GI Flashcards

(237 cards)

1
Q

What is Achalasia?

A

Osephageal dysmotility (impaired peristalsis)
-failure of the lower oesophageal sphincter to relax in response to swallowing.
- rate and idiopathic

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2
Q

Symptoms of achalasia?

A

-Non progressive dysphagia (struggle swallowing anything)
-Chesty Substernal pain
-Food regurgitation
-Aspiration pneumonia-food or liquid is breathed into the airways or lungs, instead of being swallowed.
-Weight loss

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3
Q

Investigations to diagnose Achalasia?

A

Barium swallow with “bird beak” appearance of the distal oesophagus
- manometry (measure pressure across LOS) = diagnostic

endoscopy to exclude malignancy anytime there is dysphagia

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4
Q

Complication of Achalasia?

A

May increase risk of oesphageal squamous cell lung cancer

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5
Q

Treatment for Achalasia?

A

There is no cure for achalasia, but treatment can help relieve the symptoms and make swallowing easier.

The pharmalogical agents used are either calcium-channel blockers (i.e., nifedipine, verapamil) or nitrates, taken prior to meals.- while awaiting definitive intervention.

endoscope botox to let los relax and lasts months to years

pneumatic dilatation- Air-inflated balloons are used to apply mechanical stretch to the lower oesophageal sphincter to tear its muscle fibres. Best option if surgery good option.

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6
Q

What is appendicitis?

A

Acute inflamed appendix, usually due to luminal obstruction
SURGICAL EMERGENCY

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7
Q

Epidemiology and risk factors of appendicitis?

A

10-20yrs old
Male
Frequent antibiotic use
Smoking

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8
Q

Causes of appendicitis?

A

Blockages:
- Faecolith (hard mass of stool)
- foreign body
- lymphoid hyperplasia of Peyer’s patches (teens)
- fibrous strictures

Blockage is typically infected with e.coli and as pressure inside appendix increases, so does rupture risk

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9
Q

Mechanisms of pain in appendicitis?

A

Peri umbilical pain: inflammation of appendix and visceral peritoneum irritates autonomic nerves of the embrylogical midgut —> referred pain to the umbilical region

Right iliac fossa: due to localised inflammation of the parietal peritoneum

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10
Q

Classic triad presentation of appendicitis?

A

1) central abdominal pain that migrates to right iliac fossa
2) low-grade pyrexia
3) anorexia

50% of patients present with this characteristic history

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11
Q

Symptoms of appendicitis?

A

1) periumbilical pain that migrated to the right iliac fossa (McBurney’s point) (rebound or percussion tenderness)
2) low grade fever >38°C
3) reduced appetite and anorexia
4) nausea and vomiting

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12
Q

Signs of appendicitis?

A

1) Rosving’s sign (pressing on left Illiac fossa causes right illiac fossa pain to get worse)

2) Psoas sign (pain worsened by lying on left side and extending the right leg)

3) Obturator sign (pain worsened by flexing and internally rotating the hip)

4) elevation of the neutrophil count.

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13
Q

Complications of appendicitis?

A

Perforation (15-20%) - appendiceal rupture
Appendiceal mass
Periappendical abscess

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14
Q

Investigations to diagnose appendicitis?

A

CT abdominal + pelvis = gold standard
Ab ultrasound
Pregnancy test to rule out ectopic pregnancy ( presents with right iliac fossa pain)

FBC (high neutrophil)
CRP (elevated)

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15
Q

Treatment for appendicitis?

A

-Antibiotics and then appendectomy (laproscopic)
-Must drain abcesses - resistant to antibiotics

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16
Q

Why must abscess be drained in appendicitis?

A

Abscess = walled off bacterial collection
-Resistant to systemic antibiotics so not useful
-Needs to be directly dealt with
- drainage + intra abscess antibiotic

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17
Q

What is ischemic colitis?

A

Ischemia of colonic arterial supply
- colon gets inflamed due to hypoperfusion

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18
Q

Causes of ischemic colitis?

A

Affecting inferior mesenteric artery;
- thrombosis (+/- atherosclerosis) = most common
- emboli
- decreased CO + arrhythmias (eg history of AF) or due to shock
- combined oral contraceptive pill

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19
Q

Most common sites affected with ischemic colitis?

A

Watershed areas
- splenic flexure (most common)
- sigmoid colon + cecum

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20
Q

Symptoms of ischeamic colitis?

A

LLQ pain + bright bloody stool
+/- signs of hypovolemic shock

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21
Q

Investigations to diagnose ischemic colitis?

A

Colonoscopy + biopsy = gold standard
(Only after patient is fully recovered, prevents stricture formation + normal healing)
(first rule out other causes- eg. Stool sample for h pylori)

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22
Q

Complications of ischemic colitis?

A
  • perforation
  • tissue death
  • strictures (therefore obstruction)
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23
Q

Treatment for ischeamic colitis?

A

If just symptomatic- IV fluids + antibiotics (prophylactic)
If gangrenous (infected colon)- only SURGERY

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24
Q

What is mesenteric ischemia?

A

Ischemia of small intestine

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25
Two types of mesenteric ischemia?
AMI- acute attack “abdominal MI” CMI- chronic and over a longer period of months “abdominal angina”
26
Causes of mesenteric ischemia?
Affecting superior mesenteric artery - Thrombosis (most common) - Emboli (due to AF often)
27
Symptoms of mesenteric ischemia?
Triad: 1) central/ RIF acute severe abdo pain 2) no abdo signs on exam (eg. Guarding, rebound tenderness) 3) rapid hypovolemic shock
28
Investigations to diagnose mesenteric ischemia?
CT angiogram FBC+ABG = persistant metabolic acidosis
29
Complication of mesenteric ischemia?
SBP (spontaneous bacterial peritonitis)
30
Treatment of mesenteric ischemia?
Fluid resuscitation Antibiotics IV heparin ( decrease thromboemboli) —> infarcted bowel is treated by surgery
31
What are colorectal polyps vs adenomas?
Polyps = small growths on the inner lining of the colon => very common Adenomas = type of polyp that may become cancerous => precursor - mostly spontaneous and benign - common with age
32
Risk factors for colorectal polyps and cancer?
-Familial inherited genetic predisposition -Adenomas/ polyps -Alcohol, smoking, ulcerative colitis
33
2 inherited conditions that massively increase the risk of polyps
1) familial adenomatous polyposis (FAP) - Auto dom APC gene mutation - causes 1000s of duodenal polyps - inevitably will get colorectal cancer (93% risk by 50) 2) hereditary non polyposis colon cancer (HNP C-Lynch syndrome) - auto dom MSH-1 mutation (or MSH-2) - a DNA mismatch repair gene -Rapidly increases progression adenomas-> carcinoma -MSH2 gene mutation is incorrect. This mutation is one of the mutations associated with Lynch syndrome (hereditary non-polyposis colorectal cancer), which predisposes individuals to colorectal cancer and other malignancies. Lynch syndrome typically does not present with the extensive polyposis seen in FAP.
34
Common metastases of colon polyps/adenomas?
Liver and Lung
35
Symptoms of colorectal polyps/adenomas?
Mostly in distal colon (from sigmoid onwards) => LLQ pain, bloody mucosy stools (fresh blood because in the distal colon closer to the anus) Tenesmus (if rectal involvement) - a frequent urge to go to the bathroom without being able to go. It usually affects your bowels
36
Investigations to diagnose colorectal polyps/adenomas?
FIT test (fecal occult) - screening for microscopic blood in poop - done in all 60+ with Fe deficient anaemia and change in bowel habits Gold standard= colonoscopy and biopsy Patients with a +ve FIT and suspected colorectal cancer get referred for colonoscopy/biopsy within 2 weeks
37
How are colorectal polyps/adenomas classified?
TNM system - Tumour, Node, Metastasis. T describes the size of the tumour. N describes whether there are any cancer cells in the lymph nodes. M describes whether the cancer has spread to a different part of the body.
38
Treatment for colorectal adenomas/polyps cancer?
Surgery and chemo is the only curative option if there are no metastases
39
What are gastric carcinomas?
Mostly adenocarcinomas
40
Grading of gastric carcinomas?
T1 = well differentiated = better prognosis (mc) T2 = undifferentiated “signet ring carcinomas” typically at proximal stomach = worse prognosis
41
Causes of gastric carcinomas
H.pylori Smoking CDH-1 mutation cashed in gene= 80% risk Family history Pernicious anemia (autoimmune chronic gastritis)
42
Symptoms of gastric carcinomas?
Severe epigastric pain (Same as gastritis, but worse) Anemia (Fe deffieciency, occult loss) - weight loss - Tired all the time - progressive dysphagia Metastatic signs: -jaundice due to liver metastases -krukenberg tumour due to ovarian metastases from gastric cancer
43
Investigations to diagnose gastric carcinomas?
Gastroscopy+ biopsy CT\mri for staging, PET to iD metastases Staging= TNM
44
Treatment for gastric carcinomas?
Surgery + “ECF” chemo regimen, if resectable E – epirubicin (eh-pee-roo-bih-sin) C – cisplatin (sis-pla-tin) F – fluorouracil (floor-oh-yoor-uh-sil)
45
Two types of esophageal cancer?
Adenocarcinoma Squamous cell carcinoma
46
Adenocarcinoma location and association?
Lower 2/3 of oesophagus Associated with Barrett’s oesophagus
47
Squamous cell carcinoma location and association?
Upper 2/3 esophagus Smoking and alcohol
48
Symptoms of oesophageal cancers?⏰
Presents when advanced ALARMS Anemia Loss of weight Anorexic Recent sudden symptom worsening Melaena/Haematemesis Swallowing progressive difficulty
49
Key symptom of esophageal cancer and differential diagnosis?
Progressive swallowing difficulty - first hard to swallow potatoes, now it’s hard to swallow soup If it’s non progressive it could be achalasia
50
Investigations to diagnose esophageal cancer
OGD (oesophago-gastro-duodenoscopy) + biopsy with barium swallow CT/PET for staging
51
Treatment for esophageal cancer?
Medically fit = chemo/radio + surgery Unfit = palliative
52
Chance of small intestine carcinomas?
Small intestine is pretty tumour resistant so decreased chance of tumour here 1% of all GI tumours Most are adenocarcinomas
53
Risk factors of small intestine carcinomas
Chronic SI disease: -Chron’s -Coeliac’s
54
Diagnosis and treatment of small intestine carcinoma?
Same as gastric carcinomas
55
What is Coeliac’s?
Systemic autoimmune T4 hypersensitivity to gluten that effects the small intestine
56
Pathophysiology of Coeliac’s
-Pathogenic component of gluten = gliadin -Once absorbed, it is deamidated by tissue transglutaminase (tTG) -In coeliacs, deamidated peptides are presented by antigen-presenting cells via HLA DQ2 or DQ8 to T helper cells to trigger immune response. -Immune activation —> villous atrophy, lymphocyte accumulation and intestinal crypt hyperplasia —> malabsorption
57
Risk factors for Coeliacs
Family history HLA-DQ2.5 / 2 and HLA-DQ8 Autoimmunity (thyroid disorders + addisons) IgA deficiency Down’s syndrome Turner’s syndrome
58
Signs and symptoms of coeliacs
Indigestion Diarrhoea or steatorrhoea Bloating and/or constipation Weight loss and fatigue Unexplained iron, vit b12 or folate deficiency IBS in adults Dermatitis herpetiformis- vesicular itchy rash that occurs due to IgA deposition along the dermal papillae
59
Investigations to diagnose coeliacs
*If possible patients should be on a gluten containing diet for 6 weeks prior to investigations* Screening: 1st line: serological test for IgA antibodies against tTG (anti-tTG) - total IgA must also be measured as may get false -ve in IgA deficient patients 2nd line: endomysial antibodies (IgA) if anti-tTG is weakly positive Diagnostic: gold standard Duodenal biopsy for all patients with positive serology Findings: crypt hyperplasia, villous atrophy, intraepithelial lymphocyte infiltration
60
Treatment for coeliacs
Gluten-free diet Avoid : wheat, rye, barley sometimes oats -Rice, potatoes and corn are gluten free -Replace vitamins and mineral’s deficiency if needed -Offer pneumococcal vaccination with boosters every 5 years
61
Complications of coeliacs
Dermatitis herpetiformis Malignancy Increased risk of osteoporosis Calcium and vit D deficiency
62
Differential diagnosis with coeliacsand treatment for it?
Sprue or tropical sprue (associated with tropical travel) = malabsorption syndrome -Similar biopsy to coeliacs- crypt hyperplasia and villous atrophy -Treatment = often antibiotics eg tetracycline
63
Types of diarrhoea?
- watery - secretory - osmotic - functional (IBS) - steatorrhoea - inflammatory
64
What is diarrhoea?
A presenting symptom with many differential diagnoses Classed as 3+ watery stools daily which are level 5-7 on Bristol stool chart
65
What is bloody diarrhoea?
Dysentery Eg. Amoebic dysentery E.coli + salmonella + shigella
66
Levels of diarrhoea?
Acute < 14 days Subacute 14-28 days Chronic > 28 days
67
Causes of diarrhoea?
IBD (Crohn’s, UC) Coeliac disease Hyperthyroidism Inflammation or malignancy Infective causes
68
Infective causes of diarrhoea?
Viral = most common - rotavirus (kids <3y) - norovirus (adult) Bacterial: - campylobacter (most common bacterial cause) - c. Diff - salmonella - shigella - cholera - E.coli Worms Parasites- Giardiasis (most common parasite cause)
69
Antibiotics as a cause of diarrhoea?
They increase the risk of C. Diff infection 4C’s - clindamycin, co-amoxiclav, ciprofloxacin, cephalosporins
70
Treatment of diarrhoea?
Depends on underlying cause Viral (mc) = self limiting Fluids and dioralyte to rehydrate patient
71
Complications of diarrhoea?
Dehydration Electrolyte loss
72
What is diverticular disease?
-Outpouching of colonic mucosa -Most frequently affects the sigmoid due to its small diameter -due to increased intra-colonic pressure at naturally weaker parts of the colon, where penetrating arteries enter wall of the colon
73
Define diverticulum
An outpouching at perforating artery sites
74
Define diverticulosis
An asymptomatic outpouching
75
Define diverticular disease?
A symptomatic outpouching
76
Define diverticulitis
Inflammation of outpouching - infection
77
What percentage of diverticula are asymptomatic?
95% and only 5% are symptomatic (diverticular disease)
78
What is Meckel’s diverticulum?
Paediatric disorder -Failure if obliteration of vitelline duct -Rule of 2s: 2 years old 2 inches long 2ft from ileocaecal valve (umbilical) Diagnostic= technetium scam
79
Risk factors for diverticular disease?
Connective tissue disorders (ED + M) Ageing Increased colon pressure COPD + chronic cough Age
80
Complications of diverticulitis?
SBP- Spontaneous Bacterial Peritonitis Obstruction Fistulae
81
Symptoms of diverticulitis?
1) Left lower quadrant pain 2) constipation 3) fresh rectal bleeding
82
Investigations to diagnose diverticulitis?
CT abdominal/ pelvis with contrast = gold standard
83
Treatment for diverticulosis?
Nothing, watch and wait
84
Treatment for diverticular disease
Bulk forming laxatives “isphagula husk” Surgery is gold standard
85
Treatment for diverticulitis
Antibiotics (Co amoxiclav) Paracetamol IV Fluid + liquid food Rarely surgery
86
What is dyspepsia?
Not a disease A presenting symptom of “indigestion”
87
Signs of dyspepsia?
-early satiation -epigastric pain + reflux (GORD like pain) -extreme fullness
88
Cause of dyspepsia?
Often unknown (“Functional disorder”) Maybe related to ulcers (especially gastric)
89
Diagnosis of dyspepsia?
Need endoscopy to find underlying cause
90
What is gastritis?
Mucosal inflammation and injury
91
Causes of gastritis
Autoimmune (related to pernicious anaemia + anti intrinsic factor antibodies) H. Pylori NSAIDs (causes gastropathy- injury without inflammation) Mucosal ischaemia Campylobacter (GBS) + viral (CMV)
92
Symptoms of gastritis?
Epigastric pain with diarrhoea Nausea and vomiting Indigestion
93
What is PUD (Peptic ulcer disease) a complication of?
Gastritis Peptic ulcer disease (PUD) is characterized by discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin.
94
Investigations to diagnose gastritis?
If H.pylori suspected: - stool antigen test/ urea breath test Gold standard= endoscopy + biopsy
95
Treatment for gastritis/h. pylori?
H. Pylori = triple therapy CAP Clarithromycin Amoxicillin PPI
96
Pathophysiology of H.Pylori?
Commences in stomach- not usually diarrhoea causing - Decreased virulence and is typically opportunistic 1) decreases stomatostatin 2) decreases luminal HCO3 3) secretes urease 4) inscreases gastrin release Urea —urease—> CO2 + NH3 NH3 + N+ —reversible—> NH4+ (toxic)
97
What is autoimmune gastritis?
Affects fundal portion of the stomach Especially causes atrophy of parietal cells
98
What kindof bacteria is C.difficile?
Gram +ve spore forming bacteria
99
What is C.difficile mainly induced by?
Ciprofloxacin Co-amoxiclav Cephalosporins Clindamycin 4 Cs
100
What does C. difficile cause and how?
Pseudomembranous colitis - normal GIT flora killed by antibiotics and C.diff replaces these - results in dangerous severe diarrhoea ( very watery so increased dehydration) and is highly infectious
101
Treatment for C.difficile?
Stop using these 4 antibiotics ( ciprofloxacin, Co-amoxiclav, cephalosporins, clindamycin) => give Vancomycin (now first line according to nice)
102
What is E.Coli?
Major player in UTIs also Gram -ve bacterialbacilli Often commensal flora of GIT Some strains/ “serotypes” are very virulent
103
Strains of E.coli that lead to watery diarrhoea?
ETEC EAEC EPEC
104
Strains of E.coli that lead to bloody diarrhoea?
EHEC
105
Cause of haemolytic uremic syndrome?
Serotype 0157:H7 of E.coli Leads to haemorrhagic diarrhoea Nephrotic syndrome
106
Treatment of E.coli?
Often amoxicillin, trimethoprim, nitrofurantoin
107
What is H.pylori?
Gram -ve bacteriabacillus Has a decreased virulence in the GIT
108
Pathology of H.pylori?
1) causes decreased stomatostatin 2) increased luminal gastric acid (as more gastrin) 3) urease results in ammonia generation 4) therefore decreased HCO3- secretion
109
Complications of h.pylori?
-PUD- Peptic ulcer disease -gastritis -gastric carcinomas
110
Investigations to diagnose H.Pylori?
Biopsy (Stool antigen + C-urea breath test often 1st line)
111
Treatment for H.pylori?
Triple therapy: Clarythromycin + amoxicillin + PPI
112
What is GORD
Gastric-oesophageal reflux disease = reflux of gastric contents into oesophagus due to decreased pressure across lower oesophageal sphincter
113
Causes of GORD
- raised intragastric pressure= obesity + pregnancy - hiatal hernia (mostly with LOS sliding up through diaphragm) - Drugs anti-muscarinics, CCBs - Scleroderma (LOS = scarred)
114
Symptoms of GORD
“Heartburn” -Retrosternal burning chest pain that is exacerbated by lying flat -Sour/bitter taste of acid in the back of the mouth -dysphagia -nausea -chronic cough
115
Investigations to diagnose GORD
If no red flags go straight to treatment (PPI) Red flags (dysphagia, haematemesis, weight loss) - endoscopy —> esophagitis or Barrett’s - esophageal manometry —> measure functionality of LOS and gastric acid pH
116
Treatment for GORD
-Conservative lifestyle changes (smaller meals, 3+hrs before bed, avoidance of trigger foods) -medication review: consider reducing or stoppping medications that are causing symptoms eg CCB -PPI offer full dose for 1-2 months If symptoms persists use PPI at lowest dose possible as maintenance If symptoms still persist or CI then use H2RA
117
Last resort for GORD treatment?
Surgical treatment- laparoscopic fundoplication = mobilisation of fundus of stomach which is then wrapped around the lower oesophageal sphincter to tighten it
118
Complications of GORD
-Barrett’s oesophagus -oesophageal stricture - fibrous scarring and therefore narrowing of oesophageal lumen -dental problems
119
Barrett’s oesophagus
-10-15% develop Barrett’s -Always involves hiatal hernia -Metaplasia (SSNKE —>simple columnar) -Increased risk of adenocarcinoma -Diagnose with a Biopsy Pathway for oesphagus changes: Normal—> metaplasia (Barrett’s) —> dysplasia (adenocarcinoma)
120
What is IBS?
Chronic, relapsing and often lifelong disorder that affects lower GI tract - no discernible structure or biochemical cause => considered ‘functional’
121
Cause of IBS
Multi factorial Genetics + environmental + psychological (stress, anxiety) + dietary Exact mechanism unknown
122
Categorisation of IBS
IBS-C —> mostly constipation IBS-D —> mostly diarrhoea IBS-M —> mostly mixed; alternating C/D
123
Risk factors of IBS
Young adults Females Family history Dietary factors Psychosocial cavities Drugs
124
Symptoms of IBS
-Abdominal pain and bloating relieved from defecation -Altered stool form/frequency
125
Diagnosis to exclude before diagnosing IBS
Coeliacs (serology) IBD (check fecal calprotectin) Infections (ESR/CRP/Blood cultures)
126
Investigations to diagnose IBS
IBS is a diagnosis of exclusion so no specific investigation to confirm diagnosis May use following to exclude other conditions: - FBC - ESR/CRP - coeliac serology
127
Treatment for IBS
1st line: conservative patient education, dietary advice and patient reassurance, address any cormorbid stress or anxiety For IBS-C consider more fibre and for IBS-D consider probiotics 2nd line: IBS-C —> laxatives (senna/Fybogel) IBS-D —> antimotility drug (loperamide) 3rd line: For severe abdominal pain consider low-dose trycyclic antidepressant (TCA eg amitriptyline) - consider CBT for psychological support - refer to gastroenterologist
128
Complications of IBS
Mood disorders: more severe and frequent depression and anxiety Poor quality of life: miss three times as many days off work
129
What does inflammatory bowel disease comprise of? (IBD)
Ulcerative colitis Crohn’s disease
130
Pathophysiology of IBD?
Inflamed intestines Associated with HLAB27 (Seronegative spondyloarthropathy) Has a Bimodal age distribution (15-20, 55+)
131
Extraintestinal manifestations of both Crohn’s and Ulcerative Colitis
Eyes: Episcleritis = chrons> Uveitis = UC> Cutaneous: Erythema nodosum Pyoderma gangrenosum Musculoskeletal: Arthritis (most common manifestation in both) Spondylarthritis “spine ache” Osteoporosis Clubbing Also 90% of UC patients have PSC but also sometimes present in patients with Chron’s Primary sclerosing cholangitis (PSC) is a chronic liver disease in which the bile ducts inside and outside the liver become inflamed and scarred, and are eventually narrowed or blocked. When the bile ducts are narrowed or blocked, bile builds up in the liver and causes further liver damage.
132
How to differentiate UC from Crohn’s particularly in the pediatric population?
Serum antibody markers: - pANCA more associated with UC - ASCA more associated with Crohn’s
133
How to differentiate IBD from IBS?
Faecal calprotectin Raised in IBD and not IBS
134
Cause of Crohn’s disease?
Environmental and genetic - CARD15/NOD2 mutation => strong genetic component - bacteria trigger an immune mediated response (t-cells)
135
What part of the gut does Crohn’s disease affect?
Whole gut Especially terminal ileum and proximal colon (usually rectum is spared) Throat to anus
136
Risk factors for Crohn’s
Family history Jewish HLA-B27 gene Smoking (2x as likely) Caucasian
137
Pathophysiology of Crohn’s
-Characterised by skip lesions (lesions with gaps in between) arising anywhere between the mouth and the anus -End result is transmural inflammation (in all layers) with granuloma formation => resulting in fistulas, strictures and adhesions
138
Signs and symptoms of Crohn’s disease?
-Diarrhoea- most significant symptom in adults -Abdominal pain- most significant symptom in kids -Gallstones and kidney stones -Weight loss and lethargy -B12/folate/ Fe deficiency due to malabsorption in small intestine -Apthous mouth ulcers
139
Investigations to diagnose Crohn’s
-Feacal calprotectein = raised (inflammation in GI tract + differentiates IBD from IBS) -FBC -CRP/ESR -U&Es -Colonoscopy = skip lesions, cobblestone mucosa, deep ulcers -Biopsy = transmural inflammation, granulomas and goblet cells
140
General management tips for Crohn’s
-Smoking cessation advice = crucial -Some evidence that NSAIDs and/or combined oral contraceptive pill can increase risk of relapse
141
Treatment given to induce remission in mild and moderate Crohn’s
Elemental diet (alone or with meds, particularly in young people) Mild Crohn’s: FIRST LINE : glucocorticoids (PO predinsolone or IV hydrocortisone) SECOND LINE: aminosalicylate (eg mesalazine) Moderate Crohn’s: Add in: FIRST LINE: azathioprine or mercaptopurine SECOND LINE: Methotrexate
142
Treatment for severe Crohn’s to induce remission that is unresponsive to conventional therapy
Infliximab or adalimumab as monotherapy or combined with other immunosuppressant
143
Treatment for Crohn’s if it is refractory to medical therapy or disease limited to the distal ileum to induce remission
Surgery
144
How to classify severity of Crohn’s
Mild: - first prevention or - 1 exacerbation in 12 months Moderate: - >= exacerbations in 12 months or - glucocorticoid cannot be tapered for management of mild disease Severe: - unresponsive to conventional therapy AND - >= symptoms eg weight loss, fever, severe abdominal pains - usually >3 loose stools per day
145
How to maintain remission in Crohn’s
1st line: azathioprine or metcaptopurine 2nd line: Methotrexate Post surgery: consider azathioprine with or without methotrexate
146
Frequency of surgery in Crohns patients?
Approx 80% of patients with Crohn’s will require surgery but this is not curative as entire bowel can be affected. By removing ‘x’, ‘y’ can flare up.
147
Complications of Crohn’s
Peri-anal abscess Anal fissure Anal fistula Strictures and obstruction
148
Location of ulcerative colitis
COLON ONLY start at rectum—> sigmoid colon—> proximal colon Never proximally beyond illeocaecal valve Doesn’t affect the anus
149
Aetiology of ulcerative colitis
Not well understood Autoimmune colitis associated with HLA B27 gene Involves polygenic predisposition and env factors
150
Risk factors for ulcerative colitis
Family history HLA b27 Caucasian Non-smokers Bimodal age distribution 15-25 and 55-70yrs
151
Symptoms of ulcerative colitis
-Abdominal pain in left lower quadrant -Urgency and tenesmus (pain on defecation) -Bloody mucosy watery diarrhoea
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Investigations to diagnose ulcerative colitis
-Increase in feacal calprotectin -pANCA +ve -FBCs -CSR\ESR - colonoscopy = continuous, “leadpipe sign” - biopsy = raw/red mucosal with widespread shallow ulceration with crypt abscesses and goblet cell depletion
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How is disease activity measured in ulcerative colitis patients?
Truelove and Witt’s severity index -how many bowel movements, blood?, HR, pyrexial?, anaemic?, esr?
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Treatment for ulcerative colitis to induce remission
Generally: First line: topical ASAs -acetylsalicylic acid Second line: Add high-dose oral ASA Third line: Add topical or oral corticosteroid For acute severe colitis admit into hospital and start iV corticosteroids Add ciclosprin if no improvement in 72hr Still no improvement consider surgery
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Treatment for maintenance of remission of ulcerative colitis
Low maintenance dose of ASA-aspirin
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Surgery with ulcerative colitis?
Total/partial colectomy is often curative
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Complications of ulcerative colitis
Toxic megacolon is the most common complication cause ulcerative colitis deaths
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Investigations to diagnose both types of intestinal obstruction?
1st line- X-Ray = shouldn’t be used however might be your exam answer according to lecturer but he is trying to get exam boards to change it💀💀 Gold standard = CT abdomen and pelvis with contrast, and is now often used as initial imaging modality where possible - can idenitify dilated bowel loops, evidence of ischaemia and perforation as well as underlying cause
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What is a pseudo obstruction?
No mechanical obstruction, often a result of post operative state -still have symptoms of intestinal obstruction
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Treatment for intestinal obstruction?
pain: analgesia assess food balance: nasogastric tube, urinary catheter resuscitate: iv fluids alleviate nausea: nasogastric tube, select antiemetics nutrition: if > 5 days without intake, may need parenteral feed Most patients are two days without food before admission
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Two types of intestinal obstruction?
Small Bowel Large Bowel
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Causes of intraluminal obstruction?
-tumour - carcinoma - lymphoma - diaphragm disease (becoming more common due to NSAIDs) - meconium Ileus - a baby's first stool (feces), called meconium, is blocking the last part of the baby's small intestine - gallstone disease
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Causes of intramural obstruction?
- inflammatory - Chron’s disease - diverticulitis - tumours - neural - Hirschsprung’s disease
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Causes of extraluminal obstruction?
- adhesions - volvulus - tumour - peritoneal deposits
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Percentage of intestinal obstruction cases that involve large bowel?
25-40% of all cases
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Causes of large bowel obstruction?
Malignancy (90%) Volvulus- mostly sigmoid colon, children Intussusception (bowel telescopes in on itself -> most common in children)
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Symptoms of large bowel obstruction?
First constipation Then vomiting Gross distension + pain Hyperactive, then normal, then absent bowel sounds
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Percentage of intestinal obstruction that is small bowel?
60-75% of all cases
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Causes of small bowel obstruction?
Adhesions (most common) 50% Hernias 15% Cancer 10% Crohn’s
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Symptoms of intestinal obstruction?
Vomiting then constipations Mild abdominal distension + pain Tinkeling bowel sounds (*hyperresonant bowels on percussion in both types of intestinal obstruction)
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What is small bowel obstruction?
A form of intestinal failure causing malabsorption requiring iV supplementation or replacement
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Presenting history of small bowel obstruction?
-Pain in umbilical region that comes in waves = colic -Bilious vomiting (dark green) - bloating/ distension - when did they last eat and drink?
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What to assess in a patient with potential small bowel obstruction?
- hydration status - weight loss - pulse/bp - O2 stats - scars - abdominal distension - abdominal tenderness - Hernia orifices - PR exam
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Investigations to diagnose small bowel obstruction?
Full blood count Urea and electrolytes Lactate C-reactive protein CT SCAN = 🔑 NOT X RAY
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Why use a CT scan for suspected small bowel obstruction?
3D representation of problem Localises site of obstruction Indicates cause Tells you if bowel is ischaemic: - poor enhancement - free fluid - twisted mesentery
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How to treat patients with Small bowel obstruction due to adhesions?
Gastrograffin Challenge = administer soluble contrast and do x-ray to assess if operation needed ischaemia/shock= resuscitate and operate non operative management for up to 3 days gastrografin challenge
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How to treat small bowel obstruction due to hernia?
Groin or umbilical - operate (almost always groin- ie. femoral) High risk patient- Taxis (local anaesthesia and push back in) High BMI- conservative measures Incisional hernia- treat as adhesive SBO
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Types of operation given for small bowel obstruction?
-Key hole or open -divide scar tissue -risk of future scar formation -minimally invasive surgery can help
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Most common complication of small bowel obstruction?
Renal failure
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When would you advise surgery in adhesive SBO?
Signs of ischemia on a CT scan
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Differential diagnosis for MWT?
Boerhaave’s syndrome -spontaneous perforation of the oesophagus -usually due to vomiting -ruptures all the layers of the oesophageal wall (transmural) -unlike MWT it’s a surgical emergency
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Risk factors of a Mallory Weiss Tear?
-Any condition that predisposes to retching or vomiting: gastroenteritis, bulimia, hyperemesis - Alcoholism - chronic cough - hiatus hernia - GORD - Male - age 40-60
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What if a patient has haematemesis and pulmonary hypertension?
oesophageal varices rupture
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Symptoms of MWT
Background of alcohol excess presenting with episodes of violent retching or vomiting - Haematemesis (Usually small to moderate volume of bright red blood which is self limiting) - hypotensive in severe cases but unlikely
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Investigations to diagnose MWT
Upper GI endoscopy (gold standard) required for all patients depending on the Glasgow Blatchford score - usuallay shows a single longitudinal tear (can be multiple) in the mucosa at the gastro-oesophageal junction
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Scoring system for upper GI bleeds
Glasgow Blatchford Score Score >0 means patient require admission for inpatient endoscopy Score 0 means patient can be discharged Most accurate in identifying risk patients in need of transfusion
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What is the Rockall score?
Calculated after endoscopy to identify patients at risk of adverse outcomes after treatment for an upper GI bleed
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Treatment for MWT
Most spontaneously heal within 24h!
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What is Mallory Weiss Tear?
Linear lower oesophageal mucosal tear due to sudden increase in intra-abdominal pressure at the border of the gastro-oesophageal junction Limited to mucosa and submucosa
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Typical presentation of Mallory-Weiss Tear?
Presents typically as a young male with acute history of retching and vomiting after a night out eventually causing haematemesis Causes a laceration resulting in an upper GI bleed that is usually self-limiting.
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Location of Duodenal ulcers?
-Mostly at D1 and sometimes D2 -The gastroduodenal artery is located at the posteromedial aspect of D2 so deeply penetrating ulcers in this region can result in a torrential upper GI bleed
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Causes of duodenal ulcers
H. Pylori (causes 95% of duodenal ulcers) NSAIDS ZE Syndrome
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Symptoms of duodenal ulcers
Epigastric pain - worse between meals - better with food * typically weight gain
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Investigations to diagnose duodenal ulcers
If no red flags: - non-invasive testing 1. Urea breath test 2. Stool antigen test If red flags: Urgent endoscopy + biopsy (Will see Brunner’s gland hypertrophy- more mucous production)
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What do you have to make sure of before testing for H.pylori?
If testing for h.pylori, patient must be off PPI for 2 weeks+ (all ulcers) - otherwise you can get a false -ve
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Treatment for both gastric and peptic ulcers?
Stop NSAIDs 1) H.pylori +ve -> triple therapy CAP Clarythromycin Amoxicillin PPI (omeprazole) (If they have a penicillin allergy replace amoxicillin with metronidazole) 2) H.Pylori -ve give PPI at initial high dose for a month until ulcer healed Ensure all patients who have a proven ulcer have a repeat endoscopy 6-8 weeks later to confirm healing as well as h.pylori retesting
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What type of peptic ulcer is more common?
Gastric>Duodenal Gastric is 2/3x more common
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What are peptic ulcer diseases?
Punched out round holes in either stomach or stomach or duodenum
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Where do gastric ulcers occur
Mostly at a lesser curve
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Causes of gastric ulcers
-H.pylori (causes of 75% of gastric ulcers) -NSAIDs -Zolinger Ellison syndrome: - pancreatic tumour - gastric acid hypersecretion - widespread peptic ulcers
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Symptoms of gastric ulcers
Epigastric pain - worse on eating - better between meals + with antacids * typically weight loss
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Investigations to diagnose gastric ulcers
If no red flags (55+, haematemesis/melaena, anaemia, dysphasia) - non invasive tests: c-urea breath test Stool antigen test If red flags - urgent endoscopy + biopsy
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Complications of peptic ulcer disease
-Bleeding -Perforation: life threatening as ulcer penetrates the duodenum or stomach into the peritoneal cavity; requires surgical intervention -Gastric outlet obstruction: caused by obstruction at pylorus due to an ulcer and subsequently scarring. Presents with vomiting and nausea after food
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What is an anal fissure?
Tear in anal skin lining below dentate line => very painful due to strong sensory supply
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Most common causes of anal fissure?
Hard feaces
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Other less common causes of anal fissures?
Trauma (eg childbirth) Crohn’s UC
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Symptoms of anal fissures?
-Extreme defecation pain -very itchy bum (pruritus ani) -anal bleeding
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Treatment for anal fissures?
Stool softening (increase fibre intake + more fluids) Topical creams (lidocaine ointment) Definitive treatment=surgery (not usually done)
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What is an anal fistula?
Abnormal “tracks” form between inside of anus —> elsewhere Eg subcutaneous skin (mostly)
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What does an anal fistula typically progress from?
= Perianal abscesses - abscess discharges (toxic substances) which aid fistula formation as abscess grows (Also Crohn’s and rectal cancer)
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Symptoms of anal fistulas?
Bloody/ mucosy discharge Often very viable and painful
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Treatment for anal fistula?
Surgical removal + drainage (with antibiotics if infected)
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What are haemorrhoids?
Swollen veins around anus disrupt anal cushions - parts of the anal cushions prolapse through tight anal passage (Google pics at ur own discretion 🤮)
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Most common cause of haemorrhoids?
- Constipation with increase straining - also anal sex
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2 types of haemorrhoids?
1) internal - originate above internal rectal plexus (dentate line) - less painful as has decreased sensory supply - may feel “incomplete emptying” 2) external haemrrhoids - originate below dentate line - so painful patients can’t sit down!
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Symptom of haemorrhoids?
-Bright red flesh PR bleeding and mucosy bloody stool -bulging pain +/- pruritas ani (itchy bum)
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Investigations to diagnose haemorrhoids?
External haemorrhoids = PR exam (digital) - may be visible though Internal haemorrhoids = proctoscopy
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Treatment for haemorrhoids?
Stool softener Definitive= rubber band ligation
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What is a perianal abscess?
Walled off collections of stool + bacteria around anus
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Most common cause of perianal abscess?
Anal sex causing anal gland infection
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Symptoms of perianal abscess?
Pus in stool + constant pain (tender)
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Treatment for perianal abscess?
Surgical removal + drainage if walled off and resistant to oral antibiotic therapy
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In which people are pilonidal sinus and abscess commonly seen in?
In very hairy people (eg Asians)
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Symptoms of pilondial sinus and abscesses?
Swollen pus filled smelly abscess on bum crack (Visible on exam)
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Treatment for pilondial sinus / abscess?
Surgery + hygiene advice
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What’s Meleana?
Blood in the stool that appears black
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Likely causes of GI bleeding?
Peptic ulcer= most common (50%) Osephageal varices Mallory-Weiss syndrome Gastric carcinoma (uncommon)
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How to manage patients with GI bleeds?
A B C - iv fluids, blood transfusion? D - AVPU, GCS, pupils, blood sugar E - active, melaena, haematemesis keep patient nil by mouth
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How to differentiate between variceal and non-variceal bleed?
Variceal bleed= Suspect in patients with a history of liver - disease or alcohol excess. Antibiotics and Terlipressin reduce mortality. Endoscopy within 12 hours. Non-variceal bleed Suspect in patients with a history of peptic ulcers, using certain medications; NSAIDs, anticoagulation or antiplatelets. Consider proton pump inhibitors. Endoscopy within 24 hours.
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What is most important when it comes to GI bleeding?
Initial assessment and management rather than endoscopy in most cases
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In the UK how often do you see upper GI bleeding?
Nearly one presentation every 6 minutes = very common medical emergency
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What is Zenker’s diverticulum?
A pharyngeal pouch when some food goes down the pouch instead of totally down oesphagus
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Symptoms of Zenker’s diverticulum?
Smelly breath (food is accumulating in oesphagus) Regurgitation and aspiration of food
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What are pilondial sinus/abscesses caused by?
Hair follicles that get stuck in natal cleft (bum crack) Which : 1) forms small tracts (sinus) 2) get infected (abscesses)
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What is SIBO?
Small intestinal bacterial overgrowth syndrome (SIBO) can often present with similar symptoms to IBS (bloating, abdominal pain, diarrhoea or constipation). However, bloating is often strongly related to the time of day (occurring at night time due to chronic build-up of gas). Patients with SIBO often report having nausea and gastro-oesophageal reflux. As the vignette doesn't provide any of these additional symptoms, it is more likely for the patient to be suffering from IBS than SIBO.
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Food allergies presentation
Food allergies can present in a range of ways - from abdominal bloating and change in bowel habits to anaphylaxis (with oedema, rash, and airway impairment). This patient reports a mild improvement in symptoms when avoiding nightshades, however, there are still symptoms present. This should reassure the student that this is unlikely to be the correct answer.
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Zollinger-Ellison syndrome
Zollinger-Ellison syndrome is a syndrome of excessive gastrin secretion from a gastrin secreting tumour of the pancreas or duodenum, and may be associated with MEN 1. A diagnosis is made with elevated serum gastrin at least 10 times the upper limit of normal, a reduced gastric pH, and a secretin stimulation test if those criteria are not met.