers
+ chemotherapy

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11
Q

Define dyspepsia

A

pain or discomfort in the upper epigastric region

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12
Q

List the differentials for dyspepsia

A

GORD
gastric cancer
peptic ulcers
gastritis

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13
Q

What are the red flag features that would concern you in a patient presenting with dyspepsia?

A
"ALARMS"
A- anaemia
L- loss of appetite
A- anorexia
R- recent onset in symptoms
M- melaena
S- swallowing difficulties
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14
Q

what does the ROME criteria include for dyspepsia?

A
  1. 6 months post prandial fullness
  2. early satiety
  3. epigastric pain
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15
Q

How would you investigate someone with dyspepsia?

A
  1. clinical history
  2. endoscopy if any ALARMS symptoms
  3. H. pylori testing (C13 urea breath test or stool antigen test)
  4. FBC
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16
Q

What is achalasia?

A

motility disorder of the oesophagus where there is uncoordinated peristalsis and spasm of the lower oesophagus sphincter

(damage to vagus nerve and loss of ganglia in auerbachs plexus)

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17
Q

How does achalasia present?

A

SOLID and LIQUID swallowing difficulty (dysphagia)

+ heartburn, regurg of food

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18
Q

Why is achalasia important?

A

risk factor for squamous cell carcinoma of the oesophagus

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19
Q

How is achalasia diagnosed?

A

barium swallow *- bird beak deformity

+ manometry - shows high lower oesophageal pressure and absence of peristalsis

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20
Q

How is achalasia managed?

A

endoscopic balloon dilatation of the LOS or botox injected into sphincter

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21
Q

what are the causes of acute oesophagitis

A

immunosuppression - HIV
CMV
HSV
drugs - NSAIDS, bisphosphonates

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22
Q

which scale is used to classify oesophagitis/ dyspepsia?

A

los angeles scale

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23
Q

How is acute oesophagitis managed?

A

2 month course of PPI

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24
Q

What is Barretts oesophagus?

A

metaplasia of the lower oesophagus where normal squamous epithelium is replaced by columnar epithelium

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25
Q

How is barretts oesophagus caused?

A

GORD*, smoking, obesity

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26
Q

How is barretts oesophagus managed?

A
  1. endoscopy every 3-5 years to check for cancer - it is premalignant and can cause adenocarcinoma of oesophagus
  2. long term PPI
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27
Q

What is mallory weiss tear and how is it caused?

A
mucosal linear tear in the oesophagus 
caused by increased intra abdominal pressure usually by persistent vomiting or retching...
1. excessive alcohol 
2. bulimia 
3. gastroenteritis 
4. raised ICP
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28
Q

How does mallory weiss tear present?

A

fresh red blood - haematemesis
melaena
dizziness, low BP

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29
Q

How is mallory weiss tear managed?

A
  1. endoscopy and clips
  2. FBC, cross match, monitor obs
  3. usually self limiting and no treatment needed
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30
Q

What type of bacteria is h.pylori?

A

gram negative curved bacillus

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31
Q

Describe the pathology of h.pylori and how it affects the stomach

A

h.pylori can penetrate through mucus layer
produces urease which breaksdown urea into ammonia and CO2
this causes chronic inflammation
leads to ulceration

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32
Q

What does h. pylori infection predispose you to?

A
peptic ulcer* 
gastric cancer
gastritis
B cell lymphoma of MALT tissue
anaemia** (uses iron for growth and chronic bleeding)
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33
Q

How is a suspected h.pylori infection diagnosed?

A

C13 urea breath test or H.pylori stool antigen test

  • do not take PPI for 2 weeks before or abx for 4 weeks before
  • confirms h. pylori infection
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34
Q

How is a h. pylori infection treated?

A

TRIPLE THERAPY for 7 days

PPI + amoxicillin + clarithryomycin/ metronidazole

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35
Q

what are the possible symptoms of gastritis?

A
dyspepsia
nausea
post prandial fullness
early satiety 
belching
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36
Q

What are the causes of acute or chronic gastritis?

A

acute - alcohol, NSAIDs, h.pylori

chronic - h. pylori, autoimmune conditions, GORD

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37
Q

How do you treat gastritis?

A

find out if h. pylori infection, review medications

PPI for 1 month

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38
Q

List the risk factors for GORD?

A

smoking
alcohol
foods - fatty, spicy, caffeine , large meals
obesity
pregnancy
hiatus hernia
drugs e.g. NSAIDs, anti cholinergic, Ca channel antagonists

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39
Q

What are the symptoms of gORD?

A
heart burn/ dyspepsia - worse on lying down and after eating, relieved by antacids
belching
acid regurgitation, bitter taste 
cough 
water brash - excess saliva

+ hoaresness, non cardiac chest pain, laryngitis, nocturnal asthma

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40
Q

How is GORD investigated and diagnosed?

A

CLINICAL diagnosis but if have concerns…

endoscopy if ALARMS symptoms, atypical symptoms
barium swallow - hiatus hernia
use Los Angeles classification

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41
Q

How is GORD managed conservatively?

A
smoking cessation
weight loss 
eat small regular meals
avoid precipitating foods e.g. spicy, fatty, alcohol
raise head at night so not lying flat 
take antacids e.g. gaviscon, rennies
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42
Q

How is GORD managed with medication?

A

1st line = Proton Pump Inhibitor e.g. omeprazole, lansoprazole for 1 week, if doesn’t work double dose for 1 more month

2nd line = H2 receptor antagonist e.g. ranitidine

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43
Q

What are the complications of GORD?

A
oesophagitis
barretts oesophagus 
ulcers 
anaemia
oesophageal carcinoma (adenocarcinoma)
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44
Q

What are the risk factors for peptic ulcer disease?

A
H. pylori **
smoking ** 
alcohol
stress
drugs - NSAIDs, SSRIs, pepsin
EBV infection
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45
Q

How does a peptic ulcer present and what are the types?

A

epigastric pain - can point with one finger

  1. duodenal ulcers ( more common) - pain relieved by food, pain 2-3 hours after eating, well nourished
  2. gastric ulcers - pain whilst eating, nausea and vomiting, weight loss
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46
Q

How is peptic ulcer disease managed?

A
  1. find the cause e.g. C13 urea breath test, medication review
  2. lifestyle changes - smoking cessation, reduce alcohol
  3. PPI
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47
Q

What are the complications of peptic ulcers?

A

haematemesis - if erosion of gastroduodenal artery
gastric cancers
peritonitis if perforation

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48
Q

what are the causes of an acute upper GI bleed?

A
  1. perforation of peptic ulcer**
  2. oesophageal varices -> large vol + malaena
  3. mallory weiss tear -> moderate vol of bright red blood
  4. malignancy -> small vol + ALARMS
  5. oesophagitis / gastritis -> small vol fresh blood often streaking vomit
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49
Q

How does an upper GI bleed present?

A

haematemesis - if bright red then above stomach, coffee ground is below the stomach
malaena - black tarry stools
sudden collapse
dizziness, signs of shock, pallor, postural hypotension

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50
Q

How is an upper GI bleed managed?

A
  1. admit to hospital
  2. FBC (anaemia), cross match, UandE (high urea), clotting, LFTs, low BP, tachycardia
  3. upper GI endoscopy within 24 hours
  4. adrenaline injected into identifiable bleeding points
  5. continuous infusion of PPI after endoscopy

BLATCHFORD (urea, Hb, systolic BP) - severity - how quick need endoscopy
ROCKALL - risk of rebleeding

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51
Q

Define anal fissure?

A

longitudinal tear in the squamous epithelium of the anal canal

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52
Q

List 3 causes of anal fissures?

A

constipation
IBD
STI e.g. HIV, syphilis, herpes

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53
Q

how does an anal fissure present?

A

pain of defecation “shards of glass”

fresh blood on paper

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54
Q

How is an anal fissure managed?

A

reduce constipation e.g. increase dietary fibre, lots of fluids, warm baths , bulk forming laxatives

pain relief e.g. paracetemol, GTN ointment

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55
Q

Define anal fistula

A

track communicating from the skin to the anal canal due to a discharging abscess

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56
Q

what are the causes of an anal fistula?

A

abscess
crohns
rectal carcinoma

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57
Q

How are anal fistulas managed?

A
  1. MRI

2. surgery: fistulotomy and excision

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58
Q

Define anorectal abscess

A

collection of pus in anal or rectal region

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59
Q

What are the causes of an anorectal abscess?

A

infection of fissure, fistula
STI
blocked anal gland
pinonidal sinus infected

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60
Q

What are the risk factors for an anorectal abscess?

A

diabetes
immunocompromised e.g. HIV
IBD
anal sex

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61
Q

How does an anorectal abscess present?

A

pus discharging from rectum
fever, unwell
perianal pain - worse on sitting, tender

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62
Q

How is an anorectal abscess managed?

A
  1. DRE (hardened tissue) and MRI for fistula
  2. incision and drainage under local anaesthetic
  3. pain relief
  4. antibiotics if infected
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63
Q

define pilonidal sinus

A

small hole in skin caused by obstruction of hair follicles at nasal cleft which can lead to abscess formation

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64
Q

How are haemorrhoids graded?

A
  1. no prolapse
  2. prolapse on strain, resolves spontaneously
  3. prolapse on strain, resolves manually
  4. prolapse permanent
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65
Q

How do haemorrhoids present?

A

painless (if above dentate line) / painful (if below dentate line)
bright red blood on paper (not mixed in with stool)
anal itch

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66
Q

What are the risk factors for haemorrhoids?

A

constipation
prolonged straining
increased abdo pressure e.g. pregnancy, chronic cough, ascites, portal hypertension

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67
Q

How are haemorrhoids managed?

A
  1. refer on 2 week wait if concerned about anal cancer
  2. prevent constipation - lots of fluids, bulk forming laxatives, dietary fibre increase
  3. topical local anaesthetic
  4. rubber band ligation
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68
Q

Define constipation

A

infrequent (<3 stools/ week) difficult (straining and discomfort) and incomplete stools

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69
Q

What are the risk factors for constipation?

A
Lack of fibre in diet
dehydration
elderly
drugs - opioids, iron supplements, anti psychotics, tricyclic anti depressants 
spinal or pelvic nerve injury
metabolic - hypercalcaemia, hypothyroid
70
Q

What are the complications of constipation?

A

haemorrhoids
anal fissure
acute urinary retention
overflow diarrhoea

71
Q

How is constipation managed?

A
  1. treat cause
  2. increase fluids, increase dietary fibre, mobilise
  3. laxatives - bulk forming, stool softener, stimulant, osmotic or enema
72
Q

Name a bulk forming laxative

A

methylcellulose (citrucel)

increase faecal mass and stimulate peristalsis

73
Q

Name a stool softener

A

colace, surfak

74
Q

Name a stimulant laxative

A

senna, docutose

75
Q

Name a osmotic

76
Q

What is irritable bowel syndrome?

A

functional disorder where abdo pain is related with defecation and change in bowel habit, caused by psychological stress , common in women 20-30 y/o

77
Q

What is the criteria/ symptoms of IBS?

A

6 month history of:

  1. abdominal pain
  2. change in bowel habit e.g. increased frequency, urgency
  3. bloating

+ relieved by defecation

+ >2 of the following:

  1. mucus in stool
  2. worse on eating
  3. abdo bloating and distension
  4. altered passage or straining
78
Q

What are the differentials for IBS and which tests should be done to exclude them?

A

DIFFERENTIALS: coeliac, IBD, gynae (ovarian cancer, endometriosis), depression

  1. FBC
  2. tissue transglutaminase antibodies (IgA tTGA)
  3. CRP/ ESR
  4. Ca 125
  5. faecal calprotectin
79
Q

How is IBS managed with lifestyle measures?

A
  • manage stress and anxiety
  • increase fluid intake
  • dietary advice: limit high fibre foods, regular meals, probiotic supplements, avoid fizzy drinks and too much fresh fruit , less caffeine and alcohol
  • regular exercise
  • relaxation techniques
80
Q

How can IBS be managed with medication?

A

for constipation -> linaclotide (laxative)
for diarrhoea -> loperamide
for abdo pain -> anti spasmodics e.g. buscopan

81
Q

What is coeliac disease?

A

autoimmune condition where antibodies are against the protein gliadin found in gluten causing chronic inflammation and villous atrophy in the small intestine

82
Q

What are the associations with coeliac disease?

A

other autoimmune conditions e.g. type 1 diabetes, autoimmune thyroid disease, vitiligo, addisons
HLA DQ2
1st degree relatives

83
Q

What are the symptoms and signs that make you suspect coeliac disease?

A
chronic diarrhoea 
steattorhoea
abdo pain/ cramping / distension 
nausea and vomiting
weight loss / failure to thrive
fatigue
84
Q

What are the possible complications associated with coeliac disease?

A
  1. ANAEMIA - iron, vit B12 and folate deficiency (mixed deformity = increase distribution of RBC width)
  2. osteoporosis
  3. dermatitis herpetiformis
  4. T cell lymphoma of small bowel (hodgkins and non hodgkins)
  5. hyposplenism
  6. lactose intolerance
85
Q

Which skin condition is associated with coeliac disease, describe the rash?

A

dermatitis herpetiformis - caused by IgA deposits under the skin

causes a blistering itchy vesicular rash on extensor surfaces

86
Q

If suspect coeliac disease, what test would you initially do?

A

TISSUE TRANSGLUTAMINASE ANTIBODIES (IgA tTGA) and total IgA

87
Q

if IgA tTG comes back positive, what would you then do to confirm coeliac disease?

A
  1. refer to gastroenterologist
  2. endomysial antibody
  3. endoscopy and biopsy of small intestine (eaton gluten for 6 weeks before duodenal biopsy)
88
Q

what would the biopsy show in coeliac disease?

A

villous atrophy
crypt hyperplasia
lamina propria infiltration with lymphocytes

89
Q

How is coeliac disease managed?

A

gluten free diet (avoid bread, wheat, barley, rye, oats)

review annually adherence to diet (refer to dietician if poor), bloods and signs/ complications of coeliac disease

90
Q

What are the symptoms and signs of vitamin C deficiency?

A

bleeding gums
lethargy
arthralgia
easy bruising

91
Q

who is at risk of vitamin C deficiency?

A

low income
elderly
alcoholics
poor diet

92
Q

what is the difference between the course of disease in crohns and ulcerative colitis?

A

crohns - inflammation affects FULL THICKNESS of bowel wall, anywhere from MOUTH -> ANUS in SKIP LESIONS (with healthy bowel in between)

UC - inflammation is SUPERFICIAL TO MUCOSA of bowel wall, starts at the RECTUM (will not spread past ileocaecal valve) and is CONTINUOUS inflammation

93
Q

DEscribe the initial symptoms of crohns disease

A

diarrhoea (with mucus or blood but not as common as UC)
abdo pain
weight loss
fatigue

94
Q

what complications can you get in crohns?

A
strictures
abscesses
fistulas 
malnutrition 
perianal disease; skin tags, ulcers
95
Q

What are the extra intestinal signs and complications of crohns disease?

A
  1. arthritis
  2. pyoderma gangrenosum
  3. erythema nodosum
  4. osteoporosis
  5. anterior uveitis, conjunctivitis
  6. mouth ulcers
  7. clubbing
  8. iron deficiency anaemia
96
Q

list the possible risk factors for crohns disease

A

smoking
family history of IBD
previous gastroenteritis
NSAIDS

97
Q

How is crohns disease investigated?

A
  1. refer to gastroenterologist if suspect
  2. colonoscopy and biopsy
  3. FBC (anaemia), raised CRP, vitamin B12/D deficiencies
98
Q

describe the pathology seen on biopsy in crohns disease?

A

non caseating granulomas
goblet cell increase
mucus cobblestone appearance
skip lesions

99
Q

How is crohns managed during inducing emission?

A

1st line = corticosteroids e.g. prednisolone, budesonide

if >2 exacerbations in 12 months, add azathioprine
if steroids not tolerated, use 5-ASA e.g. mesalazine

100
Q

How is crohns managed during maintaining remission?

A

1st line = monotherapy azathioprine and smoking cessation

surgical resection

101
Q

Describe the main symptoms of UC?

A
bloody diarrhoea / rectal bleeding ** >6 weeks
abdominal pain (LLQ)
tenesmus, faecal urgency, incontinence 
weight loss
fatigue
fever
102
Q

Describe the extra intestinal symptoms of UC?

A
  1. erythema nodosum
  2. pyoderma gangrenosim
  3. primary sclerosing cholangitis
  4. uveitis
  5. anaemia
  6. clubbing
  7. inflammatory arthritis
  8. malnutrition
103
Q

What is the main concern with UC?

A

risk of colorectal cancer !!

104
Q

How is the severity assessed in UC?

A

MILD - <4 stools/ day, small amount of blood
MODERATE - 4-6 stools/ day, no systemic upset
SEVERE- >6 bloody stools/day + systemic upset

105
Q

Which initial tests are carried out if suspect UC?

A

FBC, high CRP, U&E, TFT, ferritin, coeliac serology, vit B12, folate, stool culture (for c diff and faecal calprotectin)

106
Q

How is UC diagnosed?

A

sigmoidoscopy and biopsy

107
Q

Describe the pathology shown on the biopsy in UC?

A

widespread ulceration
pseudopolyps
crypt abscesses
goblet cell depletion

108
Q

How is UC managed?

A

inducing remission
1st line = RECTAL aminosalicyclates e.g. mesalazine
2nd line = oral prednisolone (if no improvement in 4 weeks)
if systemic upset = admit to hospital, IV hydrocortisone, iV fluids

maintaining remission
1st line = ORAL aminosalicylates e.g. mesalazine
cure = surgery

109
Q

What is the most common type of colorectal cancer?

A

adenocarcinoma

110
Q

What are the risk factors for colorectal cancer?

A
family history - 1st degree relative
familial adenomatous polyposis 
HNPCC (lynch syndrome)
smoking
alcohol
diet high in red meat and processed food
Ulcerative colitis 
obesity
111
Q

What are the risk factors for anal cancer?

A

** HPV infection **

immunocompromised e.g. HIV , autoimmune, medications
homosexual men

112
Q

How does colorectal cancer present?

A

rectal bleeding
change in bowel habit , abdo pain
anaemia
weight loss

113
Q

Which classification system is used in colorectal cancer?

A

DUKES classification

stage A -> limited to mucosa

stage B -> extending into muscularis propria (penetrating though or not)

stage C -> penetrating/ extending into muscularis propria with nodes involved

Stage D -> distant metastatic spread

114
Q

When should patients be referred under the 2 week wait for colorectal cancer?

A
  1. positive occult blood in faeces
  2. > 40 y/o + unexplained weight loss + abdo pain
  3. > 50 y/o + unexplained rectal bleeding
  4. > 60 y/o + iron deficiency anaemia + change in bowel habit
115
Q

Who and when is offered screening for colorectal cancer?

A

age 60 - 74 y/o every 2 years have a “faecal immunochemical test” done at home

if abnormal result, have a colonoscopy

ALSO one off sigmoidoscopy if >55 y/o to detect and treat polyps

116
Q

How is possible colorectal cancer investigated?

A
  1. refer under 2 week wait
  2. colonoscopy and biospy
  3. faecal occult blood
  4. carcinoembryonic antigen
  5. CT/ PET scan - for staging and spread
117
Q

How is colorectal cancer managed?

A

resectional surgery +/- chemotherapy

118
Q

How is anal cancer managed?

A

chemo + radiotherapy

119
Q

What are the mechanical (dynamic) causes of bowel obstruction?

A

mechanical - peristalsis still working but there is a mechanical block

Intraluminal: inside the lumen
foreign material, meconium (CF), faecaliths , gallstones

Intramural : in the lumen
malignancy **, diverticular disease, strictures (inflammatory bowel)

extramural: outside wall of lumen
Adhesions** (from surgery), volvulus, intussusception, hernias

120
Q

What are the non mechanical “pseudo- obstructions” of bowel obstruction?

A

“adynamic” - absent peristalsis

paralytic ileus 
post op 
hirschsprungs 
bowel infarction
ogilvies
121
Q

Explain what paralytic ileus is and how it it caused?

A

partial or complete paralysis of the intestinal muscles resulting in lack of peristalsis

most commonly caused by laparotomy ** and bowel surgery

122
Q

What is found on examination of paralytic ileus?

A

silent bowel

123
Q

What is ogilvies syndrome?

A

acute colonic pseudo obstruction associated with massive dilatation in absence of mechanical obstruction

124
Q

What are the signs and symptoms of ogilvies syndrome ?

A

abdo pain, bloating, nausea and vomiting, constipation

O/E: normal bowel sounds, minimal tenderness, distension

125
Q

How does bowel obstruction present on examination?

A

high pitched bowel sounds
tachycardia
dehydration
hypotension

126
Q

How is suspected bowel obstruction investigated?

A
  1. FBC (anaemia, platelets - tells you health of pt)
  2. cross match (bags of blood ready), group and save *(find pt blood type)
  3. CRP
  4. UandE
  5. ABG - lactate acidosis
  6. cultures
  7. urinalysis
  8. Imaging: abdo x ray (dilated loops of bowel with gas) + abdominal contrast enhanced CT scan *** (better test - tells you what is causing obstruction)
127
Q

Define diverticular disease and diverticulitis?

A

diverticular disease = presence of diverticula (outpouching of the wall of gut in weak spots) causing symptoms

diverticulitis = inflammation of the diverticula (usually from obstruction of faeces)

128
Q

What are the risk factors for diverticular disease?

A
>50 y/o
smoking
NSAIDs use 
low dietary fibre
obesity
129
Q

What are the common symptoms associated with diverticulitis?

A

nausea and vomiting
change in bowel habit + bleeding ?
abdo pain - tenderness, guarding
fever, tachycardia

130
Q

What are the possible complications of diverticulitis?

A
POFAS:
P - perforation
O - obstruction
F- fistula
A - abscess
S - stricture
131
Q

How is possible diverticular disease investigated?

A

colonoscopy - rule out colorectal cancer

132
Q

How is diverticular disease managed?

A
if asymptomatic, no Rx needed
high fibre diet
stop smoking
bulk forming laxatives
paracetamol
133
Q

How is acute diverticulitis managed?

A

broad spec abx (co-amoxiclav 7 days)
clear fluids
surgery in 30%

134
Q

What are common causes of peritonitis?

A

perforated peptic ulcer
perforated appendicitis
surgeru

+ diverticulitis, crohns, pancreatitis

135
Q

How does peritonitis present?

A

abdo pain, fever, anorexia, nausea and vomiting

O/E: pyrexia, tachycardia, hypotension, tenderness, rebound guarding

136
Q

How is peritonitis managed?

A
  1. septic screen - FBC, U&E, LFT, ABG, blood cultures, amylase, abdo x-ray
  2. IV fluid resus
  3. metronidazole + cefotaxime
  4. surgery
137
Q

How does appendicitis present?

A

abdo pain: starts in umbilical area and localises to RIF at McBurneys point (1/3 between anterior superior iliac spine and umbilicus)
vomiting, nausea
mild pyrexia
anorexia

138
Q

How is appendicitis diagnosed?

A

clinical diagnosis + raised inflammatory markers

+/- ultrasound

139
Q

How is appendicitis managed?

A
  1. IV fluids
  2. analgesia
  3. metronidazole and cefotaxime pre operative prophylaxis
  4. appendicectomy
140
Q

Define volvulus

A

torsion of the colon around its mesenteric axis resulting in obstruction and occlusion of blood vessels supplying the bowel
—-> can cause peritonitis and gangrene

141
Q

What are the 2 types of volvulus and which is most common?

A

sigmoid (80%)

caecal (20%)

142
Q

List the risk factors for a sigmoid volvulus?

A

elderly
constipation **
neurological conditions e.g. parkinsons, Duchenne muscular dystrophy
previous volvulus

143
Q

List the risk factors for caecal volvulus?

A

adhesions

pregnancy

144
Q

List the presenting features of a volvulus?

A

sudden onset abdo pain , colicky, RIF
nausea and vomiting
constipation - no flatus
abdo distension and bloating

145
Q

How is a volvulus diagnosed and what is it characteristic sign?

A

abdominal x ray -> coffee bean sign

146
Q

How is a volvulus managed?

A

urgent admission -> rigid sigmoidoscopy with rectal tube insertion

147
Q

What is the difference between acute and chronic mesenteric ischaemia?

A

they are both caused by impaired blood flow to the intestine and an inflammatory response

acute = embolism causes total occlusion of blood supply to the intestines e.g. mesenteric artery embolism

chronic = chronic atherosclerotic disease causing impaired blood flow to the intestines

148
Q

What are the risk factors for chronic mesenteric ischaemia?

A

atherosclerotic disease = hypertension, hypercholesterolaemia, smoking, diabetes

149
Q

what are the risk factors for acute mesenteric ischaemia?

A

AF
malignancy
post MI
endocarditis

(things causing thrombus / embolus)

150
Q

How does chronic mesenteric ischaemia present?

A

“intestinal angina”
chronic intermittent colicky abdo pain
post prandial pain -> fear of eating

151
Q

How is chronic mesenteric ischaemia managed?

A
  1. arteriography **
  2. nitrate therapy
  3. anticoagulation
  4. bypass surgery
152
Q

How does acute mesenteric ischaemia present?

A

sudden onset severe abdo pain out of proportion of symptoms

153
Q

How is acute mesenteric ischaemia managed?

A
  1. angiography
  2. resus - oxygen, fluids, analgesia
  3. papaverine -> relieve spasm
  4. urgent surgical angioplasty
154
Q

What is ischaemic colitis?

A

acute but transient compromise in the blood flow to the large bowel causing inflammation and ulceration - occurs in water shed areas e.g. splenic flexure

155
Q

What would you seen on x ray of ischaemic colitis?

A

thrumbprinting due to mucosal oedema and haemorrhage

156
Q

what is a pharyngeal poach and how would it present?

A

= diverticulum through Killians dehiscence

dysphagia, regurgitation, aspiration, halitosis

157
Q

list the differentials for dysphagia?

A
oesophageal cancer
oesophagitis
oesophageal candidiasis
achalasia
pharyngeal pouch
systemic sclerosis
myasthenia graves 
globus hystericus 
neuro - MS, parkinsons
158
Q

what are oesophageal varices?

A

dilated veins at junction between portal and systemic venous circulation

159
Q

what are the risk factors for oesophageal varices?

A
  1. chronic liver disease ** - causes portal HTN

2. schistosomiasis

160
Q

How does oesophageal varices present?

A

haematemesis
melaena
abdo pain
signs of liver disease

161
Q

How are oesophageal varices managed?

A
  1. endoscopy
  2. FBC, group and save, cross match, clotting , LFT
  3. resus
  4. restore blood volume, fluids
  5. elastic band ligation (endoscopic banding) or vasoconstrictor drugs (Beta blocker)
162
Q

List the 6 types of cell in the stomach?

A
  1. chief cells -> pepsinogen -> digest protein
  2. G cells -> gastrin -> increase acid production
  3. parietal cells -> intrinsic factor / Hal
  4. enterochromaffin cells -> histamine
  5. goblet cells -> mucus + bicarbonate -> neutralise acid
  6. D cells -> somatostatin -> decrease acid production
163
Q

how is the stomach supplied?

A

coeliac trunk

164
Q

How is perforation diagnosed?

A

abdo x ray - air under diaphragm

165
Q

List examples of drugs causing constipation?

A
opioids
calcium supplements 
TCA
anti psychotics 
iron supplements 
bisphosphonates
166
Q

what are the signs on x ray of small bowel obstruction?

A

dilated loops of bowel proximal to obstruction

central dilated loops >2.5cm

167
Q

What are the 4 cardinal symptoms of bowel obstruction?

A
  1. colicky abdominal pain (as bowel is contracting and relaxing to try and overcome obstruction)
  2. abdo distension
  3. vomiting
  4. constipation
168
Q

Describe the particular symptoms of a small bowel obstruction?

A

HIGH - in jejunum
pain ** and vomiting ** early (closer to the stomach)
distension minimal

LOW - in ileum
pain is predominant**, central distension
vomiting is delayed

169
Q

Describe the particular symptoms of a large bowel obstruction?

A

distension is early ** and pronounced
constipation ** earlier sign
less pain (as large bowel has larger capacity than small obstruction)
mild vomiting - dehydration late

170
Q

How is a bowel obstruction described?

A

simple - blood supply intact

strangulated - direct interference to blood flow
(veins more likely to become obstructed as thinner and lower pressure -> causes congestion in the bowel of waste products and deoxygenated blood -> toxic and acidotic)

takes any organ 4 hours to die if no oxygenated blood

mechanism - volvulus, obstruction and intussusception

distension - gas, fluid

171
Q

How is bowel obstruction managed?

A
  1. analgesics - IM/IV morphine
  2. nil by mouth NG tube to decongest stomach
  3. IV cannula (green or pink) + fluid resus + correct electrolytes
  4. close monitoring of vital signs (hourly) and input/output (catheterise)
  5. relief of obstruction -> surgery