GI Flashcards
(186 cards)
1
Q
What is coeliac disease?
A
Inflammation of the mucosa of the upper small bowel in response to gluten
2
Q
Which part of the GIT does coeliac affect?
A
Duodenum
3
Q
What substance is gluten broken down into as it crosses the luminal enterocytes?
A
Gliadin
4
Q
What enzyme deaminates gliadin?
A
Transglutaminase
5
Q
What produces the pro-inflammatory cytokines in coeliac?
A
Gluten sensitive CD4+ tcells
6
Q
What changes occur to the bowel as a result of coeliac?
A
Villous atrophy and crypt hyperplasia.
7
Q
What does villous atrophy cause?
A
Malabsorption
8
Q
Clinical presentation of coeliac disease
A
Steatorrhoea, stinking stools, weight loss, fatigue, diarrhoea, abdo pain, bloating, nausea and vomiting
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
10
Q
What are the first-line investigations for coeliac?
A
IgA tissue transglutaminase, and EMA
11
Q
What is the gold standard investigation for coeliac disease?
A
Dudonal biopsy endoscopically
12
Q
What findings are there in coeliac on a duodenal biopsy?
A
Villous atrophy, crypt hyperplasia, increased epithelial WBC’s
13
Q
How do you manage coeliac disease?
A
Lifelong gluten free diet and correct vitamin deficiency
14
Q
Which part of the GIT does ulcerative colitis affect?
A
Large bowel only
15
Q
To which level does the inflam reach in UC?
A
Mucosa only inflamed
16
Q
What are the characteristics of inflammation in UC>
A
Circumferential and contiuous with no skip lesions
17
Q
What else is sometiems seen in UC alongside the inflam?
A
Ulcers and pseudopolyps, crypt abscesses and depleted goblet cells
18
Q
Which part of the GIT does crohns affect?
A
Any part from the mouth to the anus.
19
Q
Which parts of the GIT does crohns most commonly affect>
A
Terminal ileum and proximal colon
20
Q
What layers of the bowel does crohns affect?
A
Can affect all layers, is transmural
21
Q
What are the characteristic sof inflammation on crohns?
A
Non-continuous skip lesions, cobblestone appearance with ulcers and fissure in mucosa.
22
Q
What is the cause of ulcerative collitis>
A
Inappropriate immune response against colonic flora in genetically susceptible individuals
23
Q
What are risk factors for UC?
A
Family hostory, NSAIDS, Chronic stress and depression
24
Q
What is the epidemiology of UC?
A
Northern european and north american; males and females affected equally, presentation between 20-40 years
25
What are the symptoms of UC?
pattern of remission and exacerbations, abdominal pain in the lower left quadrant, episodic or chronic diarrhoea
Blood or mucus in stool.
26
Signs of UC?
Fever, tacchycardia, tender distended abdomen in acute
| Clubbing, oral ulcers, nutritional deficits
27
What are the skin and colon complications of UC?
```
Blood loss, perforation, toxic dilation, colorectal cancer
Erythema nodosum (tender red bumps and pyoderma gangrenosum (painful ulcers on the skin
```
28
Joint, liver and eye complications of UC?
Joints: AS, arthritis
Eyes: iritis, uveitis, episcleritis
liver: fatty change, chronic pericholangitis, sclerosing cholangitis.
29
Blood test results for UC
Raised white cells, raised platelets, raised CRP and ESR. May show normocytic anaemia of chronic disease
30
Why are stool samples taken in UC?
To exclude c.diff, campylobacter and others
31
What is faecal calprotectin?
An inflammatory marker in the stool, indicates inflammatory bowel disease if raised but can't differentiate between UC and Crohn's
32
What is the gold standard investigation for UC?
Sigmoidoscopy with biopsy, full colonoscopy may be done to define extent.
33
What is an aminosalicyclate?
It aims to reduce inflammation by inhibiting prostaglandins and is used first line to treat UC
Sulfasalazine
34
What is used seocnd line in mild/moderate UC if they don't respond to 5-ASA's?
Oral prednisolone
35
What would you use in severe cases of UC?
IV hydrocortisone, ciclosporin, infliximab
36
What would you do in seveer UC with no response to treatment?
Colectomy with the whole colon removed.
37
What are the risk factors for crohns?
FH, Smoking, NSAIDS, chronic stress and depression
38
What populations are more likely to be affected with Crohn's?
Northern european and north america, femals and between 20-40 years.
39
If crohns affects the small bowel what clinical symptoms are commonly seen?
Abdopain and weight loss, right iliac fossa pain mimicking appendicitis
40
If crohns affects the colon which symptoms are more likely to be seen?
Bloody diarrhoea, urgency, pain on defecation.
41
Signs of crohn's dsease
Bowel ulceration, abdo tenderness, abdomass, perianal disease
42
Extraintestinal signs of crohns?
CLubbing, oral apthous ulcers, skin, joint and eye problems
43
Complications of crohns
Malabsorption, abscess formation, fistula formation, colorectal cancer, anaemia, perianal disease.
44
What would blood tests show for crohn's?
Raised WCC, raised platelets, raised CRP and ESR, abnormal liver biochem, anaemia
45
Which antibody will defintely be negative in crohns?
pANCA negative
46
What's the gold standard investigation for Crohns?
colonoscopy with biopsy
47
First line treatment of crohns?
Oral prednisolone, smoking cessation, correct nutritional deficiencies.
48
Management of crohns if its not responding to steroids?
Anti-TNF (infliximab)
49
Which drugs to maintain remission of crohns?
AzathioprIne
50
What is IBS?
Mixed group of abdominal symptoms with no organic cause
51
Whats the average age of onset for ibs?
under 40 years
52
What are the risk factors for IBS?
GI infections, previous severe long term diarrhoea, anxiety and depression, psychological stress, trauma, abuse, eating disorders
53
What ar ethe 3 types of IBS?
IBS-c, IBS-D, IBS-M
54
When do you consider IBS?
Abdominal pain/discomfort; Bloating and change in bowel habit
55
How do you diagnose IBS?
Abdominal pain/discomfort associated with: Relieved by defecation, altered stool form, altered bowel frequency.
56
What other multisystem associations are there with IBS?
Painful periods, bladder symptoms, back pain, joint hypermobility, fatigue, nausea.
57
What are differential diagnoses for IBS?
COeliac disease, lactose intolerance, bile acid malabsorption, IBD, colorectal cancer, GI infection
58
What are the red flag symptoms for colon cancer?
Unexplained weight loss, bleeding on defecation, abdo/rectal mass, anaemia, raised inflam markers, FH, aged over 50.
59
What investigations would you do in IBS?
FBC, anaemia; ESR and CRP for inflam, tTG/EMA for coeliac disease
Faecal calprotectin is raised in IBD
60
How to manage mild IBS?
Education and reassurance, dietary modification, avoid FODMAPS
61
What drugs are used for pain and bloating in IBS?
Antispasmodics, mebeverine and buscopan
Loperamide for diarrhoea
Macrogol, docusate and senna for constipation.
62
If the IBS doesnt improve with diet and other changes what next?
TCA's, amytriptaline or SSRI's
63
What's the most common age to have appendicitis?
10-20
64
Where is the appendix located?
McBurney's point
65
Where in the abdomen is mcBurney's point?
2/3 of the way from the umbilicus to the ASIS
66
Why does appendicitis occur?
Obstruction within the appendix
67
Why does obstruction lead to appendicitis?
Obstruction results in the invasion of gut organisms into the appendix wall. This leads to inflammation, necrosis and eventually perforation
68
What can cause an obstruction in the appendix?
Faecoliths (hard mass of faeces), foreign bodies, trauma, intestinal worms, lymphoid hyperplasia.
69
How does appendicitis present?
Early pain around the umbilicus that migrates to the right iliac fossa
70
Other symptoms of appendicitis?
Guarding, pyrexia, nausea and vomiting.
71
Differential diagnoses for appendicitis?
Acute crohns disease, ectopic pregnancy, UTI, diverticulitiis, perforated ulcer, constipation, food poisoning
72
Whats the gold standard test for appendicitis>
CT scan
73
Other investigations for appendicitis?
raised WCC, raised CRP and ESR.
Ultrasound
Pregnancy test to exclude
Urinalysis to exclude UTI
74
Managment of acute appendicitis
Appendicectmy, IV antibiotics pre and post op
75
What are some complications of an appendicectomy
Perforation, adhesions
76
What is a bowel obstruction ?
The arrest of the onward propulsion of intestinal contents
77
What is the most common cause of small bowel obstruction?
Adhesions from previus abdo surgery, or caused by previous infections
78
What are other causes of small bowel obstruction?
Hernias, malignancy, crohns disease
79
Why does bowel obstruction lead to necrosis?
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
What is the pain like in small bowel obstruction?
Initially collicky then diffuse, higher in the abdomen than lbo
81
What other presentations are there in small bowel obstruction?
Vomiting which occurs earlier than LBO, tinkling bowel sounds
82
When does constipation occur in SBO?
Later on, there is no passage of gas either
83
What does tenderness suggest in SBO?
Strangulation or risk of perforation
84
What would an abdominal x-ray show in SBO?
Central gas shadow that completely crosses the lumen, no gas in large bowel, distended loops proximal to obstruction, may see fluid levels
85
What other investigations can be done for SBO?
FBC, examinations looking for hernia, non-contrast CT (gold standard)
86
How to manage a SBO?
IV fluids, Nasogastric decompression to prevent vomiting, analgesia and anti emetics, surgery to remove the obstruction.
87
What is the most common cause of LBO?
Malignancy
88
Other causes of LBO
Volvulus (twisting of the bowel on its mesenteric axis), diverticulitis, crohns disease, intussusception
89
What is the abdo pain like in LBO?
More constant and diffuse than SBO, occurs lower in the abdomen, especially the LIF
90
What other symptoms are there of LBO?
constipatino earleir than LBO, much more abdo distension
91
When does vomiting occur in LBO?
Much later than SBO and may be absent
92
What are the bowel sounds like in LBO?
Normal initially, then increased, then silent when there is no movement.
93
What is the first line investigation for LBO?
Abdo x-ray showing a peripheral gas shadow proximal to the blockage.
94
What other investigations would you do in LBO?
DRE (empty rectum, hard compacted stools, maybe blood) FBC
95
Whats the gold standard investigation for LBO?
CT
96
LBO management?
Fluids, nasogastric decompression, analgesia and anti emetics, surgery
97
What is a pseudo bowel obstruction?
Obstruction caused by a misfunctioning of the muscle wall of the colon
98
What are the causes of pseudo bowel obstruction?
Intra abdo trauma, paralytic ileus, sepsis, drugs i.e. opiates or antidepressants, electrolyte imbalances
99
How long does acute diarrhoea last?
Less than 2 weeks
100
How long does chronic diarrhoea last?
More than 2 weeks
101
Which bacteria are associated with bloody diarrhoea?
Salmonella, E.coli and shigella
102
Which bacteria can cause diarrhoea?
Campylobacter jejuni, e.coli, salmonella and shigella.
103
What is the most common cause of viral adult diarrhoea?
Norovirus
104
What is the most common cause of parasitic diarrhoea?
Giardia lamblia
105
How would you manage diarrhoea?
Anti emetics, Oral rehydration therapy, Loperamide (antimobility agent)
106
How would you treat bacterial diarrhoea?
Metronizadole
107
Which ischaemic bowl disease afects the small bowel>?
Acute and chronic mesenteric ischaemia
108
Which ischaemic bowel disease affects the large bowel?
Ischaemic collitis
109
Which parts of the bowel are most susceptible to ischaemia>
Splenic flexture and caecum as these are watershed areas (furthest away from a blood supply)
110
What is the most common cause of acute mesenteric ischaemia?
Superior mesenteric arterty embolism due to AF
111
Other causes of acute mesenteric ischaemia?
Mesenteric vein thrombosis, non-occlusive disease, thrombosis of SMA
112
What is the classical triad for acute mesenteric ischaemia?
Acute, severe abdo pain, no abdosigns on exam and raised hypovolaemia
113
Which disease is commonly associated with acute mesenteric ischaemia?
AF
114
Investifations for AMI?
Abdo x-ray (rule out bowel obstruction), CT/MRI angiography (non-invasive way to look at arteries to see blockages.
115
How would you manage AMI?
Fluid resuscitation, Antibiotics, IV heparin and surgery to remove necrotic bowel.
116
What is chronic mesenteric ischaemia?
Much slower onset compared to AMI, due to build up of plaques in mesenteric arteries.
117
What are the causes of ischaemic collitis?
Thrombosis, emboli, low flow states, surgery, vasculitis
118
What is the presentation of ischaemic collitis?
Sudden onset LIF pain, pasage of bright red blood, signs of hypovolaemic shock
119
What investigations for ischaemic collitis?
Urgent CT to rule out perforation, colonoscopy with biopsy when patient has recovered.
Barium enema
120
How do you treat ischaemic collitis?
Symptomatic treatement, fluid replacement, antibiotics,
121
Complications of ischaemic collitis?
Strictures at the site of disease, gangrenous ischaemic collitis
122
What is GORD?
Lower oesophageal sphincter dysfunction leading to a reflux of gastric contents leading to symptoms of oesophagitis.
123
What are some causes of GORD?
Hiatus hernia, smoking, alcoholism, obesity, pregnancy
124
How does GORD oresent>
HEartburn (retrosteronal chest pain) related to meals and worse when lying
Belching
Odynophagia (painful swallowing)
125
Extra oesophageal presentations of gord?
Nocturnal asthma, chronic cough, laryngitis, sinusitis
126
How to diagnose GORD?
Clinical diagnosis, only do endoscopy when there are red flags
127
What are the red flags for endoscopy?
Dysphagia, older than 55, weight loss, epigastric pain, , treatment resistant dyspepsia, N&V, anaemia, raised platelts.
128
How to manage GORD non-pharmacologically?
Stop smoking, alcohol and weight loss. Also change sleeping position
129
What pharmalogical measures can help GORD?
PPI's and H2 receptor antagonists or surgery
130
What is barrets oesophagus?
Acid reflux leading to metaplasia in the lower 1/3 of the oesophagus
131
What epithelium changes occur in barrets oesophagus?
Stratifies squamous to stratified columnar
132
What are oesophageal strictures?
Narrowing of the oesophagus
133
WHo is more likley to get barrets oesophagus>
GORD, Caucasion ,males
134
Lifestyle to manage Barrets
Weight loss, stop smoking, reduce alcohol, small regular meals, avoid hot drinks
135
Pharmalogical management of barrets
Endoscopic surveillance with biopsies, High dose PPI
136
What are the 2 types of oesophageal cancer?
Adenocarcinoma and squamous
137
Whereabouts is adenocarcinoma found?
lower 1/3 of the oesophagus near the GO junction.
138
What are the causes of adenocarcinoma?
GORD, barrets, smoking, obestiy
139
Whereabouts is squamous oesophageal cancer found?
Upper 2/3 of the oesophagus
140
What are the causes of squamous oesophageal cancer?
Smoking, alcohol, obesity, low fibre diet, hot drinks
141
What is the presentation of oesophageal cance?
Vomiting, progressive dysphagia, weight loss, horseness, cough, odynophagia (painful swallowing)
142
What is the mneumonic for symptoms of oesophageal cancer?
ALARMS
143
What does alarms stand for?
```
Anaemia
Loss of weight
Recent nset progressive symptoms
Melaena (black sticky faeces due to swallowing blood)
Swallowing difficulties
```
144
1st line Investigations for oesophageal cancer?
Upper GI endoscopy and biopsy
145
How to stage oesophageal cancer?
CT scan or endoscopic ultrasound, to assess which level of mucosa it gotten to
146
What is a peptic ulcer>
Break in the lining of the gastric or duodenal mucosa
147
What are the most common causes of peptic ulcers?
H.pylori, NSAIDS, ZE syndrome
148
What are the investigations for peptic ulcers?
H.pylori breath test and endoscopy if red flags
149
How to manage peptic ulcers?
Lifestyle modification (weight loss and smoking cessation), Treat cause stop NSAIDS and erdicate H.pylori
150
Whats the difference in presentation between gastric and duodenal ulcers?
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
What is gastritis?
Inflammation of the stomachs mucosal lining
152
What are the causes of gastritis?
NSAIDS, AID, H.pylori, bile reflux, Stress
153
Presentatiom of gastritis?
Epigastric pain, N&V, dyspepsia
154
How to investigate gastritis?
H.pylori detection, Endoscopy and biopsy
155
How to manage gastritis?
Address sc ause, H.pylori eradication PPI, Correct vit D deficiency
156
What is a diverticulum/
An outpouching of the gut mucosa where the blood vessels penetrate
157
What is diverticulosis?
Presence of multiple diverticula
158
What is diverticulitis?
Inflammation/infection of diverticulum
159
What is meckels diverticulum?
COmmon congenital abnormality of the GI tract
160
Where are diverticulum most likely to form?
Sigmoid colon as it has the smallest luminal diameter and therefore highest pressure
161
What are some of the causes of diverticulitis>
Low fibre diet, obesity, smoking and NSAIDS
162
Presnetation of diverticulitis?
LIF pain with tenderness, palpable LIF mass, constipation, tachycardia, fever
163
Investigations for Diverticulitis?
Raised ESR/CRP; Erect CXR, AXR and CT
164
Management of diverticulitis?
Oral/IV antibiotics, analgesia, liquid diet, fluid resus, surgical ressection
165
Presentation of diverticular disease?
Altered bowel habit, abdo pain, pr bleeding
166
Management of diverticular disease?
High fibre diet and fluids
167
What are the risk factors for colon cancer?
Family history, IBD, High fat and red meat diet, Obesity and lack of exercise, DM, radiotherapy, Other cancers, hormonal factors
168
How do you diagnose colon cancer?
Faecal occult blood test, colonoscopy and flexible sigmoidoscopy.
169
Symptoms of colon cancer?
Pain, change in bowel habit, rectal bleeding, weight loss
170
What system is used for staging colon cancer?
Dukes staging
171
What is Stage A dukes?
Confined to submucosa
172
What is Dukes B?
Invasion through muscularis without lymph node involvement
173
What is Dukes C?
Invasion through muscularis with regional lymph node involvement
174
What is Dukes D?
Presence of distant metastases.
175
What is a mallory weiss tear?
Haematemesis from tear in oesophageal mucosa
176
Causes of mallory weiss tear?
Alcoholism, gastroenteritis, bulimia, chronic cough
177
Presentation of a mallory weiss tear
Haematemesis, melaena, hypovolaemic shock
178
How to investigate a mallory weiss tear?
Rockall score to assess blood loss, FBC, U&E coag studies, ECG and cardiac enzymes
179
Management of a mallory weiss tear?
ABCDE, Terlipressin (causes vasocontriction to stop bleeding) banding/clipping, adrenaline, thermocoag.
180
What are oesophageal varices?
Dilated veins at sites of portosystemic anastomosis
181
clinical presentatio of oesophageal varices?
Haematemesis or melena, epigastric discomfort, sudden collapse
182
Investigations for oesophageal varices
Urgent endoscopy, FBC, U&E, clotting, LFT's
| CXR
183
Management of oesophageal varices?
ABCDE, Rockall score, Terlipressin and prophylactic antibiotics for bleeding varices
184
What are the red flags for upper GI cancer?
Dysphagia of any age, over 55 with weight loss and any of the following:
Upper abdo pain
Reflux
Dyspepsia.
185
Presentations of gastric cancer
Late presentation, nausea, weight loss, anaemia, dysphagia, vomiting, epigastric pain,
186
Management of gastric cncer?
Nutritional support, surgical resection and chemo
