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Phase 2a medicine > GI > Flashcards

GI Flashcards

1
Q

What is coeliac disease?

A

Inflammation of the mucosa of the upper small bowel in response to gluten

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2
Q

Which part of the GIT does coeliac affect?

A

Duodenum

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3
Q

What substance is gluten broken down into as it crosses the luminal enterocytes?

A

Gliadin

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4
Q

What enzyme deaminates gliadin?

A

Transglutaminase

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5
Q

What produces the pro-inflammatory cytokines in coeliac?

A

Gluten sensitive CD4+ tcells

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6
Q

What changes occur to the bowel as a result of coeliac?

A

Villous atrophy and crypt hyperplasia.

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7
Q

What does villous atrophy cause?

A

Malabsorption

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8
Q

Clinical presentation of coeliac disease

A

Steatorrhoea, stinking stools, weight loss, fatigue, diarrhoea, abdo pain, bloating, nausea and vomiting

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9
Q

Signs of coeliac disease?

A

Aphthous ulcers, angular stomatitis, osteomalacia, failure to thrive.
Raised red patches of skin with blisters that burst with scratching, anaemia

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10
Q

What are the first-line investigations for coeliac?

A

IgA tissue transglutaminase, and EMA

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11
Q

What is the gold standard investigation for coeliac disease?

A

Dudonal biopsy endoscopically

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12
Q

What findings are there in coeliac on a duodenal biopsy?

A

Villous atrophy, crypt hyperplasia, increased epithelial WBC’s

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13
Q

How do you manage coeliac disease?

A

Lifelong gluten free diet and correct vitamin deficiency

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14
Q

Which part of the GIT does ulcerative colitis affect?

A

Large bowel only

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15
Q

To which level does the inflam reach in UC?

A

Mucosa only inflamed

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16
Q

What are the characteristics of inflammation in UC>

A

Circumferential and contiuous with no skip lesions

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17
Q

What else is sometiems seen in UC alongside the inflam?

A

Ulcers and pseudopolyps, crypt abscesses and depleted goblet cells

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18
Q

Which part of the GIT does crohns affect?

A

Any part from the mouth to the anus.

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19
Q

Which parts of the GIT does crohns most commonly affect>

A

Terminal ileum and proximal colon

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20
Q

What layers of the bowel does crohns affect?

A

Can affect all layers, is transmural

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21
Q

What are the characteristic sof inflammation on crohns?

A

Non-continuous skip lesions, cobblestone appearance with ulcers and fissure in mucosa.

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22
Q

What is the cause of ulcerative collitis>

A

Inappropriate immune response against colonic flora in genetically susceptible individuals

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23
Q

What are risk factors for UC?

A

Family hostory, NSAIDS, Chronic stress and depression

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24
Q

What is the epidemiology of UC?

A

Northern european and north american; males and females affected equally, presentation between 20-40 years

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25
Q

What are the symptoms of UC?

A

pattern of remission and exacerbations, abdominal pain in the lower left quadrant, episodic or chronic diarrhoea
Blood or mucus in stool.

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26
Q

Signs of UC?

A

Fever, tacchycardia, tender distended abdomen in acute

Clubbing, oral ulcers, nutritional deficits

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27
Q

What are the skin and colon complications of UC?

A 
Blood loss, perforation, toxic dilation, colorectal cancer 
Erythema nodosum (tender red bumps and pyoderma gangrenosum (painful ulcers on the skin
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28
Q

Joint, liver and eye complications of UC?

A

Joints: AS, arthritis
Eyes: iritis, uveitis, episcleritis
liver: fatty change, chronic pericholangitis, sclerosing cholangitis.

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29
Q

Blood test results for UC

A

Raised white cells, raised platelets, raised CRP and ESR. May show normocytic anaemia of chronic disease

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30
Q

Why are stool samples taken in UC?

A

To exclude c.diff, campylobacter and others

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31
Q

What is faecal calprotectin?

A

An inflammatory marker in the stool, indicates inflammatory bowel disease if raised but can’t differentiate between UC and Crohn’s

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32
Q

What is the gold standard investigation for UC?

A

Sigmoidoscopy with biopsy, full colonoscopy may be done to define extent.

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33
Q

What is an aminosalicyclate?

A

It aims to reduce inflammation by inhibiting prostaglandins and is used first line to treat UC
Sulfasalazine

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34
Q

What is used seocnd line in mild/moderate UC if they don’t respond to 5-ASA’s?

A

Oral prednisolone

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35
Q

What would you use in severe cases of UC?

A

IV hydrocortisone, ciclosporin, infliximab

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36
Q

What would you do in seveer UC with no response to treatment?

A

Colectomy with the whole colon removed.

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37
Q

What are the risk factors for crohns?

A

FH, Smoking, NSAIDS, chronic stress and depression

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38
Q

What populations are more likely to be affected with Crohn’s?

A

Northern european and north america, femals and between 20-40 years.

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39
Q

If crohns affects the small bowel what clinical symptoms are commonly seen?

A

Abdopain and weight loss, right iliac fossa pain mimicking appendicitis

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40
Q

If crohns affects the colon which symptoms are more likely to be seen?

A

Bloody diarrhoea, urgency, pain on defecation.

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41
Q

Signs of crohn’s dsease

A

Bowel ulceration, abdo tenderness, abdomass, perianal disease

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42
Q

Extraintestinal signs of crohns?

A

CLubbing, oral apthous ulcers, skin, joint and eye problems

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43
Q

Complications of crohns

A

Malabsorption, abscess formation, fistula formation, colorectal cancer, anaemia, perianal disease.

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44
Q

What would blood tests show for crohn’s?

A

Raised WCC, raised platelets, raised CRP and ESR, abnormal liver biochem, anaemia

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45
Q

Which antibody will defintely be negative in crohns?

A

pANCA negative

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46
Q

What’s the gold standard investigation for Crohns?

A

colonoscopy with biopsy

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47
Q

First line treatment of crohns?

A

Oral prednisolone, smoking cessation, correct nutritional deficiencies.

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48
Q

Management of crohns if its not responding to steroids?

A

Anti-TNF (infliximab)

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49
Q

Which drugs to maintain remission of crohns?

A

AzathioprIne

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50
Q

What is IBS?

A

Mixed group of abdominal symptoms with no organic cause

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51
Q

Whats the average age of onset for ibs?

A

under 40 years

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52
Q

What are the risk factors for IBS?

A

GI infections, previous severe long term diarrhoea, anxiety and depression, psychological stress, trauma, abuse, eating disorders

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53
Q

What ar ethe 3 types of IBS?

A

IBS-c, IBS-D, IBS-M

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54
Q

When do you consider IBS?

A

Abdominal pain/discomfort; Bloating and change in bowel habit

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55
Q

How do you diagnose IBS?

A

Abdominal pain/discomfort associated with: Relieved by defecation, altered stool form, altered bowel frequency.

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56
Q

What other multisystem associations are there with IBS?

A

Painful periods, bladder symptoms, back pain, joint hypermobility, fatigue, nausea.

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57
Q

What are differential diagnoses for IBS?

A

COeliac disease, lactose intolerance, bile acid malabsorption, IBD, colorectal cancer, GI infection

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58
Q

What are the red flag symptoms for colon cancer?

A

Unexplained weight loss, bleeding on defecation, abdo/rectal mass, anaemia, raised inflam markers, FH, aged over 50.

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59
Q

What investigations would you do in IBS?

A

FBC, anaemia; ESR and CRP for inflam, tTG/EMA for coeliac disease
Faecal calprotectin is raised in IBD

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60
Q

How to manage mild IBS?

A

Education and reassurance, dietary modification, avoid FODMAPS

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61
Q

What drugs are used for pain and bloating in IBS?

A

Antispasmodics, mebeverine and buscopan
Loperamide for diarrhoea
Macrogol, docusate and senna for constipation.

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62
Q

If the IBS doesnt improve with diet and other changes what next?

A

TCA’s, amytriptaline or SSRI’s

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63
Q

What’s the most common age to have appendicitis?

A

10-20

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64
Q

Where is the appendix located?

A

McBurney’s point

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65
Q

Where in the abdomen is mcBurney’s point?

A

2/3 of the way from the umbilicus to the ASIS

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66
Q

Why does appendicitis occur?

A

Obstruction within the appendix

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67
Q

Why does obstruction lead to appendicitis?

A

Obstruction results in the invasion of gut organisms into the appendix wall. This leads to inflammation, necrosis and eventually perforation

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68
Q

What can cause an obstruction in the appendix?

A

Faecoliths (hard mass of faeces), foreign bodies, trauma, intestinal worms, lymphoid hyperplasia.

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69
Q

How does appendicitis present?

A

Early pain around the umbilicus that migrates to the right iliac fossa

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70
Q

Other symptoms of appendicitis?

A

Guarding, pyrexia, nausea and vomiting.

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71
Q

Differential diagnoses for appendicitis?

A

Acute crohns disease, ectopic pregnancy, UTI, diverticulitiis, perforated ulcer, constipation, food poisoning

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72
Q

Whats the gold standard test for appendicitis>

A

CT scan

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73
Q

Other investigations for appendicitis?

A

raised WCC, raised CRP and ESR.
Ultrasound
Pregnancy test to exclude
Urinalysis to exclude UTI

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74
Q

Managment of acute appendicitis

A

Appendicectmy, IV antibiotics pre and post op

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75
Q

What are some complications of an appendicectomy

A

Perforation, adhesions

76
Q

What is a bowel obstruction ?

A

The arrest of the onward propulsion of intestinal contents

77
Q

What is the most common cause of small bowel obstruction?

A

Adhesions from previus abdo surgery, or caused by previous infections

78
Q

What are other causes of small bowel obstruction?

A

Hernias, malignancy, crohns disease

79
Q

Why does bowel obstruction lead to necrosis?

A

The blockage causes distension due to build up of contents.
This increases pressure and leads to the blood vessels becoming compressed
this cause ischaemia and infarction of the bowel

80
Q

What is the pain like in small bowel obstruction?

A

Initially collicky then diffuse, higher in the abdomen than lbo

81
Q

What other presentations are there in small bowel obstruction?

A

Vomiting which occurs earlier than LBO, tinkling bowel sounds

82
Q

When does constipation occur in SBO?

A

Later on, there is no passage of gas either

83
Q

What does tenderness suggest in SBO?

A

Strangulation or risk of perforation

84
Q

What would an abdominal x-ray show in SBO?

A

Central gas shadow that completely crosses the lumen, no gas in large bowel, distended loops proximal to obstruction, may see fluid levels

85
Q

What other investigations can be done for SBO?

A

FBC, examinations looking for hernia, non-contrast CT (gold standard)

86
Q

How to manage a SBO?

A

IV fluids, Nasogastric decompression to prevent vomiting, analgesia and anti emetics, surgery to remove the obstruction.

87
Q

What is the most common cause of LBO?

A

Malignancy

88
Q

Other causes of LBO

A

Volvulus (twisting of the bowel on its mesenteric axis), diverticulitis, crohns disease, intussusception

89
Q

What is the abdo pain like in LBO?

A

More constant and diffuse than SBO, occurs lower in the abdomen, especially the LIF

90
Q

What other symptoms are there of LBO?

A

constipatino earleir than LBO, much more abdo distension

91
Q

When does vomiting occur in LBO?

A

Much later than SBO and may be absent

92
Q

What are the bowel sounds like in LBO?

A

Normal initially, then increased, then silent when there is no movement.

93
Q

What is the first line investigation for LBO?

A

Abdo x-ray showing a peripheral gas shadow proximal to the blockage.

94
Q

What other investigations would you do in LBO?

A

DRE (empty rectum, hard compacted stools, maybe blood) FBC

95
Q

Whats the gold standard investigation for LBO?

A

CT

96
Q

LBO management?

A

Fluids, nasogastric decompression, analgesia and anti emetics, surgery

97
Q

What is a pseudo bowel obstruction?

A

Obstruction caused by a misfunctioning of the muscle wall of the colon

98
Q

What are the causes of pseudo bowel obstruction?

A

Intra abdo trauma, paralytic ileus, sepsis, drugs i.e. opiates or antidepressants, electrolyte imbalances

99
Q

How long does acute diarrhoea last?

A

Less than 2 weeks

100
Q

How long does chronic diarrhoea last?

A

More than 2 weeks

101
Q

Which bacteria are associated with bloody diarrhoea?

A

Salmonella, E.coli and shigella

102
Q

Which bacteria can cause diarrhoea?

A

Campylobacter jejuni, e.coli, salmonella and shigella.

103
Q

What is the most common cause of viral adult diarrhoea?

A

Norovirus

104
Q

What is the most common cause of parasitic diarrhoea?

A

Giardia lamblia

105
Q

How would you manage diarrhoea?

A

Anti emetics, Oral rehydration therapy, Loperamide (antimobility agent)

106
Q

How would you treat bacterial diarrhoea?

A

Metronizadole

107
Q

Which ischaemic bowl disease afects the small bowel>?

A

Acute and chronic mesenteric ischaemia

108
Q

Which ischaemic bowel disease affects the large bowel?

A

Ischaemic collitis

109
Q

Which parts of the bowel are most susceptible to ischaemia>

A

Splenic flexture and caecum as these are watershed areas (furthest away from a blood supply)

110
Q

What is the most common cause of acute mesenteric ischaemia?

A

Superior mesenteric arterty embolism due to AF

111
Q

Other causes of acute mesenteric ischaemia?

A

Mesenteric vein thrombosis, non-occlusive disease, thrombosis of SMA

112
Q

What is the classical triad for acute mesenteric ischaemia?

A

Acute, severe abdo pain, no abdosigns on exam and raised hypovolaemia

113
Q

Which disease is commonly associated with acute mesenteric ischaemia?

A

AF

114
Q

Investifations for AMI?

A

Abdo x-ray (rule out bowel obstruction), CT/MRI angiography (non-invasive way to look at arteries to see blockages.

115
Q

How would you manage AMI?

A

Fluid resuscitation, Antibiotics, IV heparin and surgery to remove necrotic bowel.

116
Q

What is chronic mesenteric ischaemia?

A

Much slower onset compared to AMI, due to build up of plaques in mesenteric arteries.

117
Q

What are the causes of ischaemic collitis?

A

Thrombosis, emboli, low flow states, surgery, vasculitis

118
Q

What is the presentation of ischaemic collitis?

A

Sudden onset LIF pain, pasage of bright red blood, signs of hypovolaemic shock

119
Q

What investigations for ischaemic collitis?

A

Urgent CT to rule out perforation, colonoscopy with biopsy when patient has recovered.
Barium enema

120
Q

How do you treat ischaemic collitis?

A

Symptomatic treatement, fluid replacement, antibiotics,

121
Q

Complications of ischaemic collitis?

A

Strictures at the site of disease, gangrenous ischaemic collitis

122
Q

What is GORD?

A

Lower oesophageal sphincter dysfunction leading to a reflux of gastric contents leading to symptoms of oesophagitis.

123
Q

What are some causes of GORD?

A

Hiatus hernia, smoking, alcoholism, obesity, pregnancy

124
Q

How does GORD oresent>

A

HEartburn (retrosteronal chest pain) related to meals and worse when lying
Belching
Odynophagia (painful swallowing)

125
Q

Extra oesophageal presentations of gord?

A

Nocturnal asthma, chronic cough, laryngitis, sinusitis

126
Q

How to diagnose GORD?

A

Clinical diagnosis, only do endoscopy when there are red flags

127
Q

What are the red flags for endoscopy?

A

Dysphagia, older than 55, weight loss, epigastric pain, , treatment resistant dyspepsia, N&V, anaemia, raised platelts.

128
Q

How to manage GORD non-pharmacologically?

A

Stop smoking, alcohol and weight loss. Also change sleeping position

129
Q

What pharmalogical measures can help GORD?

A

PPI’s and H2 receptor antagonists or surgery

130
Q

What is barrets oesophagus?

A

Acid reflux leading to metaplasia in the lower 1/3 of the oesophagus

131
Q

What epithelium changes occur in barrets oesophagus?

A

Stratifies squamous to stratified columnar

132
Q

What are oesophageal strictures?

A

Narrowing of the oesophagus

133
Q

WHo is more likley to get barrets oesophagus>

A

GORD, Caucasion ,males

134
Q

Lifestyle to manage Barrets

A

Weight loss, stop smoking, reduce alcohol, small regular meals, avoid hot drinks

135
Q

Pharmalogical management of barrets

A

Endoscopic surveillance with biopsies, High dose PPI

136
Q

What are the 2 types of oesophageal cancer?

A

Adenocarcinoma and squamous

137
Q

Whereabouts is adenocarcinoma found?

A

lower 1/3 of the oesophagus near the GO junction.

138
Q

What are the causes of adenocarcinoma?

A

GORD, barrets, smoking, obestiy

139
Q

Whereabouts is squamous oesophageal cancer found?

A

Upper 2/3 of the oesophagus

140
Q

What are the causes of squamous oesophageal cancer?

A

Smoking, alcohol, obesity, low fibre diet, hot drinks

141
Q

What is the presentation of oesophageal cance?

A

Vomiting, progressive dysphagia, weight loss, horseness, cough, odynophagia (painful swallowing)

142
Q

What is the mneumonic for symptoms of oesophageal cancer?

A

ALARMS

143
Q

What does alarms stand for?

A 
Anaemia
Loss of weight 
Recent nset progressive symptoms 
Melaena (black sticky faeces due to swallowing blood)
Swallowing difficulties
144
Q

1st line Investigations for oesophageal cancer?

A

Upper GI endoscopy and biopsy

145
Q

How to stage oesophageal cancer?

A

CT scan or endoscopic ultrasound, to assess which level of mucosa it gotten to

146
Q

What is a peptic ulcer>

A

Break in the lining of the gastric or duodenal mucosa

147
Q

What are the most common causes of peptic ulcers?

A

H.pylori, NSAIDS, ZE syndrome

148
Q

What are the investigations for peptic ulcers?

A

H.pylori breath test and endoscopy if red flags

149
Q

How to manage peptic ulcers?

A

Lifestyle modification (weight loss and smoking cessation), Treat cause stop NSAIDS and erdicate H.pylori

150
Q

Whats the difference in presentation between gastric and duodenal ulcers?

A

Gastric: Epigastric pain is worse on eating and relieved by antacids
Duodenal: epigastric pain is worse before meals and at night and relieved by eating or milk

151
Q

What is gastritis?

A

Inflammation of the stomachs mucosal lining

152
Q

What are the causes of gastritis?

A

NSAIDS, AID, H.pylori, bile reflux, Stress

153
Q

Presentatiom of gastritis?

A

Epigastric pain, N&V, dyspepsia

154
Q

How to investigate gastritis?

A

H.pylori detection, Endoscopy and biopsy

155
Q

How to manage gastritis?

A

Address sc ause, H.pylori eradication PPI, Correct vit D deficiency

156
Q

What is a diverticulum/

A

An outpouching of the gut mucosa where the blood vessels penetrate

157
Q

What is diverticulosis?

A

Presence of multiple diverticula

158
Q

What is diverticulitis?

A

Inflammation/infection of diverticulum

159
Q

What is meckels diverticulum?

A

COmmon congenital abnormality of the GI tract

160
Q

Where are diverticulum most likely to form?

A

Sigmoid colon as it has the smallest luminal diameter and therefore highest pressure

161
Q

What are some of the causes of diverticulitis>

A

Low fibre diet, obesity, smoking and NSAIDS

162
Q

Presnetation of diverticulitis?

A

LIF pain with tenderness, palpable LIF mass, constipation, tachycardia, fever

163
Q

Investigations for Diverticulitis?

A

Raised ESR/CRP; Erect CXR, AXR and CT

164
Q

Management of diverticulitis?

A

Oral/IV antibiotics, analgesia, liquid diet, fluid resus, surgical ressection

165
Q

Presentation of diverticular disease?

A

Altered bowel habit, abdo pain, pr bleeding

166
Q

Management of diverticular disease?

A

High fibre diet and fluids

167
Q

What are the risk factors for colon cancer?

A

Family history, IBD, High fat and red meat diet, Obesity and lack of exercise, DM, radiotherapy, Other cancers, hormonal factors

168
Q

How do you diagnose colon cancer?

A

Faecal occult blood test, colonoscopy and flexible sigmoidoscopy.

169
Q

Symptoms of colon cancer?

A

Pain, change in bowel habit, rectal bleeding, weight loss

170
Q

What system is used for staging colon cancer?

A

Dukes staging

171
Q

What is Stage A dukes?

A

Confined to submucosa

172
Q

What is Dukes B?

A

Invasion through muscularis without lymph node involvement

173
Q

What is Dukes C?

A

Invasion through muscularis with regional lymph node involvement

174
Q

What is Dukes D?

A

Presence of distant metastases.

175
Q

What is a mallory weiss tear?

A

Haematemesis from tear in oesophageal mucosa

176
Q

Causes of mallory weiss tear?

A

Alcoholism, gastroenteritis, bulimia, chronic cough

177
Q

Presentation of a mallory weiss tear

A

Haematemesis, melaena, hypovolaemic shock

178
Q

How to investigate a mallory weiss tear?

A

Rockall score to assess blood loss, FBC, U&E coag studies, ECG and cardiac enzymes

179
Q

Management of a mallory weiss tear?

A

ABCDE, Terlipressin (causes vasocontriction to stop bleeding) banding/clipping, adrenaline, thermocoag.

180
Q

What are oesophageal varices?

A

Dilated veins at sites of portosystemic anastomosis

181
Q

clinical presentatio of oesophageal varices?

A

Haematemesis or melena, epigastric discomfort, sudden collapse

182
Q

Investigations for oesophageal varices

A

Urgent endoscopy, FBC, U&E, clotting, LFT’s

CXR

183
Q

Management of oesophageal varices?

A

ABCDE, Rockall score, Terlipressin and prophylactic antibiotics for bleeding varices

184
Q

What are the red flags for upper GI cancer?

A

Dysphagia of any age, over 55 with weight loss and any of the following:
Upper abdo pain
Reflux
Dyspepsia.

185
Q

Presentations of gastric cancer

A

Late presentation, nausea, weight loss, anaemia, dysphagia, vomiting, epigastric pain,

186
Q

Management of gastric cncer?

A

Nutritional support, surgical resection and chemo

Phase 2a medicine (14 decks)

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