GI Flashcards
1
Q
What is an inflammatory bowel disease?
A
Inflammatory Bowel Disease: Autoimmune-mediated intestinal inflammation primarily due to either Crohn’s disease or ulcerative colitis.
2
Q
What are the 2 types of inflammatory bowel disease
A
- Crohn’s
- Ulcerative colitis
3
Q
Risk Factors for IBD
A
4
Q
Signs and symtpoms for IBD
A
5
Q
Differential diagnosis for IBD
A
6
Q
Investigations for IBD
A
7
Q
Pathology for IBD
A
8
Q
Management of IBD
A
9
Q
Complications and Prognosis of IBD
A
10
Q
What is irritable bowel syndrome
A
Functional Disorder where there is recurrent abdominal pain + abnormal bowel motility causing constipation and/or diarrhoea
11
Q
Symptoms of Irritable Bowel Syndrome
A
Abdominal pain, Bloating and Change in bowel habit are classic features of irritable bowel syndrome
12
Q
Risk Factors for IBS
A
13
Q
Differential diagnosis of IBS
A
Coeliac Disease
Lactose Intolerance
Inflammatory Bowel Disease - Crohn’s Disease or Ulcerative Collitis
Infective Colitis
Lymphocytic Collagenous Colitis
Colon cancer
Drug effects (e.g. Proton Pump Inhibitors, NSAIDS, metformin)
Choledocholithiasis
14
Q
Investigations for IBS
A
15
Q
Pathophysiology of IBS
A
The pathophysiology of IBS is unclear. There are no specific anatomical, endoscopic, microbiological or histological findings that indicate a clear pathophysiology.
According to current understanding, IBS arises due to multiple factors that contribute to alteration of:
The Brain-gut axis: Bidirectional communication between the brain and the GIT. Involves the ANS, the neuroendocrine system and neuroimmune pathways
Gut sensitivity: Sensation of the GIT.
Gut reactivity: Mobility and secretion of the GIT.
Psychological functioning
16
Q
Treatment for IBS
A
Only a fraction of patients with IBS-like symptoms (∼50%) seek medical care
Education and reassurance
Dietary alterations
Pharmacotherapy
Behavioural and psychological therapy
17
Q
What is coeliac disease
A
Inflammatory process which occurs in susceptible individuals in response to ingestion of wheat protein (gluten-gliaden)
18
Q
Small Intestine: Anatomy and Physiology
A
-
19
Q
Risk Factor for coeliac disease
A
Family history
IgA deficiency
Type 1 diabetes
Autoimmune diseases - autoimmune thyroid, Sjogren’s syndrome, Addison’s disease
Inflammatory Bowel disease
Genetic disorder - Down’s syndrome, Turners syndrome
20
Q
Clinical Presentation of coeliac disease
A
A 30-year-old woman presents with foul smelling oily diarrhoea, abdominal bloating, fatigue and weight loss. On examination she has papulovesicular lesions on the extensor aspects of her arms - coeliac disease
Splenic atrophy may occur in coeliac disease together with the appearance of Howell-Jolly bodies in erythrocytes
21
Q
Differential diagnosis for coeliac disease
A
Childhood other food-sensitive enteropathies (milk sensitivity)
Adults
Lymphoma
Whipple’s disease
Crohn’s Disease
Giardiasis
Irritable Bowel Syndrome
22
Q
Investigations for coeliac disease
A
Gold Standard: Endoscopy
23
Q
Management for coeliac disease
A
Management is ongoing
Gluten Free diet
Calcium Supplements
Iron Supplements
Vitamins
Coeliac Crisis Management:
Rehydration
Electrolytes
Corticosteroids
24
Q
Pathology of coeliac disease
A
25
Complications of coeliac disease
Coeliac disease is most associated with osteomalacia, osteporosis, small bowel lymphoma, lactose intolerance
26
What type of HLA allele is most associated coeliac disease?
HLA-DQ2/DQ8
27
What is gastritis
Inflammation of the stomach lining that’s associated with mucosal injury.
28
isk Factors for Gastritis
H. Pylori infection
Alcohol
NSAIDs use
Previous gastric surgery
Autoimmune disease
29
Causes of gastritis
Caused by things that cause inflammation to stomach e.g -
H.Pylori - lives in gastric mucus
Autoimmune gastritis
Viruses e.g. CMV and HSV
Duodenogastric reflux
Crohn’s disease
Mucosal ischaemia
↑ Stomach acid
Aspirin and NSAIDs
Alcohol
30
Pathophysiology of Gastritis
31
Clinical manifestations for Gastritis
Key presentations: Epigastric pain, Recurrent upset stomach
Signs: Abdominal bloating, Haematemesis
Symptoms: Loss of appetite, Vomiting, Indigestion, Nausea
32
Investigations of gastritis
33
Differential Diagnosis of gastritis
Peptic Ulcer disease
GORD
Non-ulcer dyspepsia
Gastric lymphoma
Gastric carcinoma
34
Treatment for Gastritis
35
Complications gastrits
Achloridya
B12 deficiency
Peptic Ulcer disease
36
What is GORD
Gastric Oesphageal Reflux Disease
37
What are symptoms of GORD caused by?
backflow of gastric acid and other gastric contents into oesphagus due to incompetent barriers at the gastroesophageal junction
38
Anatomy of oesphagus
39
What factors contribute to GORD
Decrease in oesphageal sphincter tone
Increase in intra-gastric volume pressure
40
What factors increase intra-gastric volume pressure
Cough
Large meals
Delayed gastric emptying
41
What factors decrease oesophageal sphincter tone
Alcohol
Drugs: Tricyclic antidepressants
Previous surgery
Peptic strictures
42
Pathological Features of GORD
By reflux oesphagitis: develops when mucosal defences are unable to counteract the damage done by acid pepsin and bile. This causes inflammation
Oesphageal strictures: results from fibrosis that causes luminal constriction. Occur in 10% of patients with untreated GORD and distal oesphagous near the squamous columnar junction
43
Clinical Presentation of GORD
Heart Burn: after meal, lying
Acid Brash
Water Brash
Ooynophagia
Chronic cough
Laryngitis
Sinusitis
44
Investigations-Diagnosis of GORD
Young <40
PPI trial
Elderly/not received by medication
1. Endoscopy
2. Barium Swallow
3. 24hr pH monitoring
45
Lifestyle management for GORD
1.weight loss
2. smoking cessation
3. small regular meals
4. avoid meals before sleep
5. avoid:
fizzy drinks
alcohol
coffee
citrus fruits
spicy foods
46
Pharmacological management for GORD
Proton Pump Inhibitor
Antacids
H2 Receptor Blocker
47
Surgical Management for GORD
Only if medical management has failed
1. Nissen's operation
48
Complications of GORD
Oesophagitis -> metaplasia/dysplasia (Barrett's oesophagus) -> Adenoma
49
What is peptic ulcer disease
Defect which develops in the mucous membrane of the stomah or duodenum
50
What are peptic ulcers
Having one or more sores in the stomach (gastric ulcers), or in the duodenum (duodenal ulcers)
51
Stomach: Anatomy and Physiology
52
Risk Factors for peptic ulcer disease
H. pylori
NSAIDs
Smoking
>Age
History of peptic ulcer
Family History of peptic ulcer
Alcohol
Patient in ICU on mechanical ventilation or with coagulopathy
Chronic obstructive lung disease
Chronic renal insufficiency
53
Causes of peptic ulcer disease
1. H.Pylori Bacterial infection:
2. NSAIDs
3.Zollinger-Ellison Syndrome
54
Differential diagnosis for peptic ulcer disease
Oesophageal Cancer
Gastric Cancer
GORD/GERD
Gallstone Disease
Acute Pancreatitis
Coeliac Disease
Irritable Bowel Syndrome
Pericarditis
Lower lobe Pneumonia
Achalasia
55
Investigations peptic ulcer disease
H.pylori breath test or stool antigen test
Upper Gastro endoscopy
FBC
Fasting serum gastrin level – hypergastrinaemia in Zollinger-Ellison syndrome
Abdominal X-ray
Abdominal CT
56
Pathophysiology of peptic ulcer disease
57
Complication of peptic ulcer disease
58
Management peptic ulcer disease
59
Symptoms for peptic ulcer disease
60
What is appendicitis
Inflammed appendix
Affects 10% of population
61
Signs and symptoms of appendicitis
62
Differential Diagnosis of appendicitis
63
Investigations of appendicits
64
Management for Appendicitis
65
Complication for appendicitis
Perforation
Appendix mass
Appendix abscess
Portal Venous thrombosis
Liver Abscess
Bacteraemia - sepsis
Fistula
Pyelonephritis
PE/DVT following hospitalization
66
What is diverticular disease
67
What is diverticula/diverticulum?
abnormal sac-like protrusion from the wall of a hollow organ
68
Diverticulosis
Diverticulosis: presence of multiple diverticula, not symptomatic
69
Diverticulitis:
inflammation of diverticula
70
Diverticular Disease:
Complication of diverticulosis
71
What are a true diverticula?
Contain all layers of the colonic wall, often right-sided (i.e Merkel's Diverticulum)
72
False diverticulum
False (acquired) diverticuli: contain mucosa and submucosa, often left-sided (highest pressure)
73
Merkel's Diverticulum:
A true diverticulum, it is a reminant of proximal part of the yolk-stalk. May present with symptoms in a small majority of patients.
74
What are most colonic diverticula
False
75
Colon Anatomy and physiology
76
Risk Factor for diverticular disease
Age >50
Low fiber diet
Western diet
Obesity
NSAIDs
77
Signs and symptoms of diverticular disease
Clinical Presentation of Diverticular Disease, one of four: Asympstomatic (majority), Painful Diverticular Disease, Bleeding Diverticular Disease or Diverticulitis
78
Differential diagnosis for diverticular disease
Ectopic Pregnancy
Colorectal Cancer
Meckel’s diverticulum
Appendicitis
Inflammatory Bowel Disease
Mesenteric Ischaemia
Pyelonephritis
Urinary Tract infection
Pelvic Inflammatory Disease
Irritable Bowel Syndrome
79
Investigations for diverticular disease
Investigations depend on suspected complication and for diagnosis of diverticular disease. Diverticulosis may be an incidental finding on colonoscopy. Laboratory tests include FBC and CRP to check for bleeding and signs of inflammation/infection/malignancy. CT scan can help identify complications. A Chest x-ray can also be used which may reveal free air under the diaphragm (sign of perforation)
80
Pathophysiology of diverticular disease
81
Management for diverticular disease
82
Complications of diverticular disease
83
What is Merkels diverticulitis
Meckel’s diverticulum is the remnant of the vitellointestinal duct of the embryo. It lies on the antimesenteric border of the ileum and, as an approximation, occurs in 2% of the population, arises 55cm (2 feet) from the caecum, and averages 5 cm (2 inches) in length.
Remember Merkel's Diverticulum is a true diverticulum
84
Right Lower-quadrant pain common differential
85
Difference between diverticula vs diverticulosis, diverticultis
86
What is Helicobacter Pylori (H.Pylori)
Helicobacter pylori is a Gram-negative bacteria associated with a variety of gastrointestinal problems, principally peptic ulcer disease.
87
How is H.pylori infection spread?
88
Pathology of H.pylroi infection
89
Association of H.pylori
90
Consequence of H.pylori infection
91
Clinical presentation of H.pylori
92
Diagnosis of H.pylori infection
93
Treatment for H.pylori infection
Clarithromycin
Amoxycillin
PPI
94
What is intestinal obstruction
A condition that comes from either a mechanical blockage of the bowels or a functional issue (Pseudo) where the bowels no longer propel digested content properly through the G.I tract
95
Several categories have been used to classify differences in the various presentations of intestinal obstruction. Ask yourself:
Cardinal features of bowel obstruction present?
Degree of obstruction to flow (partial or complete)
Site of obstruction (small bowel or large bowel)
Mechanical obstruction or ileus?
Absence or presence of intestinal ischemia (simple or strangulated).
96
Cardinal features of bowel obstruction
Colicky abdominal pain
Distension
Absolute constipation/obstipation
Nausea and Vomiting
97
Pathophysiology of intestinal obstruction
Disruption of the normal flow of intestinal contents leading to proximal dilatation and distal decompression may take 12-24 h to decompress. Therefore passage of faeces and status may occur and the onset of obstruction. Bowel ischemia may occur if blood supply is strangulated or if the bowel wall in ammation leads to venous congestion, bowel wall oedema, and disruption of normal bowel absorptive function can lead to increased intraluminal uid and transudative fluid loss into the peritoneal cavity, electrolyte disturbances.
98
Is it a partial or complete bowel obstruction?
Partial Obstruction - still can pass gas +/- diarrhoea
Complete Obstruction - can not pass gas or poo
99
Is it obstruction of the small or large bowel?
100
Mechanical obstruction or ileus?
101
Radiography Bowel obstruction
102
Treatment for intestinal obstruction
103
Bowel obstruction table
104
What is diarrhoea
Loose stools 3< Times per day. 200g/24hr (Not commonly used)
105
Classifications of diarrhoea
106
How to distinguish between functional/organic diarrhoea
107
Small Bowel vs Large Bowel diarrhoea
108
What do you do once you have identified small bowel vs large bowel and Organic vs Functional diarrhoea
109
Types of diarrhoea based on pathophisiology
110
Gastric cancer
Gastric cancer accounts for around 2% of all cancer diagnoses in the developed world, making it much less common than colorectal and slightly less common than oesophageal cancer. It is a cancer of older people (half of patients are > 75 years) are has a male predominance (2:1).
111
Risk Factors of gastric cancer
1. Age - Median age 70
2. Sex - 2:1 Male: Female
3. Helicobacter Pylori infection- 60%
4. Smoking
5. Alcohol
6. Obesity
7. Diet - Pickled/cured/processed
8. Family History: 10%, 1% syndromic: hereditary diffuse gastric cancer
9. Pernicious anaemia
10. Gastritis
112
Most common sites of gastric cancer
113
Most common types of gastric cancer
95%: Adenocarcinoma
5%: Lymphoma, carcinoid, stromal tumours
114
Signs and symptoms of gastric cancer
abdominal pain
typically vague, epigastric pain
may present as dyspepsia
weight loss and anorexia
nausea and vomiting
dysphagia: particularly if the cancer arises in the proximal stomach
overt upper gastrointestinal bleeding is seen only in a minority of patients
if lymphatic spread:
left supraclavicular lymph node (Virchow's node)
periumbilical nodule (Sister Mary Joseph's node)
115
Investigations of gastric cancer
Endoscopy + Biopsy are the gold standard
CT imaging
Diagnosis: oesophagus-gastro-duodenoscopy with biopsy
signet ring cells may be seen in gastric cancer. They contain a large vacuole of mucin which displaces the nucleus to one side. Higher numbers of signet ring cells are associated with a worse prognosis
staging: CT.
116
How to identify different stages of gastric cancer
Stage 3 is most common
117
Survival of gastric cancer
West - 30% 5 Year survival
Japan/Korea - 45% 5 Year survival
*Stage 0/1 5 Year survival is ~90%
118
Treatment for gastric cancer
surgical options depend on the extent and side but include:
endoscopic mucosal resection
partial gastrectomy
total gastrectomy
chemotherapy
119
Colorectal cancer significance
Colon cancer is the second most commonly diagnosed cancer. 1/12 people will develop bowel cancer before the age of 85. However, there are Survival rates are increasing. Early bowel cancer is cured by surgery alone (screening is important!!). If untreated, or diagnosed when distance metastases are present, >98% pf patients die in <5 years.
Cancer of the colon and/or rectum usually at an advanced age. It is an adenoma and the primary site of metastasis is the liver.
120
Risk Factors for Large Bowel Cancer
Diet Poor in fiber
Age
Male
Smoking
Family History
Polyposis syndrome: FAP, HNPCC
History of polyps
History of colon cancer
Ulcerative colitis
Crohn's
121
Differential diagnosis of colorectal cancer
122
Clinical Presentation of Colorectal Cancer
Clinical Examination
Anaemia
Palpable mass on abdominal examination
Palpable nodular liver (metastasis)
Pigmentation (Peutz-Jeghers syndrome)
Discrete black brown lesion on lips
123
Pathology of Large Bowel Cancer
Pathology Colorectal cancer are primarily adenocarcinoma. Coloncancer can be polyploid, ulcerative, stenosing or infiltrative.
Remember Blumer’s shelf: A firm lump felt in the perirectal pouch on rectal examination. It is a rare physical finding in patients with metastatic adenocarcinoma from the GIT usually the stomach.
124
Investigations for large bowel cancer
Rectal examination
FBC
Faecal occult blood testing (not done if symptomatic)
Tumour markers
CT imaging
Colonoscopy
Investigation
Remember Screening for colon cancer is available: FOBT. Done yearly after 50yo (Australia).
Diagnosis Colon cancer is usually diagnosed with colonoscopy and biopsy (takes 1-2 days for pathology results)
125
Investigations for staging large bowel cancer
126
Treatment for Large bowel cancer
127
Complications and prognosis of colorectal cancer
128
What is oesophageal cancer, and what are the different types
Until recently, oesophageal cancer was most commonly due to squamous cell carcinoma, but the incidence of adenocarcinoma is rising rapidly. Adenocarcinoma is now the most common type of oesophageal cancer and is more likely to develop in patients with a history of gastro-oesophageal reflux disease (GORD) or Barrett's.
The majority of adenocarcinomas are located near the gastroesophageal junction, whereas squamous cell tumours are most commonly found in the upper two-thirds of the oesophagus.
129
Squamous cell carcinoma orginates
in squamous epithelium
130
Risk Factors of squamous cell carcinoma
Alcohol
Smoking
Hot fluids
131
Squamous cell carcinoma mutations occur in
132
Adenomcarcinoma
Originates in columnar glandular epthelium
Affects lower 1/3 of oesphagus
Consequence of GORD
133
Risk Factors of oesphageal cancer
134
Symptoms of oesophageal cancer
dysphagia: the most common presenting symptom
anorexia and weight loss
vomiting
other possible features include: odynophagia, hoarseness, melaena, cough
135
Diagnosis of oesophageal cancer
Upper GI endoscopy with biopsy is used for diagnosis
Endoscopic ultrasound is the preferred method for locoregional staging
CT scanning of the chest, abdomen and pelvis is used for initial staging
FDG-PET CT may detect occult metastases if metastases are not seen on the initial staging CT scans.
Laparoscopy is sometimes performed to detect occult peritoneal disease.
136
Treatment for oesophageal cancer
The operable disease is best managed by surgical resection - the most common procedure is an Ivor-Lewis type oesophagectomy.
The biggest surgical challenge is an anastomotic leak, with an intrathoracic anastomosis resulting in mediastinitis.
In addition to surgical resection, many patients will be treated with adjuvant chemotherapy.
137
What is Meckel's Diverticulum
Abnormal pouch on antimesenteric side of ileum
138
Complications of Meckel's Diverticulum
Diverticulitis
139
Signs and symptoms of Meckel's Diverticulum
Usually asymptomatic
Abdominal pain/distension, melena, vomiting, constipation
140
Diagnosis of Meckel's Diverticulum
141
Treatment for Meckel's Diverticulum
142
What is achalasia?
Rare disorder that results from progressive destruction of the ganglion cells in the myenteric plexus in the oesphogeal wall.
The destruction of these cell leads to the inability of the lower oesphageal sphincter to relax and leads to the loss of peristalsis of the distal oesphagus
143
What is the result of achalasia
Dilatation of the distal oesphagus
144
Clinical Presentation of achalasia
dysphagia of BOTH liquids and solids
typically variation in severity of symptoms
heartburn
regurgitation of food
may lead to cough, aspiration pneumonia etc
malignant change in small number of patients
145
What is a misdiagnosis for achalasia
Gastrooesophageal reflux
146
Aetiology of achalasia
1.Idiopathic
2.Viral/parasitic cause
3.Autoimmune
4.Neurodegenerative disorder
5.Trypanoma cruzi -> Chagos disease
6.Antibodies against:
-HSV
-HPV
-Rubeola
Remember : Both myenteric antibodies and HSV-1 infection were found in 100% of patients with achalasia
147
Investigations for achalasia
1.oesophageal manometry
excessive LOS tone which doesn't relax on swallowing
considered the most important diagnostic test
2.barium swallow
shows grossly expanded oesophagus, fluid level
'bird's beak' appearance
3.chest x-ray
wide mediastinum
fluid level
148
Pseudo achalasia
Due to an obstructed distal oesophagus from causes other than destruction of the myenteric plexus at the distal oesophagus.
Due to obstruction by a malignant mass, scleroderma, strictures, toxins, reflux malignancies.
Also due to lymphoma, oesophageal carcinoma, gastric carcinoma
Investigations include:
CT
Endoscopic ultrasound
149
Treatment for achalasia
1.pneumatic (balloon) dilation is increasingly the preferred first-line option
less invasive and quicker recovery time than surgery
patients should be a low surgical risk as surgery may be required if complications occur
2.surgical intervention with a Heller cardiomyotomy should be considered if recurrent or persistent symptoms
3.intra-sphincteric injection of botulinum toxin is sometimes used in patients who are a high surgical risk
4.drug therapy (e.g. nitrates, calcium channel blockers) has a role but is limited by side-effects
150
What is intestinal ischaemia
group of conditions where there is inadequate blood flow to large or small intestine
151
Classifications of intestinal ischaemia
Ischaemic collitus: affects large intestine
Acute/Chronic mesenteric ischaemia: Affects small intestine
152
Areas most prone to intestinal ischaemia
Splenic Flexture (Griffiths point)
Rectosigmoid junction (Sudeck's point)
153
Causes of intestinal ischaemia
Acute mesenteric ischemia can result from occlusion of a mesenteric vessel arising from an embolus, which may emanate from an atheroma of the aorta or cardiac mural thrombus, or primary thrombosis of a mesenteric vessel, usually at a site of atherosclerotic stenosis. Embolic occlusion is more common in the superior mesenteric artery than the celiac or inferior mesenteric artery, presumably because of the less acute angle of the superior mesenteric artery of the abdominal aorta.
Remember: AF with abdominal pain think mesenteric ischaemia.
154
Signs and symtoms of intestinal ischaemia
Depends on severity and time of occlusion
1. Abdominal pain (95%)
-Disproportionate to exam
-Widespread as ischaemia progresses
2. Nausea/Vomiting
3. Diarrhoea (Constipation is rare)
4. Rectal Bleeding
Can be sequence to the symptoms (see pic)
Chronic symptoms
-Slower onset
-Pain 30min after eating: Fear of eating & Weight loss
155
Risk Factors for intestinal ischaemia
1.Atherosclerosis
2.Age
3.smoking
4.atrial fibrillation
5.hypercoagulability
6.chronic organ failure
156
Diagnosis for intestinal ischaemia
1.HIstory + Physical Exam
2.Lab markers: Leukocytosis, Raised lactate
3.imaging:
-CT (intramural gas, portal venous gass, free air)
-Angiogrpahy
-X-Ray
-Endoscopy
157
Treatment for intestinal ischaemia:
158
What is pseudomembranous Colitis
Swelling or Inflammation of the large intestine due to disturbance of normal bacterial flora of the colon and an overgrowth of Clostridium difficile (C.diff) bacteria
159
What is pseudomembranous Colitis a common cause of
Diarrhoea after antibiotic use
160
Pseudomembranous colitis infection causes
Antibiotics: ampicillin, cindamycin, fluoroquinolone, cephalosporins
Healthcare workers: as infection is spread by faeces
161
What is C.difficle bacteria
Spore forming, anaerobic, gram positive bacilus.
Pathogenic C.difficile strains produce multiple toxins e.g entertoxins and cytotoxins both of which produce diarrhoea and inflammation in infected patients
162
Pathophysiology of C.difficile
anaerobic gram-positive, spore-forming, toxin-producing bacillus
transmission: via the faecal-oral route by ingestion of spores
releases two exotoxins (toxin A and toxin B) that act on intestinal epithelial cells and inflammatory cells resulting in colitis
163
Symptoms of pseudomembranous colitis
diarrhoea
abdominal pain
a raised white blood cell count (WCC) is characteristic
if severe toxic megacolon may develop
164
Investigations for Pseudomembranous colitis
165
Management of pseudomembranous colitis
166
What is an anal fissure
A superficial linear tear in the anoderm distal to the pectinate line (dentate line) commonly caused by passage of hard stool
167
Clinical Presentation of an anal fissure
168
Risk Factors for anal fissure
Low intake of dietary fiber
169
Differential diagnosis for an anal fissure
170
Pathophysiology of an anal fissure
Anal fissures usually occur in the anterior or posterior parts of the anus and underlies the internal anal sphincter. Muscles spasm are due to contraction of the internal anal sphincter causing ischaemia → pain
171
Complications for an anal fissure
Faecal incontinence due to sphincterotomy
172
Signs and symptoms of an anal fissure
173
Diagnosis of an anal fissure
History, examination of anal region/rectum
174
Treatment of an anal fissure
175
What is an anal fistula
abnormal connection of the anorectal epithelial surface to the perineal or vaginal skin.
176
Types of anal fistula
177
Signs & Symptoms of anal fistula
178
Differential diagnosis of an anal fistula
Anal Abscess
Anal fissure
Anal ulcer or sores (secondary to another disease or infection)
Crohn disease
179
Diagnosis of anal fistula
180
Pathophysiology of an anal fistula
181
Treatment for anal fistula
182
Complication of an anal fistula
Recurrence
Faecal incontinence from surgery
183
What is a haemorrhoid
collections of submucosal, fibrovascular, arteriovenous sinusoids that are part of the normal anorectum
184
Types of haemorrhoid
185
Risk factors for haemorrhoid
Constipation, a low fibre diet, a high Body Mass Index, pregnancy, and a sedentary lifestyle
186
Complications with haemorrhoid
Anaemia
Pain
Heavy bleeding
Chronic unremitting prolapse of mucosal tissue
Strangulation
Ulceration
Thrombosis
187
Signs and symptoms of a haemorrhoid
188
Diagnosis of a haemorrhoid
189
Treatment of haemorrhoids
190
What is an anorectal abscess
Collection of pus in the anal/rectal region
Usually an invasion of normal rectal flora
191
Signs and symtpoms of an anorectal abscess
192
Investigations for anorectal abscess
193
Diagnosis of anorectal abscess
194
Pathophisiology of anorectal abscess
Usually originates from an infected anal crypt gland
1.Infection of crypts
2.spread through anal duct and gland
3.Infection spreads:
-Submucosal
-Subcutaneous
-Transsphincter
Surrounding tissue
*the abscess collects in which ever anatomical space between the gland terminates or whichever path of least resistance is*
195
Differential diagnosis of an anorectal abscess
196
Management of an anorectal abscess
197
Complications of an anal abscess
198
What is pilonidal sinus
Obstruction of natural hair follicles above the anus
199
Clinical Presentation of pilonidal sinus
200
Pilonidal sinus pathophisiology
201
Aetiology of pilonidal sinus
Congenital
202
Diagnosis of pilonidal sinus
Diagnosis of observation
203
Treatment for a pilonidal sinus
204
Complication of pilonidal sinus
Infection
205
Venn Diagram comparing IBD
206
a 20-year-old woman presents with recurrent episodes of abdominal pain associated with bloating. The pain is relieved on defecation. She normal passes 3 loose stools with mucous in the mornings
IBS
207
Table comparing diff between IBD
208
Diverticulitis classical presentation is:
left iliac fossa pain and tenderness
anorexia, nausea and vomiting
diarrhoea
features of infection (pyrexia, raised WBC and CRP)
209
Mesenteric ischaemia: Key question features (lower gastrointestinal disorders)
abdominal pain, rectal bleeding, metabolic acidosis
210
Stereotypical histories Crohn's disease
a 20-year-old woman presents with diarrhoea. Over the past few months she has lost weight and suffered with recurrent abdominal pain and mouth ulcers
211
An elderly man complains of dysphagia, halitosis, regurgitation and cough is a stereotypical history for:
Pharyngeal pouch
212
Which antibody is most associated with ulcerative colitis?
P-ANCA
213
Palpation in LLQ causes pain in RLQ
acute appendicitis
214
What type of cancer is most associated with Helicobacter pylori?
B cell lymphoma of MALT tissue
215
What type of cancer is most associated with Helicobacter pylori?
B cell lymphoma of MALT tissue
216
Strong family history of colorectal and endometrial cancer in a question is most likely to indicate:
Hereditary non-polyposis colorectal carcinoma
217
Which one of the following tumour markers is most associated with colorectal cancer?
Carcinoembryonic antigen
218
A 17-year-old boy is admitted to hospital with suspected appendicitis. He is found to be maximally tender at McBurney's point. Where is this located?
McBurney's point is found 2/3rds of the way along an imaginary line that runs from the umbilicus to the anterior superior iliac spine on the right-hand side. The other options do not locate this anatomical site.
219
Pathophysiology of a Mallory-Weiss tear
Severe vomiting → painful mucosal lacerations at the gastroesophageal junction resulting in haematemesis. Common in alcoholics
220
Mallory Weiss tear
221
Oesphogeal Varices
Definition
Epidemiology
Aetiology
Risk Factors
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Pathophysiology of oesphogeal varices
@ oesophagogastric junction, rectum and anterior wall - portal and systemic
capillary beds meet
If portal hypertension, then blood takes path of least resistance i.e. through
systemic circulation - bypasses liver and into heart
∴ causes detoxification and nutrition issues
As portal pressure ↑, can cause oesophagogastric varices to form and rupture
∴ massive haemorrhage
—
As these vessels are not thin, not meant to transport higher pressure blood
∴ rupture
(∴ haematemesis)
(if blood digested = melaena)
223
Clinical Manifestations and Investigations for oesphageal varices
224
Differential diagnosis for oesphageal varices
Gastroenteritis
Peptic ulcer
Cancer
Mallory-Weiss tear
225
Management for oesphageal varices
Blood transfusion if anaemic
Beta blocker to reduce CO ∴ ↓ portal pressure
Nitrate to cause vasodilation ∴ ↓ portal pressure
Terlipressin (ADH analogue) ∴ ↓ portal pressure
Trans-jugular intrahepatic portoclaval shunt (TIPS)
Correct clotting abnormalities w/ vit K and platelet transfusion
Variceal banding - band put around varice using endoscopy
