GI Flashcards
What does inflammatory bowel disease comprise of? (IBD)
Ulcerative colitis Chron’s disease
Pathophysiology of IBD?
Inflamed intestines Associated with HCAB27 (Seronegative spondyloarthropathy) Has a Bimodal age distribution (15-20, 55+)
Cause of Chron’s disease?
Environmental and genetic - CARD15/NOD2 mutation => strong genetic component - bacteria trigger an immune mediated response (t-cells)
What part of the gut does Chron’s disease affect?
Whole gut Especially terminal ileum and proximal colon (usually rectum is spared)
Risk factors for Chron’s
Family history Jewish HLA-B27 gene Smoking (2x as likely) Caucasian
Pathophysiology of Chron’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
Signs and symptoms of Chron’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
Extraintestinal manifestations of both Chron’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
Investigations to diagnose Chron’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
How to differentiate UC from Chron’s particularly in the peadiatric population?
Serum antibody markers: - pANCA more associated with UC - ASCA more associated with Chron’s
How to differentiate IBD from IBS?
Faecal calprotectin Raised in IBD and not IBS
General management tips for Chron’s
Smoking cessation advice = crucial -Some evidence that NSAIDs and/or combined oral contraceptive pill can increase risk of relapse
Treatment given to induce remission in mild and moderate Chron’s
Elemental diet (alone or with meds, particularly in young people) Mild Chron’s: FIRST LINE : glucocorticoids (PO predinsolone or IV hydrocortisone) SECOND LINE: aminosalicylate (eg mesalazine) Moderate Chron’s: Add in: FIRST LINE: azathioprine or mercaptopurine SECOND LINE: Methotrexate
Treatment for severe Chron’s to induce remission that is unresponsive to conventional therapy
Infliximab or adalimumab as monotherapy or combined with other immunosuppressant
Treatment for Chron’s if it is refractory to medical therapy or disease limited to the distal ileum to induce remission
Surgery
How to classify severity of Chron’s
Mild: - first prevention or - 1 exarcerbation in 12 months Moderate: - >= exarcerbations 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
How to maintain remission in Chron’s
1st line: azathioprine or metcaptopurine 2nd line: Methotrexate Post surgery: consider azathioprine with or without methotrexate
Frequency of surgery in Chrons patients?
Approx 80% of patients with Chron’s will require surgery but this is not curative as entire bowel can be affected. By removing ‘x’, ‘y’ can flare up.
Complications of Chron’s
Peri-anal abscess Anal fissure Anal fistula Strictures and obstruction
Location of ulcerative colitis
COLON ONLY start at rectum—> sigmoid colon—> proximal colon Never proximally beyond illeocaecal valve Doesn’t affect the anus
Aetiology of ulcerative colitis
Not well understood Autoimmune colitis associated with HCA B27 gene Involves polygenic predisposition and env factors
Risk factors for ulcerative colitis
Family history HLA b27 Caucasian Non-smokers Bimodal age distribution 15-25 and 55-70yrs
Physiopathology of ulcerative colitis
Histopathology will show mucosal and submucosal ulceration as well as crypt abscesses with neutrophil infiltration
Symptoms of ulcerative colitis
Abdominal pain in left lower quadrant -Urgency and tenesmus (pain on defecation) -Bloody mucosy watery Diarrhoea
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
How is disease activity measured in ulcerative colitis patients?
Truelove and Witt’s severity index
Treatment for ulcerative colitis to induce remission
Generally: First line: topical ASAs 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
Treatment for maintenance of remission of ulcerative colitis
Low maintainance dose of ASA
Surgery with ulcerative colitis?
Total/partial colectomy is often curative
Complications of ulcerative colitis
Toxic megacolon is the most common complication cause ulcerative colitis deaths
What is Coeliac’s?
Systemic autoimmune T4 hypersensitivity to gluten that effects the small intestine
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
Risk factors for Coeliacs
Family history HLA-DQ2 and HLA-DQ8 Autoimmunity (thyroid disorders + addisons) IgA deficiency Down’s syndrome Turner’s syndrome
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
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
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
Complications of coeliacs
Dermatitis herpetiformis Malignancy Increased risk of osteoporosis Calcium and vit D deficiency
Differental diagnosis with coeliacs
Sprue or tropical sprue (associated with tropical travel) = malabsorption syndrome -Similar biopsy to coeliacs- crypt hyperplasia and villous atrophy -Treatment = often antibiotics eg tetracycline
What is IBS?
Chronic, relapsing and often lifelong disorder that affects lower GI tract - no discernible structure or biochemical cause => considered ‘functional’
Cause of IBS
Multi factorial Genetics + environmental + psychological (stress, anxiety) + dietary Exact mechanism unknown
Categorisation of IBS
IBS-C —> mostly constipation IBS-D —> mostly diarrhoea IBS-M —> mostly mixed; alternating C/D
Risk factors of IBS
Young adults Females Family history Dietary factors Psychosocial cavities Drugs
Symptoms of IBS
Abdominal pain and bloating relieved from defecation -Altered stool form/frequency
Diagnosis to exclude before diagnosing IBS
Coeliacs (serology) IBD (check fecal calprotectin) Infections (ESR/CRP/Blood cultures)
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
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
Complications of IBS
Mood disorders: more severe and frequent depression and anxiety Poor quality of life: miss three times as many days off work
What is GORD
Gastric-oesophageal reflux disease = reflux of gastric contents into oesophagus due to decreased pressure across lower oesophageal sphincter
Causes of GORD
- raised intragastric pressure= obesity + pregnancy - hiatal hernia (mostly with LOS sliding up through diaphragm) - Drugs anti-muscarinics, CCBs - Scleroderma (LOS = scarred)
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
Investigations to diagnose GORD
If no red flags go a traight to treatment (PPI) Red flags (dysphagia, haematemeis, weight loss) - endoscopy —> oesphagitis or Barrett’s - oesophagal manometry —> measure functionality of LOS and gastric acid pH
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
Last resort for GORD treatment?
Surgical treatment- laparoscopic fundoplication = mobilisation of funded of stomach which is then wrapped around the lower oesophageal sphincter to tighten it
Complications of GORD
Barrett’s oesophagus-oesophageal stricture - fibrous scarring and therefore narrowing of oesophageal lumen -dental problems
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)
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
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.
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
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
What if a patient has haematemesis and pulmonary hypertension?
oesophageal varices rupture
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
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
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
What is the Rockall score?
Calculated after endoscopy to identify patients at risk of adverse outcomes after treatment for an upper GI bleed
Treatment for MWT
Most spontaneously heal within 24h!
What type of peptic ulcer is more common?
Gastric>Duodenal Gastric is 2/3x more common
What are peptic ulcer diseases?
Punched out round holes in either stomach or stomach or duodenum
Where do gastric ulcers occur
Mostly at a lesser curve
Causes of gastric ulcers
-H.pylori (causes of 75% of gastric ulcers) -NSAIDs -Zolinger Ellison syndrome: - pancreatic tumour - gastric acid hypersecretion - widespread peptic ulcers
Symptoms of gastric ulcers
Epigastric pain - worse on eating - better between meals + with antacids * typically weight loss
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
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
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
Causes of duodenal ulcers
H. Pylori (causes 95% of duodenal ulcers) NSAIDS ZE Syndrome
Symptoms of duodenal ulcers
Epigastric pain - worse between meals - better with food * typically weight gain
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)
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
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
What is gastritis?
Mucosal inflammation and injury
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)
Symptoms of gastritis?
Epigastric pain with diarrhoea Nausea and vomiting Indigestion
What is PUD a complication of?
Gastritis
Investigations to diagnose gastritis?
If H.pylori suspected: - stool antigen test/ urea breath test Gold standard= endoscopy + biopsy
Treatment for gastritis?
H. Pylori = triple therapy CAP Clarythromycin Amoxicillin PPI
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)
What is autoimmune gastritis?
Affects funds portion of the stomach Especially causes atrophy of parietal cells
What is appendicitis?
Acute inflamed appendix, usually due to luminal obstruction SURGICAL EMERGENCY
Epidemiology and risk factors of appendicitis?
10-20yrs old Male Frequent antibiotic use Smoking
Causes of appendicitis?
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
Mechanisms of pain in appendicitis?
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
Classic triad presentation of appendicitis?
1) central abdominal pain that migrates to right iliac fossa 2) low-grade pyrexia 3) anorexia 50% of patients present with this characteristic history
Symptoms of appendicitis?
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 1) McBurney’s point 2) umbilicus 3) right ASIS
Signs of appendicitis?
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)
Complications of appendicitis?
Perforation (15-20%) - appendiceal rupture Appendiceal mass Periappendical abscess
Investigations to diagnose appendicitis?
CT abdominal + pelvis = gold standard Pregnancy test to rule out ectopic pregnancy ( presents with right iliac fossa pain)
Treatment for appendicitis?
Antibiotics and then appendectomy (laproscopic) -Must drain abcesses - resistant to Antibiotics
Why must abscess be drained in appendicitis?
Abscess = walled off bacterial collection -Resistant to systemic antibiotics so not useful -Needs to be directly dealt with - drainage + intra abscess antibiotic
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 walk of the colon
Define diverticulum
An outpouching at perforating artery sites
Define diverticulosis
An asymptomatic outpouching
Define diverticular disease?
A symptomatic outpouching
Define diverticulitis
Inflammation of outpouching - infection
What percentage of diverticula are asymptomatic?
95% and only 5% are symptomatic (diverticular disease)
What is Meckel’s diverticulum?
Paediatric disorder -Failure if obliteration of vitelline duct -Rule of 2s: 2 years old 2 inches long 2ft from illeocaecal valve (umbilical) Diagnostic= technetium scam
Risk factors for diverticular disease?
Connnective tissue disorders (ED + M) Ageing Increased colon pressure COPD + chronic cough Age
Complications of diverticulitis?
SBP Obstruction Fistulae
Symptoms of diverticulitis?
1) Left lower quadrant pain 2) constipation 3) fresh rectal bleeding
Investigations to diagnose diverticulitis?
CT abdominal/ pelvis with contrast = gold standard
Treatment for diverticulosis?
Nothing, watch and wait
Treatment for diverticular disease
Bulk forming laxatives “isphagula husk” Surgery is gold standard
Treatment for diverticulitis
Antibotics (Co amoxiclav) Paracetamol IV Fluid + liquid food Rarely surgery
Two types of intestinal obstruction?
Small Bowel Large Bowel
Percentage of intestinal obstruction that is small bowel?
60-75% of all cases
Causes of small bowel obstruction?
Adhesions (most common) 50% Hernias 15% Cancer 10% Chron’s
Symptoms of intestinal obstruction?
Vomiting then constipations Mild abdominal distension + pain Tinkeling bowel sounds (*hyperresonant bowels on percussion in both types of intestinal obstruction)
Percentage of intestinal obstruction cases that involve large bowel?
25-40% of all cases
Causes of large bowel obstruction?
Malignancy (90%) Volvulus- mostly sigmoid colon, children Intussusception (bowel telescopes in on itself -> most common in children)
Symptoms of large bowel obstruction?
First constipation Then vomiting Gross distension + pain Hyperactive, then normal, then absent bowel sounds
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
What is a pseudo obstruction?
No mechanical obstruction, often a result of post operative state -still have symptoms of intestinal obstruction
Treatment for intestinal obstruction?
Most patients are two days without food before admission
Types of diarrhoea?
watery - secretory - osmotic - functional (IBS) - steatorrhoea - inflammatory
What is diarrhoea?
A presenting symptom with many differential diagnoses Classed as 3+ watery stools daily which are level 5-7 on Bristol stool cahrt
What is bloody diarrhoea?
Dysentery Eg. Amoebic dysentery E.coli + salmonella + shigella
Levels of diarrhoea?
Acute < 14 days Subacute 14-28 days Chronic > 28 days
Causes of diarrhoea?
IBD (Chron’s, UC) Coeliac disease Hyperthyroidism Inflammation or malignancy Infective causes
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)
Antibiotics as a cause of diarrhoea?
They increase the risk of C. Diff infection 4C’s - Clarythromycin, co-amoxiclav, ciprofloxacin, cephalosporins
Treatment of diarrhoea?
Depends on underlying cause Viral (mc) = self limiting Fluids and diroalyte to rehydrate patient
Complications of diarrhoea?
Dehydration Electrolyte loss
Two types of osphageal cancer?
Adenocarcinoma Squamous cell carcinoma
Adenocarcinoma location and association?
Lower 2/3 of oesophagus Associated with Barrett’s oesophagus
Squamous cell carcinoma location and association?
Upper 2/3 oesphagus Smoking and alcohol
Symptoms of oesophageal cancers?
Presents when advanced ALARMS Anemia Loss of weight Anorexic Rescent sudden symptom worsening Melenea/Haematemesis Swallowing progressive difficulty
Key symptom of osphageal 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 aschalasia
Investigations to diagnose osphageal cancer
OGD (oesophago-gastro-duodenoscopy) + biopsy with barium swallow CT/PET for staging
Treatment for oesphageal cancer?
Medically fit = chemo/radio + surgery Unfit = palliative
What are gastric carcinomas?
Mostly adenocatcinomas
Grading of gastric carcinomas?
T1 = well differentiated = better prognosis (mc) T2 = undifferentiated “signet ring carcinomas” typically at proximal stomach = worse prognosis
Causes of gastric carcinomas
H.pylori Smoking CDH-1 mutation cashed in gene= 80% risk Family history Pernicious anemia (autoimmune chronic gastritis)
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 -krukenbergtumour due to ovarian metastases from gastric cancer
Investigations to diagnose gastric carcinomas?
Gastroscopy+ biopsy CT\mri for staging, PET to iD metastases Staging= TNM
Treatment for gastric carcinomas?
Surgery + “ECF” chemo regimen, if resectable
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
Risk factors of small intestine carcinomas
Chronic SI disease: -Chron’s -Coeliac’s
Diagnosis and treatment of small intestine carcinoma?
Same as gastric carcinomas
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
Risk factors for colorectal polyps and cancer?
Familial inherited genetic predisposition -Adenomas/ polyps -Alcohol, Smoking, ulcerative colitis
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
Common metastases of colon polyps/adenomas?
Liver and Lung
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)
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 2weeks
How are colorectal polyps/adenomas classified?
TNM system
Treatment for colorectal adenomas/polyps cancer?
Surgery and chemo is the only curative option if there are no metastases
What is dyspepsia?
Not a disease A presenting symptom of “indigestion”
Signs of dyspepsia?
early satiation -epigastric pain + reflux (GORD like pain) -extreme fullness
Cause of dyspepsia?
Often unknown (“Functional disorder”) Maybe related to ulcers (especially gastric)
Diagnosis and treatment of dyspepsia?
Need endoscopy to find underlying cause
What is H.pylori?
Gram -ve bacteria Has a decreased virulence in the GIT
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
Causes of h.pylori?
PUD -gastritis -gastric carcinomas
Investigations to diagnose H.Pylori?
Biopsy (Stool antigen + C-urea breath test often 1st line)
Treatment for H.pylori?
Triple therapy: Clarythromycin + amoxicillin + PPI
What is E.Coli?
Major player in UTIs also Gram -ve bacteria Often commensal flora of GIT Some strains/ “serotypes” are very virulent
Strains of E.coli that lead to watery diarrhoea?
ETEC EAEC EPEC
Strains of E.coli that lead to bloody diarrhoea?
EHEC
Cause of haemolytic uremic syndrome?
Serotype 0157:H7 of E.coli Leads to haemorrhagic diarrhoea Nephrotic syndrome
Treatment of E.coli?
Often amoxicillin, trimethoprim, nitrofurantoin
What is C.difficile?
Gram +ve spore forming bacteria
What is C.difficile mainly induced by?
Ciprofloxacin Co-amoziclav Cephaolosporins Clindamycin 4 Cs
What’s Meleana?
Blood in the stool that appears black
Likely causes of GI bleeding?
Peptic ulcer= most common (50%) Osephageal varices Mallory-Weiss syndrome Gastric carcinoma (uncommon)
How to manage patients with GI bleeds?
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How to differentiate between variceal and non-variceal bleed?
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What is most important when it comes to GI bleeding?
Initial assessment and management rather than endoscopy in most cases
In the UK how often do you see upper GI bleeding?
Nearly one presentation every 6 minutes = very common medical emergency
Causes of intraluminal obstruction?
tumour - carcinoma - lymphoma - diaphragm disease (becoming more common due to NSAIDs) - meconium Ileus - gallstone disease
Causes of intramural obstruction?
inflammatory - Chron’s disease - diverticulitis - tumours - neural - Hirschsprung’s disease
Causes of extraluminal obstruction?
adhesions - volvulus - tumour - peritoneal deposits
What is small bowel obstruction?
A form of intestinal failure causing malabsorption requiring iV supplementation or replacement
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?
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
Investigations to diagnose small bowel obstruction?
Full blood count Urea and electrolytes Lactate C-reactive protein CT SCAN = 🔑 NOT X RAY
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
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
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
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
Most common complication of small bowel obstruction?
Renal failure
When would you advise surgery in adhesive SBO?
Signs of ischemia on a CT scan
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
Treatment for C.difficile?
Stop using these 4 antibiotics ( ciprofloxacin, Co-amoxiclav, cephalosporins, clindamycin) => give Vancomycin (now first line according to nice)
What is Achalasia?
Osephageal dysmotility (impaired peristalsis) - LOS fails to relax - rate and idiopathic
Symptoms of achalasia?
Non progressive dysphagia (struggle swallowing anything) -Chesty Substernal pain -Food regurgitation -Aspiration pneumonia
Investigations to diagnose Achalasia?
Barium swallow with “bird beak” - manometry (measure pressure across LOS) = diagnostic
Complication of Achalasia?
May increase risk of oesphageal squamous cell lung cancer
Treatment for Achalasia?
Only surgery is curative (balloon stenting) * drugs may help pre-surgery - nitrates, nifedipine
What is ischemic colitis?
Ischemia if colonic arterial supply - colon gets inflamed due to hypoperfusion
Causes of ischemic colitis?
Affecting inferior mesenteric artery; - thrombosis (+/- atherosclerosis) = most common - emboli - decreased CO + arrhythmias (eg history of AF) or due to shock - combined oral contraceptive pill
Most common sites effects with ischemic colitis?
Watershed areas - splenic flexure (most common) - sigmoid colon + cecum
Symptoms of ischeamic colitis?
LLQ pain + bright bloody stool +/- signs of hypovolemic shock
Investigations to diagnose ischemic colitis?
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)
Complications of ischemic colitis?
Perforation - tissue death - strictures (therefore obstruction)
Treatment do ischeamic colitis?
If just symptomatic- IV fluids + antibiotics (prophylactic) If gangrenous (infected colon)- only SURGERY
What is mesenteric ischemia?
Ischemia of small intestine
Two types of mesenteric ischemia?
AMI- acute attack “abdominal MI” CMI- chronic and over a longer period of months “abdominal angina”
Causes of mesenteric ischemia?
Affecting superior mesenteric artery - Thrombosis (most common) - Emboli (due to AF often)
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
Investigations to diagnose mesenteric ischemia?
CT angiogram FBC+ABG = persistant metabolic acidosis
Complication of mesenteric ischemia?
SBP (spontaneous bacterial peritonitis)
Treatment of mesenteric ischemia?
Fluid resuscitation Antibiotics IV heparin ( decrease thromboemboli) —> infarcted bowel is treated by surgery
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 🤮)
Most common cause of haemorrhoids?
Constipation with increase straining - also anal sex
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!
Symptom of haemorrhoids?
-Bright red flesh PR bleeding and mucosy bloody stool -bulging pain +/- pruritas ani (itchy bum)
Investigations to diagnose haemorrhoids?
External haemorrhoids = PR exam (digital) - may be visible though Internal haemorrhoids = proctoscopy
Treatment for haemorrhoids?
Stool softener Definitive= rubber band ligation
What is a perianal abscess?
Walled off collections of stool + bacteria around anus
Most common cause of perianal abscess?
Anal sex causing anal gland infection
Symptoms of perianal abscess?
Pus in stool + constant pain (tender)
Treatment for perianal abscess?
Surgical removal + drainage if walled off and resistant to oral antibiotic therapy
What is an anal fistula?
Abnormal “tracks” form between inside of anus —> elsewhere Eg subcutaneous skin (mostly)
What does an anal fistual typically progress from?
Perianal abscesses - abscess discharges (toxic substances) which aid fistula formation as abscess grows (also Chron’s and rectal cancer)
Symptoms of anal fistulas?
Bloody/ mucosy discharge Often very viable and painful
Treatment for anal fistula?
Surgical removal + drainage (with antibiotics if infected)
What is an anal fissure?
Tear in abal skin lining below dentate line => very painful due to strong sensory supply
Most common causes of anal fissure?
Hard feaces
Other less common causes of anal fissures?
Trauma (eg childbirth) Chron’s UC
Symptoms of anal fissures?
extreme defecation pain -very itchy bum (pruritus ani) -anal Bleeding
Treatment for anal fissures?
Stool softening (increase fibre intake + more fluids) Topical creams (lidocaine ointment) Definitive treatment=surgery (not usually done)
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)
In which people are pilondial sinus and abscess commonly seen in?
In very hairy people (eg Asians)
Symptoms of pilondial sinus and abscesses?
Swollen pus filled smelly abscess on bum crack (Visible on exam)
Treatment for pilondial sinus / abscess?
Surgery + hygiene advice
What is Zenker’s diverticulum?
A pharyngeal pouch when some food goes down the pouch instead of totally down oesphagus
Symptoms of Zenker’s diverticulum?
Smelly breath (food is accumulating in oesphagus) Regurgitation and aspiration of food
