GI Flashcards
(134 cards)
1
Q
Crohn’s disease definition
A
A disorder of unknown aetiology characterised by granulomatous transmural inflammation of the GI tract. Usually seen in the terminal ilial, proximal colon and perianal location, but can affect ANY PART of the GI tract. Unlike ulcerative colitis, CD may have non-continuous skip lesions (normal bowel mucosa found between diseased areas). The transmural inflammation can also result in sinus tracts that burrow through and penetrate the serosa, giving rise to perforations and fistulae.
Macroscopic appearance: skp lesions, cobblestone appearance, thickened and narrowed.
Microscopic appearance: transmural, granulomas (non-ceseating), goblet cells present
2
Q
Crohn’s disease aetiology
A
Unknown
Genetic - potential: inappropriate immune response against (possibly abnormal) colonic flora in genetically susceptible individuals
Environment: smoking, oral contraceptive pill, NSAIDs, stress
3
Q
Crohn’s disease risk factors
A
Peak age of onset 14-40yrs Smoking Family history Mutation on NOD2 gene Equally present in men and women More common in white northern Europeans and N. America
4
Q
Crohn’s disease pathophysiology
A
Acute transmural inflammation results in bowel obstruction due to mucosal oedema associate with spasm. Scarring, luminal narrowing and stricture formation occur due to the chronic inflammation.
Chronic inflammation damages the mucosa leading to deficient absorptive ability
Involvement at the terminal ileum interferes with bile acid absorption, leading to steatorrhea, fat-soluble vitamin deficiency and gallstone formation
5
Q
Crohn’s disease key presentations
A
Can have mild symptoms in periods of remission followed by ‘flare ups’/exacerbatiions. Oral ulcers are common
Dependent on area affected:
Small bowel
- abdo pain
- weight loss
- right iliac fossa pain (less common)
Colon
- bloody diarrhoea
- pain on defecation
Systemic symptoms in attacks
- fever
- anorexia
- malaise
- fatigue
Signs
- bowel ulceration
- abdo tenderness
- abdo mass
- perianal disease
- extraintestinal signs: clubbing; oral apthous ulcers; more common than UC; skin, joint and eye problems
6
Q
Crohn’s disease 1st line investigations
A
Ask for travel history, family history and medications to see any contributing causes.
Blood tests - raised WCC, raised platelets, raised CRP and ESR, normocytic anaemia of chronic disease, iron, folate, B12 deficiency, hypoalbuminaemia in severe, pANCA negative
Stool sample - exclude infection
Faecal calprotectin - raised in IBD
Gold standard
Colonoscopy with biopsy - can help determine severity, further radiological examinations can determine severity and transmural complications (eg fissure)
7
Q
Crohn’s disease differential diagnosis
A
Ulcerative colitis, infective colitis, intestinal ichaemia, acute appendicitis, diverticulitis, IBS, malignancy such as tumour
8
Q
Crohn’s disease management
A
No cure so treatment is intended to manage and improve symptoms.
1st treatment: corticosteroids such as prednisolone tablets or hydrocortisone injections (severe) - reduce inflammation. Side effects: weight gain, swelling of the face and osteopenia or osteoporosis. If the case is severe, immunosuppressants are considered. Surgery can also be considered if symptoms arent relieved.
Smoking cessation, treat iron/folate/B12 deficiency
Anti-TNF antibodies if no response to steroids: inflicimac, adalimumab
Azathioprine to maintain remission
Surgery last resort to remove most damaged area - short bowel syndrome = diarrhoea and malabsorption
9
Q
Crohn’s disease monitoring
A
A surveillance colonoscopy is generally recommended eight to ten years after diagnosis of ulcerative colitis or Crohn’s disease involving the colon and every one to two years thereafter
10
Q
Crohn’s disease complications
A
SAMPANOO
Systemic - amyloidosis. Thisis where the myloid protein builds up in organs + interferes with their function
Anemia
Malabsorption - due to the reduced absorptive function
Perforation
Anal issues - fistula, abscesses, fissure and skin tags
Neoplasia - colorectal cancer
Osteoporosis
Obstruction - due to acute swelling and chronic fibrosis
11
Q
Crohn’s disease prognosis
A
Great prognosis - mortality rates low with management
12
Q
Ulcerative colitis definition
A
A type of inflammatory bowel disease that usually involves the rectum and extends proximally to affect a variable length of the colon. It is recognised as a multifactorial poygenic disease.
Macroscopic appearance: continuous inflammation (no skip lesions), ulcrs, pseudo-polyps
Microscopic appearance: mucosal inflammation (no transmural inflammation_, no granulomata, depleted goblet cells, increased crypt abscesses
13
Q
Ulcerative colitis epidemiology
A
More prevalent in Northern European population
Most patients are aged 20-40 at diagnosis with another peak at 60yrs
Uncommon in children
High incidence than Crohn’s
Smoking is protective
14
Q
Ulcerative colitis aetiology
A
Unknown, possibly autoimmune: inappropriate immune response against (possibly abnormal) colonic flora in genetically susceptible individuals
Exacerbated by NSAIDs and stress
15
Q
Ulcerative colitis pathophysiology
A
Relapses strongly associated with infectious enteritis
16
Q
Ulcerative colitis key presentations
A
Remission and exacerbation
17
Q
Ulcerative colitis signs and symptoms
A
Symptoms:
- pain in lower left quadrat
- diarrhoea with blood and mucus
- lower back pain from spondylitis (inflammation of spinal bones)
- systemic fever, anorexia, malaise, weight loss
Signs:
- fever (in acute UC)
- clubbing
- erythema nododsum (inflammation of subcutaneous fat)
- pyoderma gangrenosum - painful ulcers on skin
- malnutrition
- real ulcers
18
Q
Ulcerative colitis 1st line investigations
A
Still studies: elevated feacal calprotein (useful for DDx but seen in both UC and Crohn’s), C.difficile toxins often present and associate with increase mortality (need at least 4 sample)
FBC: ESR and CRP may be elevated in flare-up, raised WCC and platelets, normocytic anaemia of chronic disease
pANCA: antibody found in 70% of UC patient (helps with DDx of CD)
Imagining:
- plain abdominal radiography
- ab x-ray
19
Q
Ulcerative colitis gold standard investigations
A
Colonscopy with biopsy
- sigmoidoscopy for diagnosis
- full colonoscopy to define extent once controlled
20
Q
Ulcerative colitis management
A
Aminosalicylate (1st lines): mesalazine or sulfasalzine
Add oral prednisolone if no response, IV hydrocortisone if severe
Azathioprine to maintain remission
Colectomy indicated in patients with severe UC and not responding to treatment
21
Q
Ulcerative colitis complications
A
Toxic megacolon can occur with associated risk of perforation
Bpwel adenocarcinoma is a complication in 3-5% of patients
Joint problems such as arthritis
Hepatobiliary such as chronic pericholangitis and sclerosing cholangitis
22
Q
Irritable bowel syndrome defintiion
A
A chronic condition characterised by abdominal pain associated with bowel dysfunction. There are no structural abnormalities to explain the pain
IBS-C: with constipation
IBS-D: with diarrhoea
IBS-M: mixed, with alternating constipation and diarrhoea
23
Q
Irritable bowel syndrome epidemiology
A
Occurs in abotu 15% of the adult population - 1 in 5 western world
More common in female
Under 40s
24
Q
Irritable bowel syndrome aetiology
A
Likelt multifactorial
25
Irritable bowel syndrome risk factors
Stress, female, GI infection
26
Irritable bowel syndrome pathophysiology
Altered gut reactivity (motility and secretion) due to environmental effects such as stress and certain foods
27
Irritable bowel syndrome key presentations
Abdominal pain associated with 2+ of:
1. relived by defacating
2. altered stool form
3. altered bowel frequency
28
Irritable bowel syndrome signs and symptoms
ABC:
Abdominal dyscomfot
Abdominalbloating or distention
Change in bowel habits
Normal examination of abdomen
Can affect variety of other systems eg painful periods, back pain, bladder dysfunction
29
Irritable bowel syndrome 1st line investigations
FBC: normal; anaemia suggests non-IBS disease; ESR/CRP-inflammation
Faecal Calprotein - raised in IBD
Faecal occult blood: may be positive in IBS or colorectal cancer
30
Irritable bowel disease differential diagnosis
Crohn's: faecal occult blood will be positive
| Coeliac disease: usually have weight loss
31
Irritable bowel disease management
Dietary midifcations - food diary, avoid FODMAPs
Pain/bloating: antipasmodics; buscopan
Contstipation: laxative eg Senna, linaclotide
Diarrhoea: antimotility eg Loperamide
If no better: tricylic antidepressants (amitryptiline SE: drowsiness)
3rd line: SSRIs
CBT
32
Coeliac disease definition
Systemic autoimmune disease tirggered by Prolamin (dietary gluten peptide) found in wheat, rye, barley etc. Inflammation of upper small bowel mucosa
Leads to villous atrophy, hyperplasia of the intestinal crypts and increased numbers of lymphocytes in the epithelium and lamina propria. Leads to GI symptoms and malabsorption. Systemic manifestations are diverse, potentially affecting almost every organ system.
33
Coeliac disase risk factors
Family history, other autoimmune diseases
34
Coeliac disease epidemiology
Affects up to 1% of gneeral population
| Peaks at infancy + 40-60yrs
35
Coeliac disease aetiology
Almost all patient carry one of two major histocompatibility complex class-II molecules (human leukocyte antigen [HLA]-DQ2 or -DQ8)
36
Coeliac disease pathophysiology
1. Gliadin (a prolamin found in wheat) binds to secretory IgA in the mucosal membrane
2. The gliadin-IgA is transcytosed to the laminate propria
3. Gliadin binds to tTH and is deamidated
4. Deamidated gliadin is taken up by macrophages via HLA and expressed on MHC2
5. T helper cells release inflammatory cytokines and stimulate B cells
6. This causes gut damage
Note that gliadin is deamidated not deaminated
Inflammation of the mucosa of the upper small bowel in response to gluten
Autoimmune - T cell mediated
Intolerance to prolamin (in what, barely, rye, oats) - component of gluten protein
Causes villous atrophy and crypt hyperplasia
Leads to malabsorption
37
Coeliac disease signs and symptoms
Symptoms: diarrhea, bloating, abdo pain, nausea and vomiting
Signs: anaemia, weight loss, steatorrhoea and stinking stools (malabsorption), angular stomatitis, apthous stomatitis (non-contagious mouth ulcers), osteomalacia (decreased vitamin D absorption), failure to thrive (children), dermatitis herpetiformis
38
Coeliac disease 1st line investigations
IgA-tTG blood test: positive, very high sensitivity and specificity
FBC and blood smear: low Hb, folate, ferritin, B12
Genetic testing
39
Coeliac disease gold standard investigations
Duodenal biopsy:
- required for definitive diagnosis
- villous atrophy, crypt hyperplasia
- increase epithelial WBCs
40
Coeliac disase managemet
Gluten free diet
| Vitamin and mineral supplementation
41
Coeliac disease prognosis
Up to 90% of people will have complete and lasting resolution of symptoms on a gluten-free diet alone
42
GORD definition
Complications due to the reflux of gastric contents into or beyond the oesophagus
43
GORD epidemiology
GORD is common - exists when the reflux of the stomach contents become troublesome - more than 2 heartburn episodes a week
44
GORD aetiology
Usually as a result of the ring at the bottom of the oesophagus becoming weakened. Causes can include lower oesophageal sphincter hypertension, hiatus hernia
45
GORD risk factors
Overweight or obese, eating large amounts of fatty foods, smoking, alcohol, coffee, chocolate intake, pregnancy, hiatus, certain medicines such as NSAIDs
46
GORD pathophysiology
Transient lower oesophageal sphincter relaxations and other lower oesophageal sphincter pressure abnormalities. As a result, reflux of acid, bile, pepsin and pancreatic enzymes occur, leading to oesophageal mucosal injury.
47
GORD clinical manifestations
- heartburn. This is aggravated by bending, stooping and lying down. May be relieved by antacids.
- belching
- food/acid regurgitation
- increased salvation (water brash)
- odynophagia (painful swallowing)
- nocturnal asthma
- chronic cough
48
GORD investigations
Diagnosis can usually be made without investigation.
NO ALARM BELLS - weight loss, haematemesis and dysphagia require further investigation:
- endoscopy - symptoms longer than 4 weeks, persistent vomiting, GI bleed or palpable mass. Also required if symptoms persist after treatment
- barium swallow - to exclude hiatus hernia
These investigations assess the oesophagus - Barrett's oesophagus confirms reflux
49
GORD differential diagnosis
Chronic Artery Disease, biliary colic, peptic ulcer disease, malignancy
50
GORD management
LIfestyle changes: weight loss, smoking cessation, small and regular meals, avoiding hot drinks, alcohol, citrus fruits. Don't eat within 3 hours of going to bed
Pharmacology: antacids such as magnesium trisilicate mixture. This relieves symptoms by forming a gel with gastric contents to reduce reflux. Side effects could be diarrhoea.
Alginates such as gaviscon can also relieve symptoms.
PPI - proton pump inhibitors such as lansoprazole reduces gastric acid production H2 receptor antagonists - cimetidine - blocks histamine receptors on partial cells and reduces acid release.
Surgery: nissen fundoplication - laparoscopically increase the resting lower oesophageal sphincter. This is used when they aren't responding to treatment.
51
GORD monitoring
not much monitoring required if responding well to treatments. Make patient aware of increased risks and alarm bell symptoms so they know went to come back.
52
GORD complications
Peptic stricture - inflammation of the oesophagus (aka oesophagitis) due to gastric acid exposure. Results in narrowing and stricture change. Usually occurs in patients over 60. Presents as gradually worsening dysphagia.
Barrett's oesophagus - distal oesophageal epithelium undergoes metaplasia from squamous to columnar. Increased risk of oesophageal cancer.
53
GI cancers definition
Oesophageal cancers: most are mucosal lesions originating from the epithelial cells of the oesophagus. Associated with metaplastic condition. Barrett's oesophagus ('precancerous' condition) (stratified squamous to columnar epithelium with goblet cells)
Stomach cancers: most common is type 1 (interstitial/differentiated) usually in the antrum and lesser curve, type 2 (diffuse/undifferentiated) occurs anywhere but often the cardia
Colon cancer: majority are adenocarcinomas
54
GI cancers aetiology
Oesophageal cancers: most common type is adenocarcinomas (typically from Barrett's oesophagus) which are generally found in the distal oesophagus (lower 1/2), squamous cell carcinomas are less common and are more evenly distributed throughout the oesophagus.
Stomach cancers: most are adenocarcinomas.
Colon cancers: most common in the rectum, sigmoid colon and descending colon
55
GI cancers risk factors
Oesophageal cancers: rates are the fastest rising of any malignancy in the west. Male sex is a risk factor. Tobacco and alcohol use are risk factors for squamous cell carcinoma, this type is more common in non-white populations. GORD and Barrett's oesophagus are risk factors for adenocarcinoma
Stomach cancers: male, H. pylori, gastritis, blood type A
Colon cancers: family history, IBD, high fat and red meat, low fibre, folate and calcium, DM
56
GI cancers clinical manifestations
ALARMS: Anaemia, Loss of weight, Anorexia, Recent onset progressive symptoms, Melaena/haematemesis, Swollowing difficulties eg dysphagia
Oesophageal: presence or risk factors, progressive dysphagia (only occurs after obstruction so generally have advanced disease at diagnosis), odynophagia (pain on swallowing), weight loss, hoarsness and hiccups may be present
Stomach: presence of risk factors, abdo pain (tends to be epigastric and vague), weight loss, may have haematemesis, treatment resistant dyspepsia and anaemia
Colon:
- pain (most common in right sided lesions, uncommon in rectal)
- mass (common in right sides, ver uncommon in rectal)
- bleeding (most common in rectal)
- weight loss
- vomiting
- obstruction
- changes in bowel habits
57
GI cancers investigations
Oesophageal:
Oesophagogastrodueodenoscopy (OGD) with biopsy - mucosal lesion, histology shows squamous carcinoma or adenocarcinoma
CT scan or endoscopic ultrasound: for staging
58
GI cancers management
Oesophageal:
- endoscopic or major surgery for removal depending on how advanced
- may need chemo or radio
Stomach:
- surgery
- chemo or radio
Colon:
- surgery
- chemo
59
Peptic ulcers definition
A break in the epithelial cells which penetrates down to the mucosa. Duodenal ulcers are more common. Gastric ulcers are most commonly seen in the lesser curve of the stomach
60
Peptic ulcers aetiology
Helicobacter pylori (gram -ve bacteria)
Aspirin and other NSAIDs
Zollinger-Ellsion syndrome (tumours cause stomach to produce too much acid) -> treatment resistant peptic ulcer disease
61
Peptic ulcers risk factors
Smoking, age
62
Peptic ulcers pathophysiology
Result from an imbalance between factors that can damage the gastroduodenal mucosal lining and defence mechanisms that normally limit the injury
63
Peptic ulcers key presentations
Gastric
- epigastric pain worse one ating, relieve by antacids
Duodenal
- epigastric pain before mals and at night, relieved by eating or milk
64
Peptic ulcers 1st line investigations
H. pylori:
- urea breath test
- stool antigen test
- serology
FBC:
- only if patient seems clinically anaemic or evidence of gastrointestinal bleeding
- microcytic anaemia or high platelet count
65
Peptic ulcers gold standard investigations
Upper GI endoscopy (if suspected bleeding or over 55)
66
Peptic ulcers differential diagnosis
Endoscopy is used for DDx with cancers
| GORD: absence of ulcers on endoscopy
67
Peptic ulcers management
Withdraw NSAIDs
H. pylori negative:
- PPI, H2 antagonists are 2nd line
H. pylori positive:
- PPI and amoxicillin and clarithromycin
68
Peptic ulcers complications
Upper GI bleeding is main
69
Acute appendicitis definition
Sudden inflammaition of the appendix. The appendix is located at McBurney's point which lies 2/3rds of the way from the umbilicus to the anterior superior iliac spine
70
Acute appendicitis epidemiology
Can occur at any age although the highest incidence is 10-20yrs. The most common surgical emergency.
71
Acute appendicitis aetiology
Usually occurs because of an obstruction within the appendix however this obstruction can arise in many different ways
Obstruction of the appendix results in the invasion of gut organisms into the appendix wall. This leads to inflammation, necrosis and eventually perforation
72
Acute appendicitis key presentations
Early pain/discomfort around the unbilicus that migrates to the right iliac fossa. As inflammation progresses, it irritates the peritoneum causing severe localised pain at McBurney's point
73
Acute appendicitis signs and symptoms
Abdominal guarding - tensing of the abdo wall muscles
Tender mass in RIF
Pyrexia
Anorexia
Nausea and vomiting
Rosving's sign - palpation of the left lower quadrant increases pain felt in the right lower quadrant
Moving/coughing causes pain due to peritonism
74
Acute appendicitis 1st line investigations
Bloods: raised WCC, raised CRP and ESR
USS: can detect an inflamed appendix, may show appendiceal mass
Pregnancy test to exclude
Urinalysis to exclude UTI
75
Acute appendicities gold standard investigations
CT - highly sensitive and specific
76
Acute appendicitis management
Appendicetomy - gold standard
| IV antibiotics and fluids pre and post-operatively - metronidazole, cefuroxime
77
Acute appendicitis complications
Perforation
| Adhesions
78
Bowel obstructions definition
A bowel obstruction is an arrest of the onward propulsion of intestinal contents.
Common and can be separated into 3 key types:
- small bowel obstruction (most common - 60-75%)
- large bowel obstruction
- pseudo-bowel obstruction (dilatation of the colon due to an dynamic bowel in the absence of mechanical obstruction)
All can be serious and potentially fatal
79
Bowel obstructions aetiology
Small bowel obstruction:
Adhesions (60%)
- usually due to previous abdo/pelvis surgery
- can be caused by previous abdo infections eg peritonitis
Hernias
- due to intestinal contents being unable to pass through a strangulated loop
Malignancy
Crohn's disease
Large bowel obstruction:
LBOs are generally less common due to wide lumen
Malignancy (90%)
Volvulus
- rotation/twisting of the bowel on its mesenteric axis
- sigmoid colon is the most common place for this to occur
Diverticulitis, Crohn's disease and intussusception (bowel rolls inside itself, almost exclusively in neonates)
Pseudo-bowel obstruction:
Intra-abdominal trauma, post-operstive states eg paralytic ileus, intra-abdominal sepsis, drugs eg opiates, antidepressants, electrolyte imbalances
80
Bowel obstructions pathophysiology
Small bowel obstruction:
Obstruction of the bowel leads to distention above the blockage due to a buildup of fluid and bowel contents
This leads to increased pressure which pushes on the blood vessels within the bowel wall causing them to become compressed
These compressed vessels cannot supply blood resulting in ischaemia and necrosis and eventually perforation
81
Bowel obstructions signs and symptoms
Small bowel obstruction:
Pain: initially colicky then diffuse, pain is higher in the abdomen than LBO. Profuse vomiting following pain (occurs earlier than in LBO)
Abdominal distention: less than with LBO
Tenderness: suggests strangulation/risk of perforation
Constipation: with no passage of gas occurs late in SBO
Bowel sounds: increased (tinkling)
Large bowel obstruction:
Abdominal pain: more constant and diffuse than SBO, usually in lower abdomen
Abdominal distention: much more than SBO
Bowel sounds: normally initially, then increased then silent as no movement
Palpable mass: eg hernia
Vomiting: occurs much later than SBO and may be absent
Constipation: earlier than in SBO
Pseudo bowel obstructions:
Presents identically to LBOs and SBOs dependent on the location
82
Bowel obstructions investigations
Small bowel obstruction:
1st line: abdo x ray
- central gas shadows that completely cross the lumen
- no gas in large bowel
- distended loops proximal to the obstruction
Examinations of hernia orifices and rectum
FBC
Gold standard: non-contrast CT
- accurately localised the obstruction
Large bowel obstruction:
Gold standard: CT
Pseudo-bowel obstruction:
CT scan with IV contrast will show dilatation of colon and exclude mechanical obstruction
83
Bowel obstructions management
Both small and large bowel obstruction:
- aggressive fluid rescusitation
- decompression of the bowel - 'drip and suck' with NG tube and IV fluids
- analgesia and anti-emetics for symptoms
- antibiotics
- surgery to remove obstruction (usually laparotomy
Pseudo-bowel obstruction
Treat underlying cause
84
Diarrhoea definition
Acute diarrhoea = less than 2 weeks
| Chronic diarrhoea = >2weeks
85
Diarrhoea aetiology
Viral (majority)
- children = rotavirus
- adults = norovirus
Bacterial
- campylobacter
- E. coli
- Salmonella
- Shigella (these are associated with bloody diarrhoea)
Parasitic
- Giardia lamblia
Medications
- any associated: quinidine, antibiotics (primary cause or due to C. diff). NSAIDs
May be initial presentation of chronic disease such as IBD< bowel ischaemia
86
Diarrhoea key presentations
Assess dehydration, assess blood or mucus in stool
87
Diarrhoea 1st line investigations
Stool sample for faecal leukocytes if inflammatory diarrhoea is suspected
Faecal lactoferrin for ddx between inflammatory diarrhoea (bacterial colitis, IBD) and non-inflammatory (IBS)
88
Diarrhoea management
Treat underlying cause
- bacterial diarrhoea is normally treated with metronidazole
Oral rehydration therapy
Antiemetics eg metoclopramide
Antimotility agents eg loperamide
89
Diverticulitis definition
Colonic diverticulitis refers to herniation of the mucosa and submucosa through the muscular layer of the colonic wall and may be the result of smooth muscle over-activity.
Diverticular disease may be defined as any clinical state caused by symptoms pertaining to colonic diverticula and includes a wide-ranging spectrum from asymptomatic to severe and complicated disease.
Diverticulitis indicated inflammation of a diverticulum or diverticula and may be caused by infection.
Meckel's Diverticulum: common congenital abnormality, usually asymptomatic
Most common in sigmoid colon
90
Diverticulitis aetiology
Multi-factorial aetiology, low fibre intake, decreased physcial activity, obesity, NSAIDs
91
Diverticulitis pathophysiology
Food may get stuck in diverticula leading to infection, which may lead to inflammation, ischaemia and necrosis and eventually perforation
92
Diverticulitis signs and symptoms
- LLQ (lower left quadrant) abdo pain
- Leukocytes
- Fever
- Guarding in LLQ in acute diverticulitis (tensing of abdo muscles)
93
Diverticulitis 1st line investigations
FBC - polymorphonuclear leukocytosis
| CT scan of abdomen
94
Diverticulitis management
Diverticulitis
- antibiotics - ciprofloxacin, metronidazole
- analgesia and liquid diet
- sugical resection in few cases
Diverticular disease
- high fibre diet and fluids
- laxatives
- surgery
95
Diverticulitis complications
Segmental colitis, lower GI bleeding, infection, abscess, perforation, peritonitis, fistula formation and obstruction
96
Gastritis definition
Defined as the histological presence of gastric mucosal inflammation
Gastropathy is a broader term that encompasses lesion characterised by minimal or no inflammation
97
Gastritis aetiology
H. pylori infection may cause acute and chronic gastritis
Erosive gastritis from NSAID/alcohol or due to bile reflux into stomach from previous gastric surgery or cholecystectomy
Stress gastritis is seen in critically ill patients
Autoimmune gastirits is a diffuse form of mucosal atrophy characterised by auto-antibodies to parietal cells and intrinsic factor
98
Gastritis risk factors
Northern european, H. pylori
99
Gastritis key presentations
Dyspepsia/epigastric discomfort
Nausea,, vomiting and loss of appetite
No suspicious features of malignancy
100
Gastritis 1st line investigations
Helicobacter pylori urea breath test
H. pylori faecal antigen test
FBC - reduced haemoglobin and raised MCV in autoimmune gastirits
Endoscopy and biopsy - evidence of gastric erosions and/or atrophy
101
Gastritis management
H. pylori associated
- PPI, clarithromycin and amoxicillin
Erosive
- stop NSAIDs and/or alcohol
- H2 antagonist or PPI
Autoimmune
- cyanocobalamin (B12 IM)
Bile reflux
- rabeprazole
- roux-en-Y diversion
102
Gastritis complications
Atrophic gastirits
Vitamin B12 deficiency
Peptic ulcer disease
103
Clostridium difficile-assocated disease definition
Infection of the colon caused by Colostridium defficile (gram positive).
Characterised by the inflammation of the colon and formation of pseudomembranes. Pseudomembranous colitis can be used to refer to the disease caused C. diff.
104
C. diff-associated disease epidemiology
Usually a healthcare associated illness
105
C. diff-associated disease aetiology
Occurs in patients whose normal bowel flora has been disrupted by recent antibiotic use.
Common causes: ampicillin, cephalosporins, clindamycin, carbapenems and fluoroquinolones
Transmission in healthcare is likely due to faceal-oral route (hands of healthcare workers)
106
C. diff-associated disease pathophysiology
Incubation period is generally 2-3 days (normally manifests 4-9 days into abs therapy) but may be longer. Clostridium difficile produced toxins A and B.
These cause an inflammatory response in the bowel and cause increased vascular impermeability and pseudomembrane formation.
107
C. diff-associated disease clinical manifestations
Presence of risk factors: abx exposure, old age, hospitalisation or nursing home residence.
Darrhoea: range from loose stools to sever
Abdo pain: may be mold or absent but can be severe
Fever
Abdo tenderness
108
Ischaemic bowel disease definition
Can be classified into 3 main types
- acute mesenteric ischaemic
- chronic mesenteric ischaemia
- ischaemic colitis
Acute and chronic mesenteric ischaemia almost always affect the small bowel, whereas ischaemic colitis affects the large bowel
109
Ischaemic bowel disease aetiology
AMI:
- SMA thrombosis
- SMA embolism (due to AF)
- mesenteric vein thrombosis (typically young patients in a hypercoagulable state)
- non-occlusive disease (poor blood flow, poor cardiac output)
Ischaemic colitis:
- thombosis
- emboli
- low flow states - low CO/arrhythmias
- surgery
- vasculitis
- coagulation disorders
- oral contraceptive pill
- idiopathic
110
Ischaemic bowel disease key presentations
AMI
- classic triad: acute, severe abdo pain, no abdo signs on exam, rapid hypovolaemia
- symptoms are often out of proportion with clinical signs
- AF with severe abdo pain, think AMI
CMI
- very similar in presentation, except symptoms are on a lower level and persist for much longer - 'abdominal angina'
Ischaemic colitis
- sudden onset LIF pain
- passage of bright red blood
- signs of hypovolemic shock
111
Ischaemic bowel disease investigations
AMI
- bloods: persistent metabolic acidosis due to ischaemia, anaemia
- abdo x-ray - rule out bowel obstruction
- laparoscopy - visualise necrosis
- CT/MRI angiography - look at artery blockage but difficult scan to do
Ischaemic colitis
- urgent CT to rule out perforation
- flexible sigmoidoscopy w/biopsy - shows epithelial cell apoptosis
- colonoscopy w/biopsy = GOLD STANDARD - only do after recovery to exclude formation of strictures and confirm healing of mucosa
- barium enema
112
Ischaemic bowel disease manaement
AMI
- fluid resuscitation
- antibiotics - metronidazole, gentamicin
- IV heparin - reduce clotting
- surgery to remove necrotic bowel
Ischaemic colitis
- most patients will be fine with symptomatic treatment
- fluid replacement and antibiotics
113
Ischaemic bowel disease complications
AMI
- sepsis
- peritonitis
Ischaemic colitis
- strictures are common
114
Hernias definition
A hernia is the banormal exit of tissue or an organ through the wall of the cavity in which it normally resides
Inguinal: occurs when abdominal cavity contents enter into the inguinal canal (most common type of hernia)
- indirect (80%) - bowel enters inguinal canal via deep inguinal ring
- direct (20%) - bowel enters inguinal canal 'directly' through a wekness in the posterior wall of the canal, termed Hesselbach's triangle
Femoral: occurs when abdominal viscera or omentum passes through the femoral ring into the femoral cana. Relatively uncommon but have a high rate of strangulation
Umbilical: in adults most are acquired
Incisional: risk of any abdominal surgery
Epigastric: occurs in the upper midline through the linea alba. Mostly occur in middle aged men
Hiatal: protrusion of inta-abdominal contents through an enlarged oesophageal hiatus
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Hernias aetiology
Inguinal: raised inta-abdominal pressure, obesity
Femoral: female, pregnancy, raised inta-abdominal pressure
Umbilical: multiple pregnancies with difficult labor, asicies, obesity
Incisonal: failure of wound to heal after surgery
Epigastric: typically secondary to raised chronic intra-abdominal pressure due to pregnancy, obesity or ascites
Hiatal: age, pregnancy, obesity, ascites
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Hernia presentation
Inguinal: lump in the groin, will initially disappear with minimal pressure or on lying down. If it becomes incarcerated it may become painful, tender and erythematous (red from increased blood flow)
Femoral: small lump in the groin. Usually asymptomatic but may present as an emergency (obstruction or strangulation). Unlikely to be reducible.
Unbilical: bulge at umbilicus
Epigastric: typically asymptomatic but may have epigastric pain as well as bloating, nausea and vomiting after meals
Hiatal: may be associated with reflux, may be vomiting, weight loss
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Hernia diagnosis
Inguinal: normally clinical diagnosis, can do ultrasound. CT needed if obstructed or strangulated
Femoral: usually clinical diagnosis but ultrasound may be needed. CT abdomen pelvis scan
Umbilical: clinical diagnosis
Epigastric: obese patients may need ultrasound
Hiatal: oesophagogastoduodenoscopy is gold standard
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Hernia management
Inguinal: surgical if symptomatic (bowel discomfort)
Femoral: managed surgically within 2 weeks
Umbilical: surgery
Incisional: surgery, recurrence is high in very obese patients
Epigastric: surgical repair
Hiatal: PPIs are first line. Weight loss. Surgery may be needed (Nissen fundoplication)
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Mallory-Weiss tear definition
Characterised by a tear or laceration oftern along ht border of, or near, the gastro-oesophageal junction. The haemorrhage is usually self-limiting.
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Mallory-Weiss tear aetiology
Usuaully occurs after an increase in a sudden rise in the pressure gradient across the gastro-oesophageal junction, such as retching, vomiting, coughing or straining. Alcoholism, gastroenteritis, bulimia and chronic cough are all risk factors.
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Mallory-Weiss tear key presentations
Haematemesis, melaena
General symtpoms of hypovolemic shock
Lightheadedness/dizziness
Postural orthostatic hypotension
Boerhaave syndrome: a more severe tear in the oesophagus. Mackler triad: vomiting, chest pain, subcutaneous emphysema
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Mallory-Weiss tear 1st line investigations
Rockall score (assess blood loss)
FBC - anaemia may occur in some cases
Urea - high in patients with ongoing bleeding
Oesophagogastroduodenoscopy
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Mallory-Weiss tear management
Terlipression + urgent endoscopy
PPI therapy
Natiemetic
Surgical intervention may be needed
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Perinanal disorders definition
Hemorrhoids: haemorrhoidal cushions are normal anatomical structures located within the anal canal. As they enlarge they can potrude outside the anal canal causing symptoms
Perianal fistula: an abnormal connection between the anal canal and the perianal skin. The majority are associated with anorectal abscess formation
Anal fissure: a split in the skin of the distal anal canal characterised by pain on defacation and rectal bleeding
Perianal abscess: a collection of pus in the anal or rectal region. More common in men and have high rates of recurrence
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Perinanal disorders aetiology
Haemorrhoids: excessive straining due to chronic constopation or diarrhoea. Pregnancy or ascites lead to increase intra-abdominal pressure so may be a cause.
Perianal fistula: typically a consequence of perianal abscess. Other risk factors include: inflammatory bowel disease, systemic disease, trauma to the anal region.
Anal fissure: passage of hard stool , pregnancy is a risk factor
Perianal abscess: majority are due to infections of the anal glands. These may become infected when a crypt is occluded by impaction of food matter, by oedema from trauma or from inflmmatory processes such as Crohn's. Common causative organsim include E. coli, Bacteroides spp and enterococcus spp.
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Perianal disorders presentation
Haemorrhoids: rectal bleeding (associated with defecation), perianal pain/discomfort may be as, associated with feeling of incomplete evacuation, anal pruritus, tender palpable perianal lesion, anal mass
Perianal fistula: usually present with recurrent perianal abscesses, discharge onto the perineum including muscus, blood, pus or faeces
Anal fissure: pain on defecation 'like passing broken glass', tearing sensation or passing stool, fresh blood on stool or on paper, anal spasm, symptoms tend to wax and wane
Perianal abscess: perianal swelling and tenderness, low grade fever, anal fistula present, perianal or rectal induration (hardening)
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Perianal disorders diagnosis
Haemorrhoids: anoscopic exam
Perianal fistula: proctoscopy, MRI imaging to visualize the anatomy
Anal fissure: clinical diagnosis (usually no tests needed)
Perianal abscess: anorectal examination (often needs anaesthetic)
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Perianal disorders management
Haemorrhoids: fibre and adequate fluids, topical corticosteroids (hyrdoscortisone), rubber band ligation, surgical hemorrhoidectomy (for more advanced disease)
Perinanal fistula: surgery, antibiotics for any infection
Anal fissure: high fibre diet and fluids, topical glyceryl trinatrate and diltiazem, may need surgery or botulinum injections if resistant
Perianal abscess: surgical drainage of abscess, fistulotomy (if fistula present) broad spectrum abx
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Perianal disorders complications
Haemorrhoids: recurrence or worsening of symptoms, excessive bleeding, non-reducible prolapse and pelvic sepsis (rarely)
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Pilonidal sinus/abscess defintion
A disease of the inter-gluteal region characterised by the formation of a sinus in the left cleft of the buttocks. Most common in males 16-30yrs
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Pilonidal sinus/abscess aetiology
Caused by the forceful insertion of hairs into te skin of the natal cleft in the sacrococcygeal area. This promotes a chronic inflammatory reaction, causing an epithelialized sinus. More common in hirsute (hairy) people
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Pilonidal sinus/abscess presentation
Sacrococcygeal discharge
Sacrococcygeal pain and swelling (particularly on sitting)
Sacrococcygeal sinus tracts seen
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Pilonidal sinus/abscess diagnosis
Clinical diagnosis
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Pilonidal sinus/abscess management
If asymptomatic: hair removal and local hygiene
| Sugical treatment and antibiotics and pain relief
