Gastrointestinal Flashcards
1
Q
What is inflammatory bowel disease?
A
The umbrella term for two main diseases that causes inflammation of the GI tract - Crohn’s and ulcerative colitis.
2
Q
Is IBD always continuously inflamed?
A
No, associated with periods of remission and exacerbation.
3
Q
What is the acronym for remembering the features of Crohn’s disease?
A
NESTS:
-No blood or mucous.
-Entire GI tract affected.
-Skip lesions on endoscopy.
-Terminal ileum most affected and Transmural inflammation.
-Smoking is a RF.
4
Q
What is the acronym for remembering features of ulcerative colitis?
A
CLOSEUP:
-Continuous inflammation.
-Limited to colon and rectum.
-Only superficial mucosa affected.
-Smoking is protective.
-Excrete blood/mucous.
-Use aminosalicyclates.
-Primary sclerosing cholangitis association.
5
Q
Who is affected most by IBD?
A
Jewish people.
6
Q
What causes IBD?
A
Unclear - autoimmune condition.
7
Q
What is IBD a big risk factor for?
A
Colorectal cancer and other autoimmune diseases.
8
Q
What is the gold standard investigation for IBD?
A
Colonoscopy and biopsy.
9
Q
Which investigation may be positive in UC but not Crohn’s?
A
May be pANCA positive in UC.
10
Q
Compare and contrast UC and Crohn’s.
A
- UC affects the bowel and rectum.
-Crohn’s affects the entire GI tract. - UC affects only the mucosa layer.
-Crohn’s is transmural inflammation. - UC has continuous inflammation.
-Crohn’s has ‘skip lesions’. - In UC, smoking is protective,
-In Crohn’s smoking is a RF. - In UC, there is blood and mucous.
-In Crohn’s there is rarely blood and mucous.
11
Q
What is the main risk factor for IBD?
A
Family history.
12
Q
Has Crohn’s or UC more genetic association?
A
Crohn’s has a stronger genetic link.
13
Q
Explain the epidemiology of Crohn’s.
A
Presents ages 20-40.
Northern European.
-Affects females more than male.
-More Jewish people affected.
14
Q
Explain the epidemiology of UC.
A
Presents ages 20-40y.
-Affects females and males equally.
-More common in Jewish people.
-Incidence 3x higher in non-smokers.
15
Q
Is UC or Crohn’s more common?
A
Ulcerative colitis is more common.
16
Q
How does ulcerative colitis usually present?
A
LLQ pain, cramps and discomfort.
-Episodic diarrhoea with blood and mucous.
-Fever, anorexia, malaise and weight loss.
17
Q
Which condition is commonly associated with ulcerative colitis?
A
Primary sclerosing cholangitis (90%).
18
Q
What are the blood and stool results in someone with IBD?
A
Raised WCC, platelets, CRP and ESR in blood.
Raised foecal calprotectin in stool.
19
Q
What is used to rule out infections in IBD?
A
Stool samples to test for bacteria.
20
Q
What is the aim of treatment for IBD?
A
To induce remission of the disease.
21
Q
What are the 1st and 2nd line treatments for UC?
A
1st - aminosalicyclate.
2nd - Steroids.
22
Q
How is remission maintained in ulcerative colitis?
A
With immunosuppressants:
-Azathioprine and methotrexate.
23
Q
What is a curative option for UC?
A
Surgery - to remove the inflamed bowel portion and making a stoma.
24
Q
What are colonic complications of IBD?
A
Colorectal cancer, blood loss and perforation.
25
Which two autoimmune conditions are associated with IBD?
Ankylosing spondylitis and arthritis.
26
What exacerbates and triggers flare ups in IBD?
NSAIDs, certain foods, chronic stress and depression.
27
Why are symptoms of Crohn's more broad than UC?
The whole GI tract is affected and symptoms will arise from where the inflammation is.
28
What are small bowel symptoms of Crohn's?
Abdominal pain, weight loss.
-Terminal ileum = RLQ pain.
29
What are colonic symptoms of Crohn's?
Bloody diarrhoea (not as common), shitting pain.
30
What are systemic symptoms in IBD attacks?
Fever, fatigue, malaise, anorexia/weight loss.
31
What are the colonoscopy and biopsy findings in IBD?
UC - Continuous and mucosal inflammation.
Crohn's - Skip lesions and transmural inflammation.
32
Why does Crohn's disease lead to anaemia and vitamin deficienies?
Inflammation affects the small intestine so vitamin absorption, leading to anaemia.
33
What is the first line treatment for Crohn's?
Steroids (prednisolone).
34
How is remission maintained in Crohn's?
Immunosuppressants:
-Azathioprine.
-Methotrexate.
35
What surgery option is available for Crohn's?
If the terminal ileum is affected, it can be removed and and an ileostomy (stoma) is done.
36
What is coeliac disease?
Autoimmune condition causing inflammation of the mucosa of the small intestine in response to gluten. Causes villous atrophy and malabsorption.
37
Where does coeliac disease affect?
Mostly the jejunum.
38
Describe the epidemiology of coeliac disease.
Equal in men and women and can start at any age.
39
When does coeliac disease usually present?
Infancy, and in middle age.
40
What type of disease is coeliacs?
Autoimmune - T4 hypersensitivity.
41
What are the two main risk factors for coeliac disease?
-Autoimmune disease (thyroid, Addison's, T1DM, auto hep, PSC, PBC).
-Family history (HLADQ2 and HLADQ8).
42
Describe the genetic associations of coeliac disease.
HLA-DQ2 (90%).
HLA-DQ8.
43
Describe the pathophysiology of coeliac disease.
T4 hypersensitivity - Autoantibodies are created in response to exposure to gluten to the small intestine.
-Villous atrophy and crypt hyperplasia.
44
Which autoantibodies are present in coeliac disease?
Anti-TTG and anti-EMA autoantibodies (IgA).
45
How does coeliac disease present in infants?
Failure to thrive.
46
How does coeliac disease present?
Diarrhoea, steatorrhoea, fatigue, weight loss, pain.
-Mouth ulcers, anaemia, dermatitis herpetiformis.
47
What are three rare symptoms of coeliac disease?
Neuro Sx:
-Peripheral neuropathy, ataxia, epilepsy.
48
Why does coeliac disease cause anaemia?
Villous atrophy causes malabsorption causing iron, folate and B12 deficiencies.
49
What is the first line investigation used in coeliac disease?
Serum antibodies:
-Total IgA.
-Anti-TTG.
-Anti-EMA.
50
What is the gold standard investigation in coeliac disease?
Duodenal biopsy.
-Crypt hypertrophy and villous atrophy.
51
What are three other investigations for coeliac disease and why?
Genetic testing (confirm gene), FBC (investigate anaemia) and DEXA scan (investigate osteoporosis).
52
How is coeliac disease managed?
Lifelong gluten free diet.
-Monitor complications and coeliac antibodies.
53
What are four complications of coeliac disease?
Vitamin deficiency, anaemia, osteoporosis, cancer (lymphoma, oesophageal, gastric, small/large bowel).
54
What is irritable bowel syndrome?
A group of functional chronic bowel disorders without an organic cause.
55
Describe the epidemiology of IBS.
Onset usually below 40y.
-More common in females.
-Affects 20% of Western world.
56
What causes IBS?
Unknown, there are theories of causes but thought to be related to psychology (stress, anxiety, drugs and a poor diet).
57
What are the types of IBS?
IBS-C - Mostly constipation.
IBS-D - Mostly diarrhoea.
IBS-M - Mixed and alternating.
58
What are the six risk factors for IBS?
GI infections, previous severe long-term diarrhoea, anxiety/depression, stress, trauma/abuse, eating disorders.
59
How does IBS usually present?
Diarrhoea, constipation, ado pain/cramps, bloating.
-Altered stool form and frequency.
-Change in bowel habit.
-Worse after eating.
-Relieved by defaecating.
60
When should IBS be considered?
ABC:
-Abdominal pain.
-Bloating.
-Change in bowel habit.
61
What type of diagnosis is IBS?
A diagnosis of exlcusion.
62
How is IBS diagnosed?
-Once all organic causes are rules out (IBD, coeliacs, cancer).
-Normal bloods (FBC, ESR, CRP, coeliac screen).
-Normal foecal calprotectin.
-Normal colonoscopy and biopsy.
63
How is IBS managed?
Eat a healthy diet and exercise.
-Regular small meals.
-Adequate fluids.
-Reduce processed foods.
-Limit caffeine and alcohol.
64
What are the medications used for IBS?
1st - loperamide (diarrhoea), laxatives (constipation).
2nd - Tricyclic antidepressants.
3rd - SSRIs.
65
What else can be used to help people with IBS who are stressed?
CBT.
66
What is GORD?
Gastro-oesophageal reflux disease.
-When stomach acid refluxes back into the oesophagus due to decreased LOS pressure and irritates the lining of the oesophagus.
67
Why is the oesophagus more sensitive to stomach acid?
The oesophagus has squamous epithelia which is more sensitive to stomach acid whereas the stomach has columnar epithelia.
68
What are the five causes of GORD?
Hiatal hernia, alcohol, obesity, pregnancy, smoking.
69
What are the symptoms of GORD?
Dyspepsia (indigestion):
-Heartburn, acid regurgitation, bloating, nocturnal cough, hoarse voice.
-Retrosternal or epigastric pain.
70
When are symptoms of GORD worse and why?
When laying down as acid refluxes easier.
71
When is endoscopy done in GORD?
When there are red flags that suggest malignancy or serious conditions.
72
What are seven red flags when investigating GORD?
Weight loss, N+V, haematemesis, dysphagia, low haemoglobin, raised platelets, resistant to treatment.
73
What is the treatment for GORD?
Lifestyle, medications (omeprazole) and surgery.
74
How is lifestyle changed in GORD?
Losing weight, avoid smoking, reduce tea/coffee and alcohol, smaller meals and avoid heavy meals before bed.
75
Which medications are used to treat GORD?
-Heartburn medication when required.
-PPIs (omeprazole/lansoprazole) to reduce acid secretion.
76
How is surgery used to treat GORD?
Laparoscopic fundoplication to tighten the LOS an d decrease the amount of acid refluxing into the oesophagus.
77
What is a complication of GORD?
Barrett's oesophagous.
78
What is Barrett's oesophagus?
Metaplasia from squamous to columnar epithelium in the lower oesophagus.
79
Do symptoms of GORD get worse in Barrett's oesophagus?
No, they typically improve.
80
Who is Barrett's oesophagus more common in?
Middle aged males.
81
What is the typical presentation of Barrett's oesophagus?
Middle aged man with a long history of GORD and dysphagia.
82
How is Barrett's oesophagus diagnosed?
OGD and biopsy.
83
What is Barrett's oesophagus a risk factor for?
Adenocarcinoma of the oesophagus as Barrett's oesophagus is premalignant.
84
What is the progression of Barrett's oesophagus?
No dysplasia - Low grade dysplasia - High grade dysplasia - Adneocarcinoma.
85
How is Barrett's oesophagus treated?
With strong PPIs to reduce acid secretion and RF ablation surgery (destroys cells so they're replaced with normal).
86
Why is Barrett's oesophagus monitored?
It is a big risk factor for oesophageal cancer (adenocarcinoma).
87
What is a peptic ulcer?
Ulceration of the mucosa of the stomach (gastric) or the duodenum (duodenal).
88
Which peptic ulcers are most common?
Duodenal ulcers are more common.
89
What are the five risk factors for peptic ulcers?
Smoking, H. pylori, stress, drugs (NSAIDs) and alcohol.
90
Describe the pathophysiology of peptic ulcers.
Mucosa is prone to ulceration from:
-Breakdown of protective layer.
-Increase in stomach acid.
91
What increases the breakdown of protective layer of the stomach/duodenum?
NSAIDs or H. pylori.
92
What increases the secretion of stomach acid?
Stress, alcohol, caffeine, smoking and spicy food.
93
How do peptic ulcers usually present?
Epigastric pain, N+V, dyspepsia, iron deficiency anaemia, haematemesis and melaena.
94
What are the red flags in peptic ulcers?
Haematemesis, coffee ground vomit, anaemia and dysphagia.
95
If no red flags are present, how are peptic ulcers investigated?
Stool antigen test and urease breath test (H. pylori).
96
If red flags are present, how are peptic ulcers diagnosed?
Endoscopy and biopsy.
97
How are peptic ulcers managed?
-If on NSAIDs, stop.
-If H. pylori - triple therapy CAP (clarythromycin, amoxicillin, PPI).
-High dose PPIs to reduce acid secretion.
98
Where are most gastric ulcers located?
The lesser curve of the stomach.
99
Where are most duodenal ulcers located?
First part of duodenum at the posterior wall.
100
Which type of peptic ulcer is worse on eating and which is better in eating?
Worse on eating - gastric.
Better in eating - duodenal.
101
Which peptic ulcer is worse between meals?
Duodenal ulcers.
102
Which peptic ulcer is relieved by anti-acids?
Gastric ulcers.
103
What is a common complication of a duodenal ulcer?
Ruptured gastroduodenal artery and bleeding.
104
What are three complications of peptic ulcers?
Bleeding, perforation and peritonitis, pyloric stenosis.
105
What is gastritis?
Inflammation of the stomach's mucosal lining.
106
What are the four main causes of gastritis?
NSAIDs, H. pylori, bile reflux and stress.
107
How does gastritis usually present?
Epigastric pain with diarrhoea, N+V and dyspepsia.
-Bloating, burping and lost appetite.
108
What is the gold standard investigation for gastritis?
Endoscopy and biopsy.
109
If H. pylori is suspected for causing gastritis, what investigation is done?
Stool antigen test and urease breath test.
110
How is gastritis treated?
Treat the cause.
-If H. pylori, triple therapy CAP (clarythromycin, amoxicillin and PPI).
111
What is the most common surgical emergency?
Appendectomy for appendicitis.
112
What is the appendix?
A vestigial organ with a disputed functionality - attached to the large intestine.
113
What is appendicitis?
Sudden inflammation of the appendix.
114
What mostly causes appendicitis?
Obstruction within the appendix.
115
What is the peak age of appendicitis?
10-20.
116
What are the most common causes of appendicitis?
Faecolith (hard solid faeces).
-Lymphoid hyperplasia, trauma and worms.
117
What is the presentation of appendicitis?
Umbilical pain which localises to McBurney's point.
-Guarding, pyrexia, N+V.
-Rosving's sign (RUQ pressure causes LLQ pain).
118
In appendicitis, what does rebound and percussion tenderness signify?
Peritonitis.
119
Where is McBurney's point?
2/3rds the way from the umbilicus to the anterior superior iliac spine (ASIS).
120
What is the gold standard investigation for appendicitis?
CT scan.
121
Why USS be used in diagnosing appendicitis?
In women to rule out pregnancy.
In children, as CT is too much harmful radiation.
122
What are the blood results in appendicitis?
Raised WCC, ESR and CRP.
123
Which other test is done in appendicitis and what does it rule out?
Urinalysis:
-Rule out UTI.
-Rule out pregnancy (HCG).
124
What is the gold standard treatment for appendicitis?
Appendectomy with IV antibiotics pre and post operatively.
125
What are two complications of appendictis?
Peritonitis and abscesses.
126
What is a diverticulum?
An outpouching of colonic mucosa.
127
What is diverticulosis?
Multiple diverticulum without inflammation or infection.
128
Is diverticulosis common? What is it associated with?
Very common above aged 50.
-Associated with higher age, low fibre diets, obesity and NSAIDs.
129
What is diverticular disease?
When diverticula cause symptoms.
130
What is diverticulitis?
Infection and inflammation of diverticula.
131
What is the most common site for diverticular diseases and why?
Sigmoid colon:
-Smallest lumen diameter, highest pressure of the colon.
132
What is Meckel's diverticulum?
Common congenital abnormality of GI tract leading to diverticula.
Affects 2% of population, normally asymptomatic.
133
Describe the pathophysiology of diverticula.
Increased pressure over time causes gaps to form in areas of circular muscles and the mucosa herniates through, forming diverticula.
134
Why don't diverticula form in the rectum?
It has an outer longitudinal muscle that surrounds the rectum.
135
Which areas of the colon are vulnerable to the development of diverticula?
Areas that aren't covered by tenia coli.
136
What are the five risk factors for diverticula?
Ageing, increased colon pressure, chronic cough and connective tissue disorders (ED, M), bad diet (no fibre, fat).
137
How does diverticulitis present?
Triad - LLQ pain, constipation and fresh rectal bleeding.
-Fever, diarrhoea, N+V.
138
What is the gold standard investigation of diverticular diseases?
CT scan.
139
What are the bloods findings in diverticulitis?
Raised ESR, CRP and WCC.
140
What is the management for diverticulosis?
Asymptomatic, watch and wait.
141
How is diverticular disease managed?
Bulk forming laxatives, high fibre diet.
Surgery considered to remove affected area.
142
How is diverticulitis treated?
Co-amoxiclav (Abx), analgesia, IV fluids and liquid food.
143
What are six complications of diverticular diseases?
Perforation, bleeding, peritonitis, fistula, obstruction, abscesses.
144
What is helicobacter pylori?
A gram negative bacteria that lives in the stomach.
145
Why is helicobacter pylori harmful?
Can cause damage to stomach lining, causing gastritis, ulcers and increasing the risk of stomach cancer.
146
How does helicobacter pylori live in the stomach?
Lives in the gastric mucosa and avoids the acid by secreting ammonia, which neutralises the acid.
147
Which tests are used to detect helicobacter pylori?
-Urea breath test.
-Stool antigen test.
-Endoscopy - rapid urease test.
148
How is helicobacter pylori treated?
Triple therapy (CAP) for 7 days:
-Clarythromycin, amoxicillin and PPI.
149
What are the two types of oesophageal cancer? Where are they found and what are they associated with?
-Adenocarcinoma (lower 1/3rd) , associated with Barrett's oesophagus
-Squamous cell carcinoma (upper 2/3rd), associated with smoking and alcohol.
150
How does oesophageal cancer present?
Presents when advanced - ALARMS:
-Anaemia, loss of weight, anorexia, recent sudden symptom worsening, melaena/haematemesis, swallowing progressively difficult.
151
What is the gold standard investigation for oesophageal cancer?
OGD and biopsy.
152
What is used in oesophageal cancer for staging?
CT/PET scan.
153
How is oesophageal cancer treated?
If fit - chemo, radio and surgery.
If unfit and old - palliative.
154
What type of tumours is gastric cancer?
Mostly adenocarcinomas.
155
What are the two types of gastric cancer? How common are they? What is the prognosis of them?
T1 - Well differentiated. 80%, better prognosis.
T2 - Undifferentiated. 20%, worse prognosis.
156
What are RFs/causes for gastric cancer?
H. pylori, smoking, gastritis, FHx.
157
How does gastric cancer usually present?
Epigastric pain, N+V, anorexia, weight loss, anaemia, TATT, dysphagia.
158
What are other signs of gastric acncer?
Signs of metastases - liver (jaundice).
159
How is gastric cancer investigated?
OGD and biopsy.
-CT/MRI/PET for staging.
160
What is the management for gastric cancer?
Nutritional support, chemo, radio, surgery.
161
What is the 5y survival for gastric cancer?
60% of people live for 5y.
162
Are small intestine cancers common?
No, rare.
-1% of all GI cancers.
163
What type of tumours are SI cancer mostly?
Mostly adenocarcinomas.
164
What are risk factors for SI cancer?
Chronic SI disease (coeliacs, Crohn's).
165
What is the diagnosis and treatment for SI cancer?
The same for gastric cancer.
166
How common is bowel cancer?
Very common, 4th most common in the UK.
167
Where does bowel cancer most commonly metastasise to?
Mostly the liver.
-Lung and bone.
168
What is the most common type of bowel cancer?
Adenocarcinoma.
169
What are common precursors to bowel cancer?
Adenomas (polyps). They are spontaneous and benign growths that are normal with age but have the ability to progress to bowel cancer.
170
What are seven risk factors for developing bowel cancer?
-Inherited genetic predisposition/family history.
-Adenomas/polyps, age.
-Alcohol and smoking.
-IBD and diet (red meat, low fibre).
171
Which two inherited conditions increase the risk of bowel cancer?
-Familial adenomatous polyposis (FAP).
-Lynch syndrome.
172
What is familial adenomatous polyposis?
An autosomal dominant mutation of the tumour suppressor gene APC which leads to 1000s of polyps developing in the bowel.
-This leads to inevitable bowel cancer usually before age 40.
173
How is FAP treated?
Prophylactic removal of the entire colon to prevent bowel cancer.
174
What is Lynch syndrome?
Hereditary non polyposis colorectal cancer.
-Autosomal dominant mutation of DNA mismatch repair gene.
-Increases risk of all cancers, but especially colorectal cancer.
-Doesn't cause polyps, but tumours in isolation.
175
What are the five red flags for bowel cancer?
-Change in bowel habit.
-Unexplained weight loss.
-Rectal bleeding.
-Unexplained abdominal pain.
-Iron deficiency anaemia.
176
Where are the most common locations for colorectal cancer?
Rectum and sigmoid colon.
177
What is a sign of colorectal cancer?
Tenesmus (needing to poo when empty).
178
What does fresh rectal bleeding mean in colorectal cancer?
Closer to the anus.
179
How is bowel cancer screened for?
FIT test - detects micro blood particles in the poo.
180
Who is bowel cancer screened in?
Everyone aged above 60y.
181
When is a FIT test used?
To screen for bowel cancer.
-In those who don't qualify for an urgent cancer referral.
182
What is the gold standard investigation for bowel cancer?
Colonoscopy/sigmoidoscopy and biopsy.
183
Who is offered colonoscopies at regular intervals?
Those at risk of developing colorectal cancer:
-FAP, Lynch syndrome, IBD.
184
When is a sigmoidoscopy used over colonoscopy?
When there is fresh rectal bleeding.
185
Which two classifications are used in staging bowel cancer?
Duke's criteria and TNM staging.
186
Describe duke's criteria for staging in bowel cancer.
A - Confined to submucosa.
B - Extends through to muscle of bowel.
C - Lymph node involvement.
D - Metastatic disease.
187
Describe TNM staging in bowel cancer.
T (tumour):
T1 - Submucosa.
T2 - Muscle layer.
T3 - Outer layer (serosa).
T4 - Through serosa and reaches other organs.
N (nodes):
N0 - No spread.
N1 - 1-3 nodes.
N2 - 3+ nodes.
M (metastases):
M0 - No metastases.
M1 - Metasatses.
188
How is colorectal cancer managed?
Surgical resection.
-Chemo, radio.
-Palliative care.
189
What is a complication of bowel cancer?
Obstruction of the large intestine (may present as this).
190
What is a Mallory-Weiss tear?
A lower oesophageal mucosal tear due to sudden increased intra-abdominal pressure.
191
How does a Mallory-Weiss tear usually present?
Young male with acute history of retching and eventually haematemesis.
192
What are the four risk factors for a Mallory-Weiss tear?
Alcohol, chronic cough, bulimia and hyperemesis gravidarum (severe N+V in pregnancy).
193
What is important in distinguishing Mallory-Weiss tear and oesophageal varices?
For Mallory-Weiss tear there is no history of liver disease and pulmonary hypertension.
194
How does a Mallory-Weiss tear usually present?
Haematemesis.
-Wretching and vomiting.
-If severe - hypotension.
195
How is Mallory-Weiss tear diagnosed?
OGD (endoscopy).
196
What is the Rockall score?
Used for patients that have had endoscopy to calculate their risk of rebleeding and mortality in upper GI bleeds.
197
What is the Glasgow-Blatchford score?
Scoring system in suspected upper GI bleeding on initial presentation.
198
How is a Mallory-Weiss tear managed?
Most spontaneously heal within 24h.
-Most require no further treatment.
199
How is a severe Mallory-Weiss tear managed?
OGD and banding/clipping.
200
What are the four most common causes of upper GI bleeding?
Peptic ulcers (stomach/duodenum), oesophageal varices, Mallory-Weiss tear, stomach/duodenum cancers.
201
How do upper GI bleeds usually present?
-Haematemesis, coffee-ground vomit, melaena, hypotension/tachycardia (if large).
-Signs of underlying pathology.
202
How often are upper GI bleeds fatal?
10% of the time.
203
What is intestine obstruction?
When there is a blockage in the bowel which prevents the passage of food, water and gas.
204
How common are SI and LI obstructions?
SI are more common than LI obstruction.
SI makes up 70% and LI makes up 30%.
205
Describe the pathophysiology of intestinal obstruction.
Obstruction results in the build up of gas and foecal matter which results in vomiting and dilation of intestines proximal to the obstruction.
206
What is the gold standard investigation for intestinal obstruction?
Non-contract CT of abdomen.
207
What is the first line investigation for intestinal obstruction and what does it show?
XRAY - dilated bowel loops and transluminal fluid gas shadows.
208
What are the blood results of intestinal obstruction?
Electrolyte imbalances, metabolic alkalosis (due to vomiting) and raised lactate (bowel ischaemia).
209
What is the initial management of intestinal obstruction?
Drip and suck:
-Nil by mouth.
-IV fluids.
-NG tube.
210
How is intestinal obstruction treated?
Surgery to correct the underlying cause.
211
What causes small intestine obstruction?
-Adhesions (mc) - scar tissue that binds contents together.
-Hernias, Crohn's and malignancy.
212
What causes large intestine obstruction?
-Malignancy (mc, 90%).
-Volvulus (twisting).
-Intussusception (mc in children) - intestine slides into itself.
-Crohn's, diverticulitis.
213
What are four serious complications of intestinal obstruction?
Hypovolaemic shock, bowel ischaemia and bowel perforation and sepsis.
214
What are the five features of intestine obstruction?
-Vomiting (bile).
-Abdominal distension.
-Diffuse abdominal pain.
-Absolute constipation.
-Tinkling sounds.
215
What are the three main causes of intestinal obstruction?
Adhesions (SI), hernias (SI) and malignancy (LI).
216
What are the four main causes of adhesions?
Abdominal or pelvic surgery/infections.
Endometriosis.
Peritonitis.
217
Compare the symptoms of SI and LI obstructions.
SI - Vomiting then constipation.
LI - Constipation then vomiting.
218
What is a pseudo-obstruction?
When there are symptoms of intestinal obstruction but no mechanical obstruction.
219
What is the definition of diarrhoea?
3 or more watery stools per day.
220
What is the difference between acute and chronic diarrhoea?
Acute - <14 days.
Chronic - >28 days.
221
What are five types of diarrhoea?
Watery, secretory, functional, steatorrhoea, inflammatory.
222
What is the most common cause of diarrhoea in adults?
Norovirus.
223
What are the six main causes of diarrhoea?
IBD, coeliac, malignancy, inflammation, hyperthyroidism and infective.
224
What is the most common cause of diarrhoea?
Viral.
225
What are the main viral causes of diarrhoea in children and adults?
Children - rotavirus.
Aduts - norovirus.
226
What are the six main bacterial causes of diarrhoea?
Campylobacter (mc), E. coli, shigella, salmonella, C. diff and cholera.
227
What three other things can cause diarrhoea?
Worms, parasites and antibiotics.
228
How does diarrhoea present?
Depends on the cause:
-Infective tends to be acute.
-Non-infective has a longer history.
229
How is diarrhoea treated?
Depends on the underlying cause:
-Viral is self limiting.
-Bacterial - antibiotics.
230
What are the two main complications of diarrhoea?
Dehydration and electrolyte loss.
231
What is achalasia?
Rare disorder where there is impaired oesophageal peristalsis and the LOS doesn't open.
232
What is the cause of achalasia?
Idiopathic.
233
How does achalasia present?
Non-progressive dysphagia, substernal pain, food regurgitation, coughing.
234
How is achalasia diagnosed?
-Manometry - measures oesophagus pressure at different points.
- X-RAY and barium swallow.
-Endoscopy.
235
How is achalasia treated?
-Nitrates - relax oesophagus.
-Balloon stenting.
-Removal of LOS.
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What is ischaemic colitis?
Ischaemia of the arterial supply to the colon, which then gets inflamed due to hypoperfusion.
237
What are the three most commonly affected sites of ischaemic colitis?
Splenic flexure (mc), sigmoid colon and caecum.
238
What causes ischaemic colitis?
Affects IMA:
-Thrombosis (mc), emboli, decreased CO and arrhythmias.
239
What are the features of ischaemic colitis?
Sudden onset LLQ pain and bright bloody stools.
-Signs of hypovolaemic shock.
240
How is ischaemic colitis diagnosed?
GS - colonoscopy and biopsy.
-Rule out other causes.
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How is ischaemic colitis treated?
IV fluid, antibiotics.
-Treat underlying cause (remove clot).
-Surgery if infarct and gangrenous.
242
What are the complications of ischaemic colitis?
Perforation, peritonitis and infarct bowel.
-Strictures and obstruction.
243
What is mesenteric ischaemia?
Ischaemia of the small intestine.
244
When should mesenteric ischaemia be suspected?
AF with severe abdominal pain.
245
What are the two types of mesenteric ischaemia?
Acute and chronic.
246
What causes mesenteric ischaemia?
Affects SMA:
-Thrombosis (mc) and emboli (due to AF).
247
What are the symptoms of mesenteric ischaemia?
Triad:
-Central acute severe abdominal pain.
-No abdominal signs of examination.
-Rapid hypovolaemic shock.
248
What are the risk factors for mesenteric ischaemia?
Same as cardiovascular disease.
249
How is mesenteric ischaemia diagnosed?
CT angiogram.
250
What is the mortality of acute mesenteric ischaemia?
50%.
251
How is mesenteric ischaemia treated?
Revascularisation and surgery if bowel is infarct.
252
What are five perianal disorders?
Hemorrhoids, perianal abscess, anal fistula, anal fissure and pilonidal abscess.
253
What is the most severe complications of ulcerative colitis?
Toxic megacolon.
254
What is toxic megacolon? What are its features?
Extreme inflammation and distention of the bowel.
-Acute colonic distention with severe bloody diarrhoea 6+ times daily.
255
How does toxic megacolon appear on AXR?
Very distended colon.
256
How does toxic megacolon appear on AXR?
Very distended colon.
257
What is the treatment of toxic megacolon?
Supportive therapy, antibiotics and aminosalicyclates, if no improvement in 36h - surgery.
258
What is Cullen's sign?
Superficial bruising in the subcutaneous fat around the umbilicus.
259
What is Grey Turner's sign?
Bruising of the flanks - between bottom rib and hip.
260
What do Cullen's and Grey Turner's signs signify?
Acute pancreatitis and intra-abodminal bleeding.
261
What does Rosving's sign signify?
Appendicitis.
262
What is Rosving's sign?
When you press the left iliac fossa, it results in pain of the right iliac fossa.
263
Describe the CMV infection.
Affects 50% of adults asymptomatically.
-Presents in HIV/AIDS as the latent infection gets reactivated and causes problems such as colitis.
-Characteristic 'owl eye' inclusions on
