GI Flashcards
(271 cards)
1
Q
What is an anal fissure?
A
Painful tear in sensitive skin-lined lower anal canal, distal to dentate line resulting in pain on defecation
2
Q
Which type of anal fissure is most common?
A
90% posterior
Anterior tend to be in childbirth
Women most affected
Isolated primary problem in young middle aged adults or can occur when associated with Crohn’s or ulcerative colitis
3
Q
What are the main causes of anal fissures?
A
Hard faeces
Spasm constricting inferior rectal artery resulting in ischaemia making healing difficult and perpetuating problem
Rare causes - syphilis, herpes, trauma, Crohn’s, anal cancer
4
Q
How do anal fissures present?
A
Extreme pain on defecation
Bleeding
5
Q
How are anal fissures diagnosed?
A
Can usually be made on history
Confirmed on perianal inspection
Rectal examination often not possible due to pain and sphincter spasm
6
Q
How are anal fissures treated?
A
Increased dietary fibre and fluids to make stools softer
Lidocaine ointment and GTN ointment or topical diltiazem
Botulinum toxin injection
Surgery if medication fails
7
Q
What is an anal fistula?
A
An abnormal connection between epithelised surface of anal canal and skin - track communicates between skin and anal canal/rectum
Blockage of deep intramuscular gland ducts thought to predispose to formation of abscesses with discharge to form fistula
8
Q
What are the main causes of anal fistulas?
A
Perianal sepsis Abscesses Crohn's TB Diverticular disease Rectal carcinoma
9
Q
How do anal fistulas present?
A
Pain
Discharge - bloody/mucus
Pruritus ani (itchy bottom)
Systemic abscess if becomes infected
10
Q
How are anal fistulas diagnosed?
A
MRI to exclude sepsis and detect associated conditions
Endoanal ultrasound - determines track location and underlying causes
11
Q
How are anal fistulas treated?
A
Surgery - fistulotomy and excision
Drain abscess with antibiotics if infected
12
Q
How common is appendicitis?
A
Most common surgical emergency
More common in men
Can occur at any age but highest incidence in 10-20 yrs
Rare before aged 2 as appendix cone shaped with larger lumen
13
Q
What can cause appendicitis?
A
Faecolith (stone made of faeces)
Lymphoid hyperplasia
Filarial worms
14
Q
What is the pathology of appendicitis?
A
Occurs when lumen of appendix becomes obstructed by one of the causes resulting in invasion of gut organisms into appendix wall
Leads to oedema, ischaemia, necrosis, and perforation as well as inflammation
If appendix ruptures then infected and faecal matter will enter peritoneum leading to life threatening peritonitis
15
Q
How does appendicitis present?
A
Pain in umbilical region that migrates to RIF, specifically McBurney's point after a few hours Colicky pain Anorexia Nausea, vomiting, occasionally diarrhoea Constipation Examination of abdomen = tenderness in RIF with guarding due to localised peritonitis Tender mass in RIF Pyrexic
16
Q
Name 5 differential diagnoses for appendicitis
A
Acute terminal ileitis due to Crohn's Ectopic pregnancy UTI Diverticulitis Perforated ulcer Food poisoning
17
Q
How is appendicitis diagnosed?
A
Bloods - raised WCC with neutrophil leucocytosis, elevated CRP with ESR USS - detects inflamed appendix CT - high sensitive and specific Pregnancy test to exclude Urinalysis to exclude UTI
18
Q
How is appendicitis treated?
A
Surgery - appendicectomy laproscopically
IV antibiotics pre-op to reduce wound infections
If appendix mass present - IV fluids and antibiotics until mass disappears over a few weeks
19
Q
What are the main complications of appendicitis?
A
Perforation - commoner with faecolith
Appendix mass - when inflamed appendix becomes covered in omentum foriming a mass - USS/CT, treat with antibiotics then surgery to remove appendix later to prevent further events
Appendix abscess - result if appendix mass fails to resolve but instead enlarged and patient gets more unwell, treat by draining appendix, antibiotics
20
Q
What is ischaemic colitis?
A
AKA chronic colonic ischaemia
Low flow to IMA territory, ranging from mild ischaemia to gangrenous colitis
21
Q
What does AF with abdominal pain suggest?
A
Mesenteric ischaemia
22
Q
Which areas of the bowel are most at risk of ischaemia?
A
Watershed areas in splenic flexure and caecum are most susceptible to ischaemia
23
Q
How common is acute mesenteric ischaemia?
A
Usually in those over 50
Almost always involves small bowel
24
Q
How common is ischaemic colitis?
A
Usually older age group
Related to underlying atherosclerosis and vessel occlusion
In young - associated with contraceptive pill use - thrombophilia and vasculitis
25
What are the main types of bowel ischaemia?
Acute mesenteric ischaemia
Chronic mesenteric ischaemia
Ischaemic colitis
26
What are the causes of acute mesenteric ischaemia?
Superior mesenteric artery thrombosis
Superior mesenteric embolism due to AF
Mesenteric vein thrombosis
Non-occlusive disease - low flow states, poor CO
27
What are the causes of ischaemic colitis?
```
Thrombosis
Emboli
Decreased CO and arrhythmias
Drugs - oestrogen, antihypertensives, vasopressin
Surgery - cardiac bypass, aortic dissection and repair, aortoiliac reconstruction
Vasculitis
Coagulation disorders
Idiopathic
```
28
What can increase your risk of getting ischaemic colitis?
Contraceptive pill
Niorandil drug
Thrombophilia
Vasculitis
29
What occurs in ischaemic colitis?
Occlusion of branch of SMA or IMA often in older age
30
How does acute mesenteric ischaemia present?
Acute severe abdominal pain - constant, central or around RIF
No abdominal signs
Rapid hypovolaemia resulting in shock - pale skin, weak rapid pulse, reduced urine output, confusion
31
How does ischaemic colitis present?
Sudden onset lower left side abdominal pain
Passage of bright red blood with/without diarrhoea
Signs of shock and evidence of underlying CVS disease
32
What could be a differential diagnosis of ischaemic colitis?
Other causes of acute colitis eg IBD
33
How is acute mesenteric ischaemia diagnosed?
Bloods - raised Hb due to plasma loss, raised WCC, persistent metabolic acidosis
Abdo x-ray - rule out other pathology, gasless abdomen
Laparotomy - to make diagnosis, may see necrotic bowel if not treated quickly
CT/MRI
34
How is ischaemic colitis diagnosed?
Urgent CT to exclude perforation
Flexible sigmoidoscopy - biopsy shows epithelial cell apoptosis
Colonoscopy and biopsy
Barium enema
35
How is acute mesenteric ischaemia treated?
Fluid resuscitation
Antibiotics
IV heparin to reduce clotting
Surgery to remove death bowel
36
How is ischaemic colitis treated?
Fluid replacement
Antibiotics
Most recover but strictures common
37
What are the potential complications of acute mesenteric ischaemia?
Septic peritonitis
Systemic inflammatory response syndrome progressive to multi-organ dysfunction syndrome, mediated by bacterial translocation across dying gut wall
38
What are the potential complications of ischaemic colitis?
Gangrenous ischaemic colitis - presents with peritonitis and hypovolaemic shock
Requires prompt resucitation followed by surgical resection of affected bowel and stoma formation
High mortality
39
What is coeliac disease?
Condition where there is inflammation of mucosa of upper small bowel that improves when gluten is withdrawn from diet and relapses when gluten is reintroduced
T cell mediated autoimmune disease of small bowel in which prolamin intolerance causes villous atrophy and malabsorption
40
What are prolamins?
Gliandin in wheat, hordeins in barley and secalins in rye
| Component of gluten protein
41
How common is coeliac disease?
1% of population affected
Occurs at any age but peaks in infancy and 50-60 years
Affects males and females equally
10% risk in 1st degree relatives with 30% risk in siblings
42
What factors can increase your risk of getting coeliac disease?
```
Other autoimmune diseases - T1DM, thyroid disease, Sjorgrens
IgA deficiency
Breast feeding
Age of introduction to gluten in diet
Rotavirus infection in infancy
Viral infections
Dysbiosis
```
43
What is the pathology of coeliac disease?
```
Prolamin a-gliandin is toxic and resistant to digestion by pepsin and chymotrypsin due to high glutamine and proline content and remain in intestinal lumen triggering immune response
Gliandin peptides pass through epithelium and deaminated by tissue transglutaminase increased immunogenicity
Gliandin peptides bind to APCs which interact with CD4+ T cells in lamina propria via HLA class II molecultes DQ2/DQ8
HLA class II molecules activate gluten sensitive T cells = pro-inflammatory cytokines initiating inflammatory cascade
Cascade releases metaloproteinkinases and other mediators which contribute to villous atrophy, crypt hyperplasia and intraepithelial lymphocytes typical of disease that result in malabsorption
```
44
What can mucosal damage lead to?
Malabsorption
Mucosa of proximal small bowel predominantly affected meaning that B12, folate and iron cannot be absorbed resulting in anaemia
Mucosal damage increases in severity towards ileum as gluten digested into small non-toxic fragments
45
How does coeliac disease present?
```
1/3 asymptomatic and only detected on routine bloods
Stinking stools/fatty stools
Diarrhoea
Abdominal pain
Bloating
Nausea and vomiting
Angular stomatitis
Weight loss
Fatigue
Anaemia
Osteomalacia - lack of phosphate, calcium and Vit D
Dermatitis hepetiformis
```
46
How is coeliac disease diagnosed?
Maintain gluten for at least 6 weeks before testing to get true results
FBC - low Hb, low B12, low ferritin
Duodenal biopsy - see villous atrophy, crypt hyperplasia and increased intraepithelial WCC
Serum antibody testing - IgA inceased (endomysial and tissue transglutaminanse antibodies)
47
How is coeliac disease treated?
Lifelong gluten free diet
Correction of vitamin and mineral deficiencies
DEXA scan to monitor osteoporotic risk
48
What are the complications of coeliac disease?
Non-responsive coeliac disease (do not improve on strict diet)
Anaemia
Secondary lactose intolerance
T cell lymphoma
Increased risk of malignancy (gastric, oesophageal, bladder, breast and brain) due to increased cell turnover
Osteoporosis
49
What is a colonic polyp?
Abnormal growth of tissue projecting from colonic muscosa
Range from a few millimetres to severe centimeters and are single or multiple
Adenomas - type of polyp, precursor lesions in most cases of colon cancer - benign, dysplastic tumour of columnar cells or glandular tissue
Most polyps asymptomatic and found by chance
50
How common are polyps?
Adenoma presence increases with age and rare before 30
Polyps removed at colonoscopy to reduce development into cancer risk
Polyps in rectum or sigmoid colon present with bleeding
51
How common is colorectal carcinoma?
```
3rd most common cancer worldwide
Usually adenocarcinoma
Majority occur in distal colon
Majority of presentations over 60
More common in men
More common in Western countries
```
52
What are the two types of inherited polyps?
Familial adenomatous polyps - autosomal dominant condtion arising from mutation in APC gene, characterised by presence of hundreds to thousands of colorectal and duodenal adenomas, develop adenomas at 16 and cancer at 39
Lynch syndrome - polyps form in colon and may rapidly progress to colon cancer, autosomal dominant condition caused by mutation in one of DNA mismatch repair genes, genes responsible for maintaining stability of DNA during replication, increased risk of DNA damage in replication and thus colorectal carcinoma development
53
What can increase your risk of developing colorectal carcinoma?
```
Increasing age
Low fibre diet
Saturated animal fat and red meat consumption
Sugar consumption
Alcohol and smoking
Colorectal polyps
Obestiy
Adenomas
UC
FHx
Genetic predisposition - FAP, lynch syndrome
```
54
What can reduce your risk of developing colorectal carcinoma?
```
Vegetables
Garlic
Milk
Exercise
Low-dose aspirin
```
55
What is the pathology of colorectal carcinoma?
Normal epithelium - adenocarcinoma - colorectal adenocarcinoma
Polypoid mass with ulceration
Spread by direct infiltration through bowel wall then spread to lymphatic and blood vessels and metastasis to liver and lung
56
How does right sided colorectal carcinoma present?
```
Usually asymptomatic until present with iron deficiency anaemia due to bleeding
Mass
Weight loss
Low Hb
Abdominal pain
```
57
How does left sided colorectal carcinoma present?
```
Change of bowel habit with blood and mucus in stools
Diarrhoea
Alternation constipation and diarrhoea
Thin/altered stools
Blood in stools
```
58
How does rectal carcinoma present?
Rectal bleeding and mucus
| When cancer grows - thinner stools and tenesmus
59
What is the emergency presentation of colorectal carcinoma?
Obstruction - absolute constipation, colicky abdominal pain, abdominal distension, vomiting
60
What could be a differential diagnosis for colorectal adenocarcinoma?
Anorectal pathology - haemorrhoids, anal fissure, anal prolapse
Colonic pathology - diverticular disease, IBD, ischaemic colitis
Small intestine and stomach pathology - massive upper GI bleed, Meckle's diverticulum
61
How is colorectal adenocarcinoma diagnosed?
```
Faecal occult blood
Tumour markers
Colonscopy - biopsy and removal of polyps
Double contract barium enema
CT colonoscopy
MRI to determine spread
```
62
How is colorectal carcinoma classified?
Dukes classification
A - limited to muscularis muscosa
B - extension through muscularis muscosa
C - involvement of regional lymph nodes
D - distant metastases
TMN system
T - primary tumour, sufficed by number denoting tumour size
N - lymph node status, number denotes number of lymph nodes/groups of lymph nodes containing metastases
M - anatomical extent of distant metastases
63
How is colorectal adenocarcinoma treated?
Surgery - only chance of cure, only indicated if no metastasis
Laproscopic
Endoscopic stenting - malignant obstruction, reduces need for colostomy
Radio/chemotherapy
Treated differentially - polyp cancers/rectal cancers
64
What is Crohn's disease?
Chronic inflammatory bowel disease characterised by transmural (deep in mucosa) granulomatous inflammation affecting any part of gut from mouth to anus
Can be unaffected bowel between areas of active disease called skip lesions
65
How common is Crohn's disease?
```
Highest incidence and prevalence in Northern Europe, UK, and North America
Lower incidence than UC per year
Prevalence less if Asian
Affects women more than men
Unknown cause
Smoking increases risk by 3-4x
1 in 5 patients have first-degree relative with disease
Presentation mostly at 20-40 years
```
66
What can increase your risk of Crohn's?
Genetic associations stronger than UC - mutations on NOD2 gene on chromosome 16 increases risk
Smoking NSAIDs may exacerbate disease
FHx
Chronic stress and depression triggers flares
Good hygiene - those in poor hygiene families have lower risk of developing CD
Appendicectomy may increase risk of CD development
67
What does Crohn's disease look like marcroscopically?
Transmural granulomatous inflammation affecting any part of gut from mouth to anus
Not continuous - skip lesions
Involved bowel usually thickened and often narrowed
Cobblestone appearance due to ulcers and fissures in muscosa
Affects any part of GI tract
68
What does Crohn's look like microscopically?
Inflammation extends through all layers (transmural) of bowel
Increase in chronic inflammatory cells and there s lymphoid hyperpalsia
Granulomas present - non-caseating epithelioid cell aggregates with Langerhan's giant cells
Goblet cells present
Less crypt abscesses' than in UC
69
How does Crohn's disease present?
```
Diarrhoea with urgency (need to go 5-6 times in 45 mins)
Bleeding
Pain due to deification
Abdominal pain
Weight loss
Malaise
Lethargy
Anorexia
Abdominal tenderness/mass
Perianal abscess
Anal strictures
Extraintestinal signs - aphthous ulcerations, clubbing, skin, joint, eye problems
```
70
What could be a differential diagnosis for Crohn's?
Alternative causes of diarrhoea
| Chronic diarrhoea
71
How is Crohn's diagnosed?
Examination - tenderness of RIF, anal exam
Bloods - anaemia due to malabsorption (iron and folate deficiency), B12 anaemia unusual, raised ESR, CRP, WCC and platelets, hypoalbuminaemia in severe disease, liver biochemistry may be abnormal, negative pANCA
Stool sample to exclude infectious causes
Faecal calprotectin - indicated IBD
Colonscopy - biopsy sses skip lesions and granulomatous transmural inflammation
Upper GI endoscopy - exclude oesophageal and gastroduodenal disease
72
How is Crohn's treated?
Smoking cessation
Anaemia treated with replacement
Mild attacks - controlled release corticosteroids
Moderate to severe - glucocorticoids
Severe - IV hydrocortisone, treat rectal disease (hydrocotisone per rectum), antibiotics (IV metronidazole for perianal disease and abscesses), if improvement transfer to oral prednisolone
If not improvement switch to anti-TNF antibodies
Maintain remission - azathioprine, methotrexate, anti-TNF antibodies
Surgery - avoided and only minimal resection, indicated in medial therapy failure, failure to thrive and perianal sepsis, temporary ileostomy
73
What are the potential complications of Crohn's disease?
```
Perforation and bleeding
Fistula formation
Anal - skin tags, fissure, fistula
Malabsorption
Small bowel obstruction as grossly dilated
Toxic dilatation of colon
Colorectal cancer
Venous thrombosis
Amyloidosis
```
74
What is diarrhoea?
Abnormal passage of loose of liquid stool more than 3 times daily
75
What are the main differences between acute and chronic diarrhoea?
Acute - lasts less than 2 weeks, usually due to infection eg Travellers diarrhoea
Chronic - lasts more than 2 weeks, organic causes, anatomical changes, must be differentiated from functional causes - no physical cause for symptoms
76
What three things can cause decreased stool consistency?
Water
Fat
Inflammtory discharge
77
What are the different types of water caused diarrhoea?
Osmotic - large quantities of non-absorbed hypertonic substances in bowel draw fluid into intestine, stops when patient stops eating or malabsorptive state discontinued - causes ingestion of non-absorbable substances, generalised malabsorption, specific malabsorptive defect
Secretory - mircoscopic colitis, active intestingla secretion of fluids and electrolytes as well as decreased absorption, continues even when patient fasts - causes enterotoxins (E coli), bile salts in colon following ileal disease, resection or idiopathic bile malabsorption, fatty acids in colon following ileal resection
78
What does steatorrhoea look like?
Increased gas, offensive smell, floating hard to flush stools
Causes - giardiasis and coeliac disease
79
Why does inflammatory discharge produce decreased stool consistency?
Damage to intestinal mucosal cells lead to fluid loss and blood and defective absorption of fluid and electrolytes
Causes - infective (shigella or salmonella) or inflammatory eg UC or Crohn's
80
How does diarrhoea present?
Sudden onset of bowel frequency associated with crampy abdominal pains and a fever will point to infective cause
Bowel frequency with loose, blood stained stools will point to an inflammatory cause
Passage of pale, offensive stools that float often accompanied by a loss of appetite and weight to steatorrhoea
81
How is acute diarrhoea diagnosed?
Flexible sigmoidoscopy with colonic biopsy performed if symptoms persist and no diagnosis made
82
How is chronic diarrhoea diagnosed?
Faecal markers of intestinal inflammation used to differentiate functional disorders from organic disease
83
How is acute diarrhoea treated?
Treatment symptomatic to maintain hydration with anti-diarrhoeal agents (loperamide hydrochloride) for short term relief and antibiotics for specific indications
84
What is diverticulitis?
Outpouching of gut wall, usually at sites of entry of perforating arteries
Diverticulosis - presence of diverticula
Diverticular disease - diverticula symptomatic
Diverticulitis - inflammation of diverticulum
85
How common is diverticulitis?
Frequently found in colon
50% patients over age 50
Most frequent in sigmoid colon, can present throughout whole colon
Diverticulum can be acquired or congenital and may occur elswehere but most important are acquired colonic diverticula
Rare in young
95% asymptomatic
86
What can cause diverticulitis?
Low fibre diet - commonly eaten in developing countries, rare in rural Africa
Obesity
Smoking
NSAIDs
87
What can increase your risk of getting diverticulitis?
Low fibre diet
| Over the age of 50
88
How do diverticula form?
Form at gap in wall of gut where blood vessels penetrate
In low fibre diet, colon must push harder to move things along (fibre helps gut motility) so pressure increases
Pressure increase results in pouches of mucosa being extruded through muscular wall through weakened areas near blood vessels leading to diverticula formation
Thickening of muscle layer
89
When does acute diverticulitis occur?
Occurs when faeces obstruct the neck of diverticulum, causing stagnation and allowing bacteria to multiply and produce inflammation
Can lead to bowel perforation, abscess formation, fistulae into adjacent organs, haemorrhage and generalised acute peritonitis and possibly death
90
How does diverticular disease present?
In 95% of cases, asymptomatic and detected incidentally on colonoscopy or barium enema examination
Intermittent LIF pain
Erratic bowel habit
Severe pain and constipation due to luminal narrowing
91
How does acute diverticulitis present?
Most commonly affects diverticula in sigmoid colon
Severe pain in LIF
Fever and constipation
Symptoms and signs similar to appendicitis but located on L side
On examination
- Febrile, tachycardia, abdominal examination (tenderness, guarding, rigidity on left side of abdomen, palpable tender mass sometimes felt in LIF)
92
How is diverticular disease diagnosed?
Colonscopy
93
How is acute diverticulitis diagnosed?
Bloods - polymorphonuclear leucocytosis (increased), ESR and CRP raised
CT colongraphy - will show colonic wall thickening and diverticucla, pericolic collections and abscesses, diagnostic
Abdominal x-ray - identify obstruction or free air
Barium enema
NO SIGMOIDOSCOPY OR COLONOSCOPY DURING ACUTE ATTACK
94
How is diverticular disease treated?
Well balanced high fibre diet with smooth muscle relaxants
95
How is acute diverticulitis treated?
Mild attacks - oral antibiotics
Those with signs of systemic upset and significant abdominal pain required bowel reset, IV fluids and IV antibiotics
Surgical resection occasionally
96
What are the complications of diverticultitis?
Perforation - paracolic or pelvic abscess or generalised peritonitis
Fistula formation into bladder resulting in dysuria or pneumaturia, vagina resulting in discharge
Bleeding
Mucosal inflammation - occurs in areas of diverticula, giving appearance of Crohn's on endoscopy
97
What is Meckle's diverticulum?
Most common congenital abnormalitiy of GI tract
| Diverticulum projects from wall of ileum
98
How common is Meckle's diverticulum?
Affects 2-3% population
99
What occurs in Meckle's diverticulum?
In 50% cases, distal ileum contains gastric mucosa that secretes HCl meaning peptic ulcers can occur which may bleed or perforated
Usually asymptomatic
Acute inflammation occurs and is indistinguishable clinically from acute appendicitis
100
How is Meckle's diverticulum treated?
Surgical removal of diverticula, often laparoscopically
101
What is the most common type of gastric cancer?
Adenocarcinoma
102
How common are gastric tumours?
4th most common cancer worldwide
More common in men
Incidence increases with age - peak at 50-70
Rare under 30
Highest incidence in Eastern Asia, Eastern Europe and South America
103
What are the two types of gastric tumours?
Intestinal (type 1) - well formed, differentiated glandular structures, tumours polypoid or ulceration lesions with heaped up, rolled edges, intestinal metaplasia seen in surrounding mucosa, often with H pylori, more likely to involve distal stomach and occur in patients with atrophic gastritis, strong environmental association
Diffuse (type 2) - poorly cohesive undifferentiated cells, tend to infitrate gastric wall, can involve any part of stomach, especially cardia, worse prognosis than intestinal
104
What can cause gastric cancer?
Smoking
H pylori infection - chronic gastritis - atrophic gastritis and pre-malignant intestinal metaplasia
Dietary factors - high salt and nitrates increase risk, non-starchy vegetables, fruit, garlic and low salt decrease risk
Loss of p53 (tumour supressor gene) and APC genes
First degree relative with gastric tumour - CDH1 gene
Pernicious anaemia - increases risk due to accompanying atrophic gastritis
105
What can increase your risk of getting gastric tumours?
First degree relative with gastric cancer
Smoking
High salt and nitrates
106
How does H pylori cause gastric cancer?
```
Acute gastritis
Chronic active gastritis
Atrophic gastritis
Intestinal metaplasia
Dysplasia
Advanced gastric cancer
```
107
How does gastric cancer present?
Most present with advanced disease
Epigastric pain indistinguishable from peptic ulcer disease, pain constant and severe
Nausea, anorexia
Weight loss
Vomiting frequent and can be severe if tumour encroaches on pylorus
Dysphagia is in fundus
Anaemia from occult blood loss
Liver metastasis resulting in jaundice
Metastases in bone, brain and lung
Palpable lymph node in supraclavicular fossa
108
How is gastric cancer diagnosed?
Gastroscopy and biopsy to histologyically confirm adenocarcinoma
Endoscopic ultrasound to evaluate depth of invasion
CT/MRI for staging
PET scan to identify metastases
109
How is gastric cancer treated?
Nutritional support
| Surgery and combination chemo - epirubiin, cisplatin and 5-glucorouracil and post-op radiotherapy
110
What is gastritis?
Inflammation asscoiated with mucosal injury
Gastropathy indicates epithelial cell damage and regeneration without inflammation - commonest cause is mucosal damage associated with aspirin/NSAIDs
111
What can cause gastritis?
H pylori infection
Autoimmune gastritis
Viruses - cytomegalovirus and herpes simplex
Duodenogastric reflux - bile salts enter stomach and damage mucin protection resulting in gastritis
Specific causes - Crohn's
Mucosal ischaemia - reduced blood supply to mucosal cells can mean less mucin produced so acid can induce gastritis
Increased acid - can overwhelm mucin resulting in gastritis, stress can increase acid production
Aspirin and NSAIDs eg naproxen
Alcohol
112
How does H pylori cause gastritis?
Causes severe inflammatory response
Gastric mucus degradation and increased mucosal permeability, directly cytotoxic to gastric epithelium (increased urease that converts urea to ammonia and CO2 which is toxic as ammonia and H+ form ammonium which is toxic to gastric mucosa resulting in less mucous produced
113
How does autoimmune gastritis work?
Affects fundus and body stomach leading to atrophic gastritis and loss of parietal cells tith intrinsic factor deficiency resulting in pernicious anaemia
Aspirin and NSAIDs inhibit prostaglandins via inhibition of COX resulting in less mucus production and therefore gastritis
114
How does gastritis present?
```
Nausea/recurrent upset stomach
Abdominal bloating
Epigastric pain
Vomiting
Indigestion
Haematemesis
```
115
Name 5 differential diagnoses for gastritis?
```
Peptic ulcer disease
GORD
Non-ulcer dyspepsia
Gastric lymphoma
Gastric carcinoma
```
116
How is gastritis diagnosed?
Endoscopy - will be able to see gastritis
Biopsy
H pylori urea breath test
H pylori stool antigen test
117
How is gastritis treated?
Remove causative agents such as alcohol
Reduce stress
H pylori eradication - confirmed by urea beath or faecal antigen test, triple therapy - PPI plus 2 metroidazole/clarithromycin/amoxicillin/tetracycline/bismuth and quinolones such as ciprofloxacin/furozolidone/rifabutin used when stanard regimens have failed such as resuce therapy
H2 antagonists
Antacids
Prevention - PPIs with NSAIDs preventing bleeding from acute stress ulcers and gastritis which if often seen with ill patients especially burns patients
118
What are gastro-oesophageal varices?
Dilated veins at risk of rupture resulting in haemorrhage and in GI system can cause a GI bleed
119
How common are gastro-oesophageal varices?
90% patients with cirrhosis will develop varices of 10 years - only 1/3 will bleed
Bleeding less likely in large varices or those with red signs at endoscopy and in severe liver disease
Tend to develop in lower oesophagus and gastric cardia
120
What can cause gastro-oesophageal varices?
Alcoholism and viral cirrhosis - leading causes of portal hypertension
Portal hypertension - pre-hepatic (thrombosis in portal/splenic vein), intra-hepatic (cirrhosis, schistosomiasis, sarcoid, congenital hepatic fibrosis), post-hepatic (Budd-Chiari syndrome, RHF, constrictive pericarditis)
121
What can increase your risk of gastro-oesophageal varices?
Cirrhosis, portal hypertension, schistosomiasis infection, alcoholism
122
How does portal hypertension lead to gastro-oesophageal varices?
Normal pressure in portal vein = 5-8mmHg
As portal pressure rises above 10-12mmHg, compliant venous system dilates and varices form within systemic venous system
Can form at gastro-oesphageal junction, rectum, left renal vein, diaphragm, anterior abdominal wall via umbilical vein
Tend to be superficial and tend to rupture resulting in GI bleeding usually when pressure exceeds 12mmHg
Following liver injury and fibrogenesis, contraction of activated myofibroblasts contributes to increased resistance to blood flow
123
How do gastro-oesophageal varices present?
If ruptured - haematemesis, abdominal pain, shock (if major blood loss), fresh rectal bleeding (associated with shock in acute massive GI bleed), hypotension and tachycardia, pallor, suspect varices as cause of GI bleed if alcohol abuse or cirrhosis
Signs of chronic liver damage eg jaundice, increased bruising and ascites
Spenomegaly
Ascites
Hyponatraemia
124
How are gastro-oesophageal varices diagnosed?
Endoscopy to find bleeding source
125
How are gastro-oesophageal varices treated?
Resuscitate if haemodynamically unstable
If anaemic - blood transfusion to get Hb to 80g/L
Correct clotting abnormalities - vit K and platelet transfusion
Vasopressin
Prophylactic antibiotics to treat and prevent infection as well as to reduce early re-bleeding and mortality
Variceal banding - banded varix will fall off after a few days
Transjugular intrahepatic protoclaval shunt - reduced portal vein pressure
126
How do you prevent gastro-oesophageal varices?
Non-selective b-blockers - reduces resting pulse rate to decrease portal pressure
Variceal banding repeatedly
Liver transplant
127
What is GORD?
Gatro-oesophageal reflux disease
When reflux of stomach contents causes troublesome symptoms and/or complications
2 or more heartburn episodes a week
Clinical symptoms when prolonged contact of gastric contents with mucosa
128
What can cause GORD?
```
Lower oesophageal sphincter hypotension
Hiatus hernia
Loss of oesophageal peristaltic function
Abdominal obesity
Gastric hypersecretion
Slow gastric emptying
Overeating
Alcohol
Pregnancy - increased abdominal pressure
Fat, chocolate, coffee, alcohol ingestion
Drugs - antimuscarincs, CCBs and nitrates
Systemic sclerosis
```
129
What is the pathology of GORD?
Much more transient lower oesophageal sphincter relaxations as LOS has reduced tone allowing gastric acid to flow back into oesophagus
Clinical features appear when anti-reflux mechanisms fail and allow gastric contents to make prolonged contact with lower oesophageal mucosa
LOS relaxes transiently, independently of a swallow after meals
Increased mucosal sensitivity to gastric acid and reduced oesophageal clearance of acid contributes
Delayed gastric emptying and prolonged post-prandial and nocturnal reflex also contribute
Hiatus hernia can impair anti-reflux mechanisms and contribute
130
How does GORD present?
```
Oesophageal
- Heartburn - aggravated by bending, stooping or lying down
- Worse with hot drinks/alcohol
- Seldom radiates to arms
- Belching
- Food/acid brash (regurgitation)
- Water brash (increased salivation)
- Odynophagia (paindul swallowing)
Extra-oesophageal
- Nocturnal asthma
- Chronic cough
- Laryngitis
- Sinusitis
```
131
What could be a differential diagnosis of GORD?
Coronary artery disease
Biliary colic
Peptic ulcer disease
Malignancy
132
How is GORD diagnosed?
Usually made w/o investigation as long as no alarm bells of oesophageal cancer
Patients under 45 treated w/o investigations
Endoscopy - symptoms for more than 4 wks, persisitent vomiting, GI bleed, palpable mass, over 55, symptoms despite treatment
Barium meal - hiatus hernia
Assess oesophagitis and hiatal hernia
Oesophagitis or Barrett's oesophagus
24 hr oesophageal pH monitoring prior to surgery to confirm reflux
Use LA classifciation of GORD when doing endoscopy to gauge extent of damage
133
How is GORD treated?
Lifestyle changes - weight loss, smoking cessation, small, regular meals, avoid hot drinks, alcohol, citrus fruits, eating less than 3 hours before bed
Drugs - antacids, alginates (gaviscon), PPI, H2 receptor antagonist
Surgery -Nissen fundoplication - increases resting LOS pressure
134
What are the possible complications of GORD?
Peptic stricture - narrowing and stricture of oesophagus
| Barrett's oesophagus - distal oesophageal epitheliun undergoes metaplasia from squamous to columnar
135
What is a haemorrhoid?
Disrupted and dilated anal cushions (masses of spongy vascular tissue due to swollen veins around anus)
Anal cushions contribute to anal closure
136
How common are haemorrhoids?
Prevalence increases with age
Peak in 45-65 year old
Equally common in men and women
137
What are the two different types of haemorrhoids?
Internal - origin above dentate line, 4 degrees
1st - remain in rectum
2nd - prolapse through anus on defecation but spontaneously redue
3rd - prolapse but can be reduced manually
4th - remain persistently prolapsed
External - origin below dentate line, visibly externally, extremely painful as sensory nerve supply below dentate line
138
What can cause haemorrhoids?
Constipation with prolonged straining key factor
Diarrhoea
Effects from gravity due to posture
Congestion from pelvis tumour, pregnancy, portal hypertension
Anal intercourse
139
How do haemorrhoids occur?
Anal cushions prone to displacement and disruption
Effects of gravity, increased anal tone and effects of straining when defecating makes them become bulky and loose so protrude to form piles
Vulnerable to trauma and bleed readily from capillaries from underlying lamina propria
Bright red blood
No sensory fibres above dentate line so not painful unless thrombus formation when they protrude and are gripped by anal sphincter, blocking venous return
Vicious circle - vascular cushions protrude through tight anus, become congested and hypertrophy, protrude again more readily
Protrusions may strangulate
140
How do haemorrhoids present?
Bright red rectal bleeding that often coats stools, seen on tissue or drips into toilet
Mucus discharge and pruritus ani
Severe anaemia
Weight loss and change in bowel habit
141
Name 3 differential diagnoses of haemorrhoids?
Perianal haematoma
Anal fissure
Abscess
Tumour
142
How are haemorrhoids diagnosed?
Abdominal exam to rule out other disease
PR exam - prolapsing piles obvious, internal haemorrhoids not palpable
Protoscopy for internal
Sigmoidoscopy to see rectal pathology higher up
143
How are haemorrhoids treated?
1st degree - increase fluid and fibre, topical anagesic and stool softner
2nd and 3rd degree - rubber band ligation infra-red coagulation
4th degree - excisional haemorrhoidectomy, staples haemorrhoidopexy
Prolapsed or thrombose piles - analgesia, ice packs, stool softners, pain usually resolves within 2-3 weeks
144
What is a hernia?
Profusion of a viscus or part of a viscus through a defect of walls and it contents into an abnormal position
Viscus = organ
145
What is an inguinal hernia?
Protrusion of abdominal contents through inguinal canal
| Contains spermatic cord, and external and internal spermatic and cremasteric fascia
146
What is a femoral hernia?
Bowel comes through femoral canal below inguinal ligament
147
What is an incisional hernia?
Tissue protrudes from surgical scar that is weak
| Complication of abdominal surgery
148
How common are inguinal hernias?
```
Commonest type of hernia
More common in men
Indirect and direct
Indirect more common than direct
70% abdominal hernias
More common over 40
Pass through internal inguinal ring and if large out external ring
```
149
How common are femoral hernias?
Less common than inguinal
More common in women
Occurs in middle age and elderly
150
How common are hiatus hernias?
30% patients above 50, especially obese women
151
How are hernias classified?
Reducible hernia - can be pushed back into abdominal cavity with manual manoeuvring
Irreducible hernia - cannot be pushed back into place, obstructed (blood flow maintained), incarcerated (contents of hernial sack stuck inside adhesions), strangulated (ischaemia)
152
What can increase your risk of getting an inguinal hernia?
```
Male
Chronic cough
Constipation
Urinary obstruction
Heavy lifting
Ascites
Past abdominal surgery
```
153
What can increase you risk of getting an incisional hernia?
Emergency surgery
Wound infection post-op
Persistent coughing and heavy lifting
Poor nutrition
154
What is the inguinal canal?
Short passage extending medially and inferiorly through inferior part of abdominal wall
Extends from deep inguinal ring to superficial inguinal ring
Pathway that structures can pass from abdominal wall to external genitalia
Potential weakness in abdominal wall
155
How does a direct inguinal hernia occur?
Where peritoneal sac enters inguinal canal through posterior wall of inguinal canal - medial to inferior epigastric vessels, rarely strangulates, reduces easily
Indirect - where peritoneal sac enters inguinal canal through deep ring to superficial ring if large enough, lateral to inferior epigastric artery, can stragnulate
156
How does a femoral hernia occur?
Bowel enters femoral canal presenting as mass in upper medial thigh or above inguinal ligament where it points down leg
Irreducible and strangulates due to rigidity of canals borders
Neck of hernia felt inferior and lateral to pubic tubercle
157
How does a hiatus hernia occur?
Sliding - gastro-oesophageal junction and part of stomach slide up chest via hiatus so lies above diaphragm, acid reflux often happens at lower oesophageal sphinter becomes less competent in many cases
Rolling - where gastro-oesophageal junction remains in abdomen but part of fundus in stomach prolapses through hiatus alongside oesophagus, reflux uncommon as junction remains in tact
158
How does an inguinal hernia present?
```
Bulging associated with coughing or straining
Appearance of lump
Rarely painful
Can usually reduce hernia themselves
Pain indicates strangulation
```
159
Name 5 differential diagnoses of inguinal hernias
```
Femoral hernia
Epididymitis
Testicular torsion
Groin abscess
Aneurysm
Hydrocele
Undescended testes
```
160
Name 5 differential diagnoses of fermoral hernia
```
Inguinal hernia
Lipoma
Femoral aneurysm
Psoas abscess
Saphena varix
```
161
How is an inguinal hernia diagnosed?
Look for lump
162
How is a hiatus hernia diagnosed?
Barium meal - confirms diagnosis
| Upper GI endoscopy - to visualise mucosa
163
How is an inguinal hernia treated?
Medial - use of truss to contain and prevent further progression of hernia
Surgery - only if symptomatic, prosthetic mesh, open repair, laparoscopy, pre-op - diet, and stop smoking
164
How is a femoral hernia treated?
Surgical repair
Herniotomy - ligation and excision of sac
Herniorrhaphy
165
How is a hiatus hernia treated?
Lose weight
Treat reflux symptoms
Surgically treat to prevent strangulation
166
What is intestinal obstruction?
Arrest/blockage of onward propulsion of intestinal contents
| One of most common causes of hospital admissions
167
How are intestinal obstructions classifed?
According to site - large/small/gastric
Extent of luminal obstruction - partial/complete
According to mechanism - mechanical (most), true, functional - paralytic ileus
According to pathology - simple, closed loop, stragulation, intussusception
168
What can cause intraluminal obstruction?
Tumour - carcinoma, lymphoma
Diaphragm disease
Meconium ileus
Gallstone ileus
169
What can cause intramural obstruction?
Disease in wall of bowel
Inflammatory - Crohn's, diverticulitis
Tumours
Neural - Hirschprung's disease
170
What can cause extraluminal obstruction?
Adhesions - fibrous tissues, not longer able to move around freely
Volvulus - twist/rotation of segment of bowel
Tumour - peritoneal tumour seen in ovarian carcinoma
171
How does intestinal obstruction sound?
Tinkling bowel sounds and tympanic percussion typical of obstruction
172
What is irritable bowel syndrome?
Mixed group of abdominal symptoms with no organic cause that can be found
173
How common is IBS?
Age of onset under 40
More common in women
Common in Western world 1 in 5
Symptoms exacerbated by stress, food, gastroenteritis or menstruation
174
What are the 3 different classifications of IBS?
IBS-C - with constipation
IBS-D - with diarrhoea
IBS-M - with both
175
What can cause IBS?
```
Depression/anxiety
Psychological stress/trauma
GI infection
Sexual, physical or verbal abuse
Eating disorders
```
176
What are the main risk factors for IBS?
Female
Severe and long diarrhoea
High hypo-chondrial anxiety and neurotic score at time of initial illness
177
What is the pathology of IBS?
Dysfunction in gut-brain axis resulting in disorder of interstinal motility and/or enhance visceral perception
178
How does IBS present?
Non-intestinal - painful period, urinary frequency, urgency, nocturia, incomplete emptying of bladder, back pain, joint hypermobility, fatigue
Abdominal pain either relieved by defecation or associated with altered stool form or bowel frequency and 2 or more of
- Urgency, incomplete evacuation, abdominal bloating/distension, muscous in stool, worsening of symptoms after food
Nausea, chronic and exacerbated by stress, menstruation or gastroenteritis
General abdominal tenderness
179
What could be a differential diagnosis for IBS?
```
Coeliac disease
Lactose intolerance
Bile acid malabsorption
IBD
Colorectal cancer
```
180
How is IBS diagnosed?
Made by ruling out differentials
Bloods - FBC for anaemia, ESR/CRP for inflammation, coeliac serology
Faecal calprotectin - IBD
Colonoscopy - IBD/colorectal cancer
Rome III diagnostic criteria
- Recurrent abdominal pain or discomfort for at least 3 days a month in past 3 months associated with 2/more of
- Improvement with defecation
- Onset with change in frequency of stool
- Onset associated with change in form of stool
181
How is IBS treated?
Mild - education, reassurance, dietary modification
Moderate - pharmacotherapy, psychological treatment
Severe - referral to pain treatment centre
Diet/lifestyle modifications - regular/small frequent meals, plenty of fluidsm reduce/avoid caffeinated drinks/alcohol/fizzy drinks
IBS-D avoid insoluble fibre intake, fruit intake more than 3 portions per day
For wind and bloating increase soluble fibre intake
For pain/bloating - anstispasmodics
For constipation - laxative
For diarrhoea - anti-motility
Still no better - tricyclic antidepressants, not to treat depression but dampen gut sensitivity
If not tolerated - SSRI
Psychological therapy
182
How common is large bowel obstuction?
Less common - 25% of all intestinal obstruction
| Acute presentation - on average 5 days of symptoms
183
Why do symptoms present slower in large bowel obstruction?
Larger lumen and circular and longitudinal muscles so ability of large bowel to distend much greater thus symptoms present slower and later
184
What can cause large bowel obstruction?
90% due to colorectal malignancy
| In African countries - volvulus
185
What occurs in large bowel obstruction?
Colon proximal to obstruction dilates
Increased colon pressure and decreased mesenteric blood flow resulting in mucosal oedema - transudation of fluid and electrolytes from lumen
Can compromise arterial blood supply and also cause mucosal ulceration resulting in full thickness necrosis as well as perforation
Bacterial translocations can also occur resulting in sepsis
186
What happens with a colonic volvulus?
Axis rotation based off mesentery and a 360 degree twist results in closed loop obstruction
Fluid and electrolyte shift into closed loop
Results in increased pressure and tension in loop causing impaired colonic blood flow
Ischaemia, necrosis and perforation of loop of bowel soon follows if untreated
187
How does large bowel obstruction present?
```
Abdominal pain more constant than SBO
Abdominal distension
Bowel sounds normal then increased then quiet
Palpable mass eg hernia, distended bowel loop or caecum
Late vomiting more faecal like
Vomiting may be absent
Constipation
Fullness/bloating/nausea
```
188
How is large bowel obstruction diagnosed?
Digital rectum exam - empty rectum, hard stools, blood
FBC essential - low Hb sign of chronic occult
Abdo x-ray - peripheral gas shadows proxiaml to blockage, caecum and ascending colon distended
CT
189
How is large bowel obstruction treated?
```
Aggressive fluid resuscitation
Bowel decompression
Analgesia and antiemetic
Antibiotics
Surgery - to remove obstruction done by laparotomy
```
190
What is a Mallory-Weiss tear?
Linear mucosal tear occuring at oesophagogastric junction and produced by a sudden increase in intra-abdominal pressure
Often follows bout of coughing or retching and classically seen after alcoholic dry heaves
191
How common are Mallory-Weiss tears?
Most common in men
| Seen mainly aged 20-50
192
What factors can increase your risk of getting a Mallory-Weiss tear?
```
Alcoholism
Forceful vomiting
Eating disorders
Male
NSAID abuse
```
193
How do Mallory-Weiss tears present?
```
Vomiting
Haematemesis after vomiting
Retching
Postural hypotension
Dizziness
```
194
What could be a differential diagnosis for a Mallory-Weiss tear?
Gastro-enteritis
Peptic ulcer
Cancer
Oesophageal varices
195
How are Mallory-Weiss tears diagnosed?
Endoscopy
196
How are Mallory-Weiss tears treated?
Most minor and heal in 24hrs
Haemorrhage may be large but tend to stop spontaneously
If surgery required - oversewing of tear rarely needed
197
What is an oesophageal tumour?
Squamous cell carcinoma occuring in middle 1/3 (40%) and in upper 1/3 (15%) of oesophagus
OR
Adenocarcinoma occur in lower 1/3 of oesophagus and at cardia (45%)
198
How common is oesophageal cancer?
6th most common cancer worldwide
Carcinoma in those 60-70
SCC - common in Ethiopia, China, South and East Africa, incidence 5-10 per 100,000, incidence decreasing in contrast to adenocarcinoma, more common in men
Adenocarcinoma - primarily arise in columnar-lined epithelium in lower oesophagus, Barrett's oesophagus (metaplasia), incidence increasing in Western countries, previous reflux symptoms increase risk 8x
Benign - 1% of all oesophageal tumours, leiomyomas most common, papillomas, fibrovascular polyps, haemangiomas, lipomas
199
What are the main causes of SCC?
High levels of alcohol consumption
Achalasia - reduced/no ability for peristalsis
Tobacco use
Obesity - increased reflux
Smoking
Low fruit/veg consumption
Diets rich in fibre, carotenoids, folate and vit C decrease risk
200
What are the main causes of adenocarcinoma?
Smoking
Tobacco
GORD
Obesity
201
What can increase your risk of getting oesophageal tumours?
```
Alcohol
Smoking
Increased reflux
Obesity
Achalasia
Diet low in Vit A and C
Barrett's oesophagus
```
202
What are benign tumours within the oesophagus called?
Leiomyomas - smooth muscle tumours arising from oesophageal wall
Intact, well encapsulated within overlying mucosa
Slow growing
203
How do oesophageal tumours present?
Most have no physical signs until cancer extremely advanced
Progressive dysphagia - initially difficulty swallowing solids, dysphagia with liquids follows within weeks
Weight loss
Lymphadenopathy
Anorexia
Pain due to impaction of food or infiltration of cancer into adjacent structures
Oesophageal obstruction - eventually difficulty swallowing saliva, coughing and aspiration to lungs
Hoarseness and cough
204
How do benign oesophageal tumours present?
```
Usually asymptomatic
Dysphagia
Retrosternal pain
Food regurgitation
Recurrent chest infection
```
205
How are oesophageal tumours diagnosed?
Oesophagoscopy with biopsy
Barium swallow to see strictures
CT scan/MRI/PET for staging
206
How are benign oesophageal tumours diagnosed?
Endoscopy
Barium swallow
Biopsy to rule out malignancy
207
How are oesophgeal tumours treated?
Surgical resection - best chance or cure if not infiltrated outside oesophageal wall - combined with chemo
Systemic chemo
Treatment of dysphagia - endoscopic insertion of expanding metal stent across tumour to ensure oesophageal patency, laser and alcohol injections cause tumour necrosis and increase lumen size, pallative care
208
How are benign oesophageal tumours treated?
Endoscopic removal
| Surgical removal of larger tumours
209
What is a peri-anal abscess?
Collection of pus in deep tissues surrounding anus
210
How common are peri-anal abscesses?
2/3 times more common in gay sex and those who have anal sex
211
How do peri-anal abscesses present?
Painful swelling
Tender
Discharge
212
How are peri-anal abscesses diagnosed?
MRI
| Endoanal ultrasound
213
How are peri-anal abscesses treated?
Surgical excision
| Drainage with antibiotics
214
What is a pilonidal sinus/abscess?
Hair follicles get stuck under skin in natal cleft (butt crack) resulting in irritation and inflammation leading to small tracts that can become infected (abscess)
215
How common are pilonidal abscesses?
Much more common in men
| Commonly presents between 20-30 years
216
What can increase your risk of getting pilonidal abscesses?
```
Obese Caucasians and those from Asia, Middle East, and Mediterranean
Large amount of body hair
Sedentary job
Occupation involving sitting or driving
FHx
```
217
Why do pilonidal abscesses form?
Ingrowing hair excites a foreign body reaction and may cause secondary tracks to pen laterally with/without abscesses with foul smelling discharge
218
How do pilonidal abscesses present?
Acute - painful swelling over days, pus filled with foul smell from abscess, systemic signs of infection
Chronic - 4 in 1- have repeated recurrent pilonidal sinus, infection never clears completely
219
How are pilonidal sinuses diagnosed?
Clinical examination
220
How are pilonidal sinuses treated?
Surgery - excision of sinus tract and primary closure and pus drainage, pre-op antibiotics
Hygiene and hair removal advice
221
What is pseudo-obstruction?
Clinical picture mimicking obstruction but with no mechanical cause
In more than 80% cases complication of other condtions
222
What other condtions may cause pseudo-obstruction?
Intra-abdominal trauma
Pelvic, spinal and femoral fractures, post-operative states eg abdominal, pelvic, cardiothoracic, orthopaedic and neuro
Intra-abdominal sepsis
Pneumonia
Drugs - opiates, antidepressants
Metabolic disorders eg electrolyte disturbance, malnutrition, DM, parkinson's disease
223
How does pseudo-obstruction present?
Rapid, progressive abdominal distension and pain
224
How is pseudo-obstruction diagnosed?
X-ray showing gas-filled large bowel
225
How is pseudo-obstruction treated?
Treat underlying problems eg withdrawal of opiate analgesia
| IV neostigmine
226
What is peptic ulcer disease?
Consists of a break in superficial epithelial cells penetrating down to muscularis mucosa of either stomach or duodenum
Most commonly found in duodenal cap
Gastric ulcers most commonly seen on lesser curve of stomach but can be found anywhere in stomach
227
How common is PUD?
Duodenal ulcers affect 10% population and 2-3 times more common than gastric ulcers
More common in elderly
More common in developing countries due to H pylori
Due to increased NSAID use
Decline in incidence in men and increasing in women
228
What can cause PUD?
```
H pylori infection
Drugs eg NSAIDs
Increased gastric acid secretion
Smoking
Delayed gastric emptying
Blood group O
```
229
What are the causes of gastric ulcers?
NSAIDs - block prostaglandin release by synthesis of COX
H pylori - inflammation, gastric cancer, peptic ulcers
Ischaemia of gastric cells - produce less mucin resulting in less protection from acid meaning acid able to damage mucosa resulting in ulcer, caused by low BP/atherosclerosis
Too much acid production - overwhelms mucin and results in ulceration, stress can result in increased acid production, PPIs and H2 blockers used to treat this
Alcohol - direct toxic effect on gastric cells in high concs
230
How does PUD present?
```
Recurrent burning epigastric pain
Night pain
Relieved by antacids
Nausea
Anorexia and weight loss
```
231
What are the red flag symptoms for cancer?
```
Unexplained weight loss
Anaemia
Evidence of GI bleeding
Dysphagia
Upper abdominal mass
Persistent vomiting
```
232
How is PUD diagnosed?
If under 55 - non-invasive testing - serological, breath tesy, stool antigen testing
Endoscopy not necessary - if found re-scopre 6-8 wks later to ensure no malignancy
Endoscopy if red flags
Serology - IgG
C-urea breath test - H pylori, measures CO2 in breath after ingestion of C-urea, used to monitor infection after eradication
Stool antigen test - immunoassay using monoclonal antibodies for H pylori detection
Invasive H pylori testing - endoscopy, biopsy urease test, histology
233
How is PUD treated?
Lifestyle adjustments - reduce stress, avoid irritating foods, reduce smoking
Stop NSAIDs
H pylori eradication triple therapy
H2 antagonists - ranitidine
Surgery if complications such as haemorrhage
234
What are the potential complications of PUD?
Deepening ulcers that hit arteries - gastroduodenal artery which can cause major haemorrhage
Peritonitis as acid enters peritoneum - air under diaphragm on erect XR
Acute pancreatitis if ulcers hits pancreas
235
How common is small bowel obstruction?
60-75% of intestinal obstruction
Majority caused by previous surgery
Crohn's disease also significant cause
236
What can cause small bowel obstruction?
Adhesions - usually secondary to previous abdominal surgery, increased incidence in pelvic, gynaecology, colorectal surgery
Hernia - can result in strangulation
Malignancy
Crohn's
237
What is the pathology of small bowel obstruction?
Mechanical obstruction most common
Leads to bowel distension above block with increased secretion of fluid into distended bowel
Proximal dilatation above block - increased secretions and swallowed air in small bowel, more dilatation results decreased absorption and mucosal wall oedema, increased pressure with intramural vessels becoming compressed resulting in ischaemia and/or perforation
Untreated leads to - ischaemia, necrosis, perforation
238
How does small bowel obstruction present?
Pain - colicky then diffuse, pain higher in abdomen than in LBO
Profuse vomiting that follows pain - earlier in SBO than LBO
Less distension than LBO
Nausea and anorexia
Tenderness suggests strangulation and urgent surgery required
Constipation with no passage of wind occurs late in SBO
Increased bowel sounds
239
How is small bowel obstruction diagnosed?
Abdo XR - shows central gas shadows that completely cross the lumen and no gas in large bowel, distended loops of bowel proximal to obstruction, fluid levels seen
Exam of hernia orifices and rectum
FBC essential
CT - helps accurately localise lesion
240
How is small bowel obstruction treated?
```
Aggressive fluid restriction
Bowel decompression
Analgesia and antiemetic
Antibiotics
Surgery - to remove obstruction done by lapartomy
```
241
How common are small intestine tumours?
Relatively resistant to development of neoplasia
Quite rare place for cancer to develop - 1% of all malignancies
Adenocarcinoma most common tumour
Lymphomas (non-Hodgkin's most frequently found in ileum and are less common that adenocarcinomas
242
What can increase your risk of getting small intestine tumours?
Coeliac disease
| Crohn's disease
243
How do small intestine tumours present?
Pain, diarrhoea, anorexia, weight loss, anaemia
| Palpable mass
244
How are small intestine tumours diagnosed?
USS
Endoscopic biopsy histologically confirms diagnosis
CT scan - may show small bowel wall thickening and lymph node involvement seen in lymphoma
245
How are small intestine tumours treated?
Surgical resection
| Radiotherapy
246
What is ulcerative colitis?
Relapsing and remitting inflammatory disorder of colonic mucosa
May affect just the rectum - proctitis
May affect rectum and left colon - left sided colitis
May affect the entire colon up to ileocaecal valve - pancolitis/extensive colitis
Never affects proximal to ileocaecal valve
247
How common is UC?
Highest incidence and prevalence in Norther Europe, UK, North America
Higher incidence than Crohn's per year
Affects males and females equally
3x more common in non/ex-smokers - symptoms relapse on stopping smoking
Cause unknown
1 in 6 will have first degree relative with UC
An appendicetomy appears to be protective against development of UC
248
What can increase your risk of developing UC?
FHx
NSAIDs - associated with onset of IBD and flares of disease
Chronic stress and depression triggers flares
249
What does UC look like macroscopically?
Affects only colon up to ileocaecal valve
Begins in rectum and extends
Circumferential and continuous inflammation - no skip lesions
Mucosa looks reddened and inflamed and bleeds easily
Ulcers and pseudo-polys in severe disease
250
What does UC look like microscopically?
Mucosal inflammation - does not go deep
No granulomata
Depleted goblet cells
Increased crypt abscesses
251
How does UC present?
Runs a course of remissions and exacerbations
Restricted pain usually in lower left quadrant
Episodic or chronic diarrhoea
Cramps
Bowel frequency linked to severty
In acute UC there may be fever, tachycardia, and tender distended abdomen
In acute attack patients have bloody diarrhoea also occurs at night, with urgency and incontinence that is severely disabiling
Extraintestinal signs - clubbing, aphthous oral ulcers, erythema nodusum and amyloidosis
252
What could be a differential diagnosis for UC?
Alternative causes of diarrhoea
253
How is UC diagnosed?
Bloods - WCC and platelets raised in moderate/severe attacks, iron deficiency anaemia, ESR/CRP raised, liver biochemistry abnormal, hypoalbuminaemia in severe disease, pANCA may be positive (negative in Crohn's)
Stoop samples - to exclude infective causes
Faecal calprotectin - indicates IBD but not specific
Colonscopy with mucosal biopsy - allows for assessment of disease activity and extent, can see inflammatory infiltrate, goblet cell depletion, crypt abscesses and mucosal ulcers
Abdo XR - excludes colonic dilatation
254
How is UC treated?
Aim to induce remission
Aminosalicylate acts topically on colonic lumen
Mild/moderate - oral 5ASA, rectal 5ASA for proctitis, glucocorticoid if don't respond
Severe - glucocorticoid
Severe with systemic features - hydrocortisone, ciclosporin, infliximab
Maintain remission - 5-ASA, azathioprine
Surgery - indicated for severe colitis that fails to respond to treatment, colectomy with ileoanal anatomosis - whole colon removed and rectum fused to ileum
Panproctcolectomy with ileostomy
255
What are the complications that can occur with UC?
Liver - fatty change, chronic pericholangitis, sclerosing cholangitis
Colon - blood loss, perforation, toxic dilatation, colorectal cancer
Skin - erythema nodusum, pyoderma gangrenosum
Joints - akylosing spondylitis, arthritis
Eyes - iritis, uveitis, episcleritis
256
Give an example of a PPI
Lansoprazole
Omeprazole
Pantoprazole
257
What are PPIs used for?
First line for prevention and treatment of peptic ulcer disease
Symptomatic relief of dyspepsia and GORD
Eradication of H pylori infection with antibioitcs
258
How do PPIs work?
Reduces gastric acid secretion by irreversibly inhibiting H+/K+ ATPase in gastric parietal cells - proton pump responsible for secreting H+ and generating gastric acid
Suppresses gastric acid production significantly
259
What are the main adverse effects of PPIs/
GI disturbances and headaches common
Increasing gastric pH may reduce body's host defence against infection, slightly higher risk of C diff
May disguise symptoms of gastric cancer
Can increase risk of fractures in elderly so use with care if have osteoporosis
PPIs especially omeprazole can reduce antiplatelet effect of colpidogrel so prescribe a different PPI if on clopidogrel
260
Give an example of an H2 receptor antagonist
Ranitidine
261
What are H2 receptor antagonists used for?
Treatment and prevention of gastric and duodenal ulcers and NSAID associated ulcers if PPIs are contraindicated
Relief of symptoms of GORD and dyspepsia if mild
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How do H2 receptor antagonists work?
Acid normally produced by proton pump of gastric parietal cell, which secretes H+ into stomach lumen in exchange for drawing K+ in
Proton pump regulated by histamine which binds to H2 receptors on parietal cell and activates the pump
So blocking the receptor reduces the activation of the cell
H2 recpetor antagonits reduce gastric acid secretion but does not completely suppress secretion as proton pump can be stimulated by other pathways - PPIs produce more complete effect
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What are the main adverse effects of H2 receptor antagonists?
Bowel disturbance, headache or dizziness
Reduce dose in renal impairment
Watch for symptoms of gastric cancer as H2 antagonist can disguise these
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Give an example of an alginate
Gaviscon
| Peptac
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What are alginates used for?
GORD disease for symptomatic relief of heartburn
| For short term relief of indigestion and dyspepsia
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How do alginates work?
Most often taken as a compound preparation of alginate with one or more antacid such as calcium bicarbonate, magnesium or aluminium salts
Alginates work to increase viscosity of stomach contents which reduces reflux of stomach acid into oesophagus
After reacting with stomach acid they form a floating raft which separates the gastric contents from the gastro-oesophageal junction to prevent mucosal damage
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What are the main adverse effects of alginates and antacids?
Magnesium can cause diarrhoea and aluminium can cause constipation
Sodium and potassium containing compounds used with caution in fluid overload or hyperkalaemia ie renal failure
Antacids may reduce concentration - ACEi, antibiotics, PPIs, bisphosphonates and digoxin so take dose at different times
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Give an example of an antimotility drug
Loperamide
| Codeine phosphate
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What are antimotility drugs used for?
Symptomatic treatment of diarrhoea, usually for IBS or gastroenteritis
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How do antimotility drugs work?
Loperamide is opioid but does not penetrate CNS so no analgesic effects - agonist of opioid receptors in GI tract which increases non-propulsive contractions of gut smooth muscle but reduces peristaltic contractions
Transit of bowel content is slowed and anal sphincter tone increased, also more water is absorbed from faeces as there is more time for this to occur so stools are hardened
Codeine phosphate has same effect but with analgesia
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What are the main adverse effects of antimotility drugs?
Most side effects of GI disturbance and are mild
Should be avoided in acute UC where inhibition of peristalsis may result in megacolon and perforation, should also be avoided if there is risk of C difficile or other bacterial infection
