GI Flashcards
What 2 conditions make up the inflammatory bowel diseases
Crohns and Ulcerative Colitis
Define Crohn’s disease with epidemiology
Inflammatory bowel disease characterised by transmural inflammation of the ENTIRE GI tract (mouth to anus). Terminal ileum and colon most commonly affected.
North Europe, UK, North America, 20-40 years
Risk factors for Crohns
- Family history
- Smoking
- White people (particularly Jewish origin)
- Oral contraceptive pill
- Diet low in fibre
- NSAID
Causes of Crohns
Genetic: NOD2/CARD15 gene mutation
Environmental:
- Smoking
- Oral contraceptive pill
- NSAIDs
Bacterial: Mycobacterium paratuberculosis, Pseudomonas and Listeria
Pathophysiology of Crohns
Chronic inflammation of the GI tract. Pathogen is presented to GI immune cells causing T helper cells to bind to it. This causes the release of inflammatory cytokines such as Interferon Gamma and TNF-a, which further stimulate immune response and inflammation
It is thought that genetic abnormalities leads to a dysfunction, causing inflammation to be unregulated.
This causes transmural inflammation with areas of healthy bowel in between, known as skip lesions, providing a cobblestone appearance of the bowel. Inflammation of the bowels can lead to malabsorption.
Signs and symptoms of Crohns
Signs
- Aphthous mouth ulcers
- Abdominal tenderness
- Perianal lesions - Skin tags, fistulae, fissures, abscesses, ulcers
Symptoms
- Diarrhoea (prolonged and often)
- Abdominal pain
- Weight loss and failure to thrive
- Several extra-intestinal manifestations affecting skin, joints, eyes (next card)
Extra-intestinal manifestations of Crohns
Skin:
- Perianal/mouth ulcers
- Erythema nodosum (swollen fat under skin, looks red, usually on shins)
- Pyoderma gangrenosum (rapidly enlarging, very painful ulcer)
Musculoskeletal:
- Arthritis of the large joints
- Seronegative spondyloarthropathies
- Clubbing
Eyes:
- Conjunctivitis
- Iritis
Investigations in Crohn’s
Faecal calprotectin (inflammatory marker in GI tract) - Raised
Serum antibodies
- pANCA negative (more in UC)
- ASCA positive (more in Crohn’s)
Endoscopy/Colonoscopy + Biopsy GOLD
- Endoscopy: Skip lesions, cobblestoning, strictures
- Biopsy: Transmural inflammation, non caseating granulomas, goblet cells present
CT/MRI can be used to find skip lesions, fistulas, abscesses
Histology of Crohn’s
Transmural inflammation, non caseating granulomas, goblet cells present
Treatment of Crohn’s
Cease NSAID, smoking
Induce remission
- Elemental diet
- Glucocorticoids: Budenoside (mild), prednisolone (moderate), IV Hydrocortisone (very severe)
- Immunosuppressants (Azathioprine or methotrexate)
- Anti TNF antibodies (infliximab)
Maintain remission
- Azathioprine
Complications of Crohn’s (6)
- Peri anal abscesses
- Anal fissure/fistula
- Small bowel obstruction
- Colorectal cancer
- Osteoporosis
- Anaemia/malnutrition
Crohns vs UC mnemonic
NESTS (Crohn’s)
N - No blood (rarer but still possible!)
E - Entire GI tract
S - Skip lesions
T - Terminal ileum and transmural inflammation
S - Smoking Risk factor
CLOSEUP (UC)
C - Continuous inflammation
L - Limited to colon and rectum
O - Only mucosa affected
S - Smoking protective
E - Excrete blood and mucus
U - Use aminosalicylates
P - Primary Sclerosing Cholangitis
Define Ulcerative Colitis with important epidemiology
Relapsing and remitting inflammatory bowel disease that characteristically involves rectum, and can extend up large bowel, up to ileocaecal valve. Doesn’t affect anus
Similar epidemiology to Crohns but 3x more common in NON SMOKERS (smoking is protective)
Risk factors for Ulcerative Colitis (6)
- Family History
- HLA-B27
- NSAIDs
- Infections
- Not smoking
- Chronic stress/depression
Pathophysiology of Ulcerative Colitis (4)
- IBD involving continuous inflammation, affecting only the colon on its mucosal layers. Usually starts at the rectum, working its way proximally to the caecum but never going past the ileocaecal valve.
- Relapsing, remitting course (Flares with new damage to bowel wall, followed by tissue healing).
- Can affect rectum only (proctitis), extend up to splenic flexure (left-sided colitis) or entire colon (pancolitis)
- Pseudopolyps develop due to regenerating mucosa that forms a kind of scar that looks like a polyp.
Signs and symptoms of UC
Signs
- LLQ pain and tenesmus (Rectal pain, feeling like you need to poo when you dont)
- Bloody, mucusy diarrhoea
- Weight loss/malnutrition
- Relapsing, remitting course
Symptoms
- Abdominal pain
- Cramping
- Diarrhoea
- Fever,malaise during attacks
Extra intestinal manifestations of UC
- Erythema nodosum
- Pyoderma gangrenosum
- Uveitis
- Colorectal cancer
- Ankylosing spondylitis
Investigations in UC
Faecal calprotectin - high
Xray, CT may be used for imaging
Check for C.diff cause of diarrhoea
Antibodies
pANCA positive
ASCA negative (Crohns)
Colonoscopy and biopsy GOLD
- Colonoscopy - Continuous mucosal ulcers and goblet cell depletion
- Biopsy - Psuedopolyps, crypt abscesses, goblet cell depletion. Inflammation limited to mucosa + submucosa
Histology in UC
Psuedopolyps, crypt abscesses, goblet cell/mucin depletion. Inflammation limited to mucosa + submucosa
What severity scoring system is used in UC
Truelove + Witts
Treatment of UC
1st (induce remission) - aminosalicylate (mesalazine/sulfasalazine) Rectal in proctitis, oral otherwise
if moderate/not responding prednisolone first.
In severe, IV hydrocortisone.
Cyclosporin (immunosuppressant) and Infliximab (TNF-a inhibitor) can also be given.
Next (Maintain remission)
- Aminosalicylate + azathioprine
If severe or non responsive,
Colectomy can be done (Curative)
Complications of UC (6)
PRIMARY SCLEROSING CHOLANGITIS!
Toxic megacolon
Bowel perforation
Colonic adenocarcinoma
Strictures or bowel obstruction
Extra intestinal manifestations
Define fulminant UC with symptoms and treatment
Sudden onset acute, severe flareup of UC.
> 10 bowel movements a day
Continuous bleeding
Abdominal tenderness
Toxicity
Colonic dilation
Hospital IV corticosteroid (hydrocortisone)
IV Ciclosporin or infliximab
Consider colectomy
Define Coeliac disease
Systemic autoimmune type 4 hypersensitivity reaction affecting the small intestine, triggered by dietary gluten peptides such as those found in rye, barley, wheat. Malabsorption is hallmark of the disease.
Pathophysiology of Coeliac
Normally, gluten containing food is broken down in stomach into gliadin. Gliadin resistant to proteases, passes to small intestine. Tissue transglutaminase (tTG) cuts off an amide group forming De-amidated gliadin.
In coeliac, this is taken up by macrophages which present it via MHC-II. T helper cells bind to it, releasing inflammatory cytokines which damage the villi of the small intestine.
IgA: Anti-tTG and Anti-EMA (Endomysial)
IgG: Anti-DGP (Deamidated gliadin peptide)
Risk factors for Coeliac
Family history
HLA-DQ2 or HLA-DQ8
Autoimmune disease
IgA deficiency
Downs syndrome
Signs/symptoms of Coeliac
Should be suspected in all diarrhoea + weight loss/anaemia
Signs
- Diarrhoea caused by common triggers
- Smelly, fatty, floaty stools (Steatorrhoea)
- Malabsorption signs (anaemia, weight loss, failure to thrive)
- Dermatitis Herpetiformis (Itchy red raised patches of skin, commonly found on extensor surfaces of arms and legs. Suggests active disease)
Symptoms
- Anaemia (iron, B12, folate deficiency)
- Weight loss
- Fatigue
- Osteomalacia (softening of bones due to lack of phosphate, vit D, calcium)
- Abdominal bloating, constipation
Common triggers of coeliac
Gliadin
Wheat, barley, rye (gluten rich foods)
Investigations in Coeliac
Antibodies:
- IgA- Anti tTG (tissue transglutaminase)
- Anti EMA (East mids airport (but also Endomysial))
IgG (if IgA deficiency)- Anti DGP (Deamidated gliadin peptide)
Small bowel endoscopy+biospy:
Villous atrophy, crypt hyperplasia, increased intraepithelial lymphocytes, lamina propria infiltration with lymphocytes
Coeliac histology
Villous atrophy, crypt hyperplasia, intraepithelial lymphocytes, lamina propria infiltration with lymphocytes
Management of Coeliac
Gluten free diet (pasta, bread, flour, barley, rye)
Vitamin/mineral supplementation
Dexa scan to check osteoporosis risk
Define Irritable bowel syndrome (IBS), with 3 types
Chronic condition featuring abdominal pain and bowel dysfunction. Functional bowel disorder (has no identifiable/known pathology - Tests always come back normal)
Has 3 types
IBS - C: Constipation
IBS - D: Diarrhoea
IBS - M: Mixed/alternating
Exacerbators and risk factors of IBS
- Stress
- Microbial dysbiosis
- High FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides and polyols) diet (short chain carbs)
- Gastroenteritis
- Menstruation
- PTSD
- Family history
- History of abuse
- Previous enteric infection
Signs/symptoms of IBS
- Chronic abdominal discomfort and abnormal bowel habits
- Abdominal bloating, distention and tenderness
- Urgency of defecation
- Symptoms worse after eating, relieved by defecation
- Mucus in faeces
- Altered stool appearance
Pathophysiology of symptoms of IBS
Visceral hypersensitivity - Sensory nerves in bowel wall have strong response to stimuli (stretching during/after meal)
Abnormal bowel motility - Fodmaps act as solutes and draw water into GI tract. Excess water causes smooth muscle spasms of intestines
Spasm/pain/bloating - GI flora metabolise FODMAPS producing gas
Investigations in IBS
“Diagnosis of exclusion”
- Faecal calprotectin, ESR and CRP - Rule out IBD
- Coeliac serology - Rule out Coeliac autoimmunity
- Abdominal X ray - Check obstruction
- Colonoscopy - Rule out IBD or bowel cancer
- FBC - Check for anaemia
Management of IBS
1st - Lifestyle advice (seperate card)
IBS-D - Loperamide - opioid receptor agonist, decreases muscular contraction in intestine. (Material stays in bowel so more water absorbed)
IBS - C - Laxatives (linaclotide)
AVOID lactulose
2nd line
If severe, tricyclic antidepressants (amitriptyline) reduces gut sensitivity
Lifestyle advice in IBS
Adequate fluid intake
Small, regular meals
Reduced processed foods
Limit caffeine and alcohol
Low FODMAP diet
Increase fibre if constipated, reduce if diarrhoea
Eat oats
Reduce stress
Lose weight
Crohns vs Colitis vs Coeliac Histology
Crohns - Transmural inflammation, non caseating granulomas, goblet cells present
Colitis - pseudopolyps, goblet cell depletion, crypt abscesses. Inflammation is mucosa/sub only
Coeliac - Villous atrophy, crypt hyperplasia, intraepithelial lymphocytes, lamina propria infiltration with lymphocytes
Give the infective causes of diarrhoea
Viral
- Rotavirus (MC children)
- Norovirus (MC Adults)
Bacterial
- Campylobacter jejuni (MC, travel associated)
- C.diff
- E. coli (children)
- Salmonella
- Shigella
Infective condition causing diarrhoea, nausea vomiting
Gastroenteritis - Inflammation from stomach to intestines
How do antibiotics cause diarrhoea
Antibiotics beginning with C (in general) can cause C. diff
- C. diff replaces normal gut flora, causing necrosis and giving rise to pseudomembranous colitis, causing diarrhoea
Risk factors for infective diarrhoea/gastroenteritis and pseudomembranous colitis
Foreign travel
Poor hygiene
Crowded area
Pseudomembranous colitis
- Elderly
- Antibiotics
- Long hospital admission
- PPI/H2 antagonist acid suppression
What are the 3 cell layers of the stomach and what do they contain?
Epithelial Layer (innermost) - Absorbs/secretes mucus and digestive enzymes
Lamina propria - Blood/lymph
Muscularis mucosa (outermost) - Smooth muscle
What are the 4 regions of the stomach and what do they contain
Cardia - Foveolar cells (secrete mucus)
Fundus and body - Parietal cells that secrete HCl and chief cells that secrete pepsinogen
Antrum - G cells that secrete gastrin (which stimulates parietal cells to secrete HCl)
Duodenum contains Brunner glands which secrete mucus rich in bicarbonate to neutralise acid
Prostaglandins function
The stomach and duodenum also secrete prostaglandins which:
- stimulate mucus and bicarbonate secretion,
- vasodilate nearby blood vessels allowing more blood to flow to the area,
- promote new epithelial cell growth
- inhibit acid secretion.
Causes of gastritis
Acute
- H pylori, NSAID, alcohol
Chronic
- Long term H pylori, chronic alcohol, bile reflux
Autoimmune
- Antibodies against parietal cells
- Caffeine
- Smoking
- Extreme stress
- Increased acid
Risk factors for gastritis
Alcohol
NSAIDs
H Pylori infection
CMV and herpes
Reflux
Hiatus hernia
Zollinger-Ellison syndrome (tumours cause stomach to release too much acid)
Signs/symptoms of gastritis
Epigastric pain
Vomiting
Indigestion
Signs of B12 deficiency
Bloating
Investigations for gastritis
Endoscopy and biopsy - Will show gastritis
H pylori investigations
- H Pylori Urea breath test/ CLO test (patient given a meal containing radioactively labelled 13C urea. H Pylori will break the urea into radioactive CO2 which can be detected on exhalation)
- H Pylori Stool antigen test
Anti parietal cell/ anti IF antibodies - check for autoimmune cause
Differentials of Gastritis pain
Peptic ulcer disease
GORD
Non-ulcer dyspepsia
Gastric cancer (lymphoma, carcinoma)
Management of gastritis
Lifestyle: Reduce stress, alcohol, caffeine, NSAID
If H pylori
1st - H pylori eradication therapy (CAP - 2 antibiotic + PPI)
- Clarithromycin, amoxicillin, omeprazole
+ ciprofloxacin if fails
H2 receptor antagonist - Ranitidine
If autoimmune,
B12 injections for malabsorption
What is phlegmonous gastritis and how is it treated
Staph. Aureus, Streptococci, E. coli, Enterobacter infection. Normally, gastric acid prevents growth of bacteria, but in atrophic gastritis, less acid produced so ingested bacteria can invade and form pus on the gastric walls
- ICU admission and surgical resection of stomach
H. pylori Pathophysiology
- H Pylori secrete urease, splitting urea in stomach into CO2 and ammonia
- Ammonia + H+ = Ammonium and ammonium is toxic to the gastric mucosa > less mucous produced
- Somatostatin decreased, so less inhibition of acid secretion
- G cells stimulated to release more gastrin and histamine, so acid release from parietal cells increased
- Inflammatory effects further weaken mucosal protection
- Destruction to mucin layer causes decrease in HCO3-, less buffering of acid
What does H pylori do to substances in stomach (put simply)
- Releases urease, causing Ammonium production, damaging mucus
- Increases gastrin production, increasing stomach acid release by parietal cells
- Decreases somatostatin and HCO3-, so acid is inhibited/neutralised less
H Pylori investigations (3)
H pylori investigations
- H Pylori Urea breath test/ CLO test (patient given a meal containing radioactively labelled 13C urea. H Pylori will break the urea into radioactive CO2 which can be detected on exhalation)
- H Pylori Stool antigen test
- Biopsy urease test can be done too but is invasive
How is a H. pylori infection treated
H pylori eradication therapy (CAP - 2 antibiotic + PPI)
- Clarithromycin, amoxicillin, omeprazole
+ ciprofloxacin if fails
Consequences of H. pylori infection
Inflammation (Gastritis)
Peptic ulcer disease
Gastric carcinoma
Define a peptic ulcer
A break in mucosal lining of stomach or duodenum of 5mm in diameter or more. Usually due to an imbalance in factors promoting mucosal damage (NSAID, H. pylori, gastric acid) and protective defences (prostaglandins, mucus, bicarbonate (HCO3-))
Causes of peptic ulcers
- H. pylori
- NSAID
- Zollinger-Ellison syndrome (Gastrinoma causing excess acid release)
- Smoking and alcohol
- Stress
Where are Gastric and Duodenal ulcers commonly found?
Gastric ulcers usually found in lesser curvature of antrum
Duodenal found just after pyloric sphincter and usually Brunner gland hypertrophy (glands which secrete bicarbonate rich mucous)
Pathophysiology of peptic ulceration causes (3)
H pylori - release adhesins to adhere to foveolar cells and proteases causing damage to mucosal membrane
NSAIDs - Inhibit COX, causing indirect inhibition of prostaglandin synthesis.
ZE syndrome - Tumour in stomach, duodenal wall or pancreas, which secretes abnormal amounts of gastrin
How do gastric and duodenal ulcers cause bleeding
Very deep ulcers cut into arteries
Gastric ulcers affect left gastric artery
Duodenal ulcers affect gastroduodenal artery
What are the pain characteristics of gastric and duodenal gastric ulcers?
Burning epigastric pain
Gastric - Worse after eating
Duodenal - Worse when hungry, food provides some relief
(posterior penetration into pancreas may make pain radiate to back)
Other signs/symptoms of peptic ulcers
Nausea/vomiting
Dyspepsia (indigestion)
Weight loss (secondary to eating less in gastric ulcer)
Epigastric tenderness
Haematemesis
If bleeding
Anaemia
Malaena
Hypotension/tachycardia (shock) if bleeding acute and severe
Red flag symptoms in peptic ulcers
ALARM D
Require urgent endoscopy
- Anaemia
- Loss of weight
- Anorexia
- Recent onset/progressive symptoms
- Malaena/haematemesis
- Dysphagia
Investigations in peptic ulcer disease
If >55, Red flag symptoms, bleeding or dysphagia
- Endoscopy and biopsy, to check for malignancy or H pylori (biopsy urease clo test) (Will also show Brunners gland hypertrophy in duodenal!)
- Repeat to confirm healing/no malignancy after 4-6 weeks
<55, no red flags, non invasive fine
- H Pylori urease breath test
How can a false negative be prevented when testing for H pylori
Patient must be off PPI for 2 weeks.
Treatment of Peptic ulcer disease (no bleeding)
1 - Risk factor minimisation (NSAID, stress, alcohol)
H pylori negative - PPI (Omeprazole) 1 month
H2 antagonist (Ranitidine) can also be used
2- H pylori positive
CAP - Clarithromycin, amoxicillin, omeprazole (metronidazole in penicillin allergy)
Treatment of peptic ulcer disease (bleeding)
IV crystalloid
Upper GI endoscopy with:
- Mechanical therapy (clipping) or
- Thermal coagulation
High dose PPI
Complications of peptic ulcer disease
Perforation - Perforation into peritoneal cavity is life threatening and can cause peritonitis.
Bleeding - (more common in duodenal ulcers)
Gastric cancer
Pyloric stenosis - scar tissue can block pylorus
What do these secrete?
G cells
Parietal cells
Chief cells
Foveolar cells
G - Gastrin
Parietal - HCl
Chief - Pepsinogen
Foveolar cells - Mucus
Define GORD and direct causes
Reflux of stomach contents into the oesophagus, usually due to a weak lower oesophageal sphincter (LOS)
Caused by:
- Lower oeseophageal hypotension
- Oesophageal dysmotility
- Gastric acid hypersecretion
Risk factors for GORD
High BMI
Pregnancy
Smoking
NSAID, coffee, alcohol
Hiatus hernia (part of stomach pushes up through diaphragm, lowering LOS pressure)
Scleroderma (LOS muscle replaced with connective tissue)
Zollinger Ellison syndrome
Pathophysiology of GORD
- Reflux of stomach contents back into oesophagus. Can be due to reduced LOS pressure, meaning it relaxes more and gastric acid can get into the oesophagus.
- Persistent reflux leads to oesophagitis, causing oedema and erosion of mucosa
- Oesophageal stenosis can cause damaged tissue to scar, narrowing its lumen.
- Overtime, metaplasia occurs, and the stratified squamous epithelium is replaced with columnar (Barret’s oesophagus)
- This is a risk factor for adenocarcinoma
Signs and symptoms of GORD
- Heartburn (pyrosis) - worse after meals or lying down
- Regurgitation
- Indigestion
- Refluxy cough
- Difficult and painful swallowing (Dysphagia is red flag)
- Retrosternal, epigastric chest pain
- Asthma/ nocturnal asthma if reflux spreads to larynx
Red flags in GORD
- Weight loss! Suggests barrets oesophagus
- Severe dysphagia
- Haematemesis
- Palpable mass
- Anaemia
Investigations in GORD
1 - PPI Trial (8wk)
2- if red flags
- Endoscopy - check for Barrett’s
- 24 hour ambulatory pH monitoring - GOLD
Treatment of GORD
Lifestyle - Weight loss, stop smoking, spicy food, fatty food, chocolate, caffeine and alcohol cut down. Dont lie down after eating.
1- PPI: Omeprazole
2 - H2 receptor antagonist (blocks histamine receptor on parietal cells): Ranitidine
3 - Antacid: Magnesium trisilicate mixture (neutralise acids)
LAST RESORT SURGICAL
- Laparoscopic fundoplication (tie fundus of stomach around LOS to narrow it and increase LOS pressure)
Complications of GORD
Oesophagitis
Barrett’s oesophagus
Oesophageal strictures
Asthma (if reaches larynx)
How does achalasia differ to GORD
Achalasia has:
A dilated oesophagus
No apparent underlying cause
Regurgitation rather than reflux
Dysphagia affects solids more than liquids
Trialled PPIs dont help
Define achalasia
Oesophageal dysmotility where LOS fails to relax. Patient struggles to swallow anything.
Investigations and treatment in achalasia
Bird beak of barium swallow
Manometry (measure pressure across LOS)
Only treatment is balloon stenting of LOS
What are diverticula?
A diverticulum is an outpouching of colonic mucosa and underlying connective tissue of colon wall. Usually 0.5-1cm. Usually caused by weakness in circular muscle that become larger gaps over time, causing mucosal herniation through the gap.
Where are diverticula most likely to occur
Sigmoid (MC) also right colon (ascending/transverse)
Through colonic weak points such as where blood vessels pass through muscle, or gaps in taeniae coli muscle
Give the types of diverticular disease
Diverticulosis - Presence of diverticula, asymptomatic patient
Diverticular disease - Diverticula cause milder symptoms, e.g. intermittent abdominal pain without inflammation or infection
Diverticulitis - Diverticula become inflamed and infected, causing more severe symptoms
What is a false diverticulum
Not all layers involved in the outpouching (in true diverticula, ALL Layers involved)
False are most common.
Causes/risk factors of diverticular disease
- Low fibre diet
- Old age
- NSAID
- Connective tissue disorders (Ehlers-Danlos/Marfans)
- Obesity
- Smoking
What are 2 possible consequences of diverticula
- Blood vessels supplying colon can rupture, allowing blood into lumen, causing haematoschezia
- Diverticula themselves can rupture, causing fistula formation, usually with bladder (colovesicular fistula), causing gas in bladder or stool in urine
Signs/symptoms of diverticulitis
Asymptomatic - Detected incidentally on colonoscopy
Diverticulosis:
- LLQ abdominal pain
- Rectal bleeding possible
Diverticulitis:
- LLQ/LIF pain and guarding (If Sigmoid. Right sided if right colon affected)
- LIF tender mass (if abscess)
- Constipation
- Fresh rectal bleeding
- Diarrhoea
Investigations in Diverticulitis
CT abdomen/pelvis with contrast
- Identify divertcula/diverticulitis and complications
Differentials for diverticulitis
Colorectal cancer
Appendicitis
UTI
Pyelonephritis
Management of diverticulitis
Diverticulosis - No treatment
Diverticular disease - Increase fibre, hydration, cut out smoking. Analgesia such as paracetamol and anti-spasmodic such as mebeverine may be used
Diverticulitis:
- Analgesia/anti-spasmodic. Fluid or low residue diet, to rest bowel.
- Co- amoxiclav
- Surgery if complications
Complications of diverticulitis
Colovesical fistula - Faecaluria, pneumaturia (stools and gas in urine)
Abscess
Perforation/ rupture onto peritoneum -> Bacterial peritonitis
Bowel obstruction
Define appendicitis
Inflammation of the appendix, most often due to obstruction of it’s lumen by either stool masses (faecalith), worms, or lymphoid hyperplasia secondary to infection. Associated with E. coli infection.
Pathophysiology of Appendicitis
Obstruction of appendix causes resident bacteria (e.coli) to be trapped. Mucus and fluid builds, increasing pressure. Appendix grows and pushes on afferent visceral nerve fibres causing pain. Pushing on blood vessels causes ischaemia, so mucosa dont secrete mucus anymore. This allows bacteria to multiply further. Appendix can rupture, causing peritonitis.
Signs and symptoms of appendicitis
- Central abdominal pain which radiates to right iliac fossa (McBurney’s point - 2/3 of the way from belly button to ASIS (anterior superior iliac spine))
- Fever
- Tachycardia
- Anorexia
- Guarding
- Rovsing’s sign: Pain felt in RIF when LIF palpated
- Rebound tenderness in RIF suggests peritonitis
Pain signs in appendicitis
Rosving - Pressing on RIF/RLQ worsens LIF/LLQ pain
Obturator - pain is worsened by flexing and internally rotating the hip
Psoas - pain is worsened by extending the hip
What is the Alvarado score?
A prediction score of the likelihood of appendicitis. >7 = very likely
5-6 may warrant ultrasound or CT
Investigations in appendicitis
FBC - Leukocytosis
ESR/CRP - Raised
Urinalysis - Exclude renal colic (no nitrates)
Pregnancy test - Exclude ectopic pregnancy
Ultrasound in children and pregnancy
CT GOLD
Differentials of appendicitis
Ectopic pregnancy
Ovarian cysts
Meckel’s diverticulum (paediatric disorder, failure of obliteration of vitelline duct)
UTI
Perforated ulcer
Management of appendicitis
Appendectomy first line
- IV antibiotics before surgery to reduce wound infections (amoxicillin and metronidazole, or piperacillin)
Complications of appendicitis
Perforation/rupture -> Peritonitis
Appendix abscess
Appendectomy complications
- Bleeding, infection
- Damage to nearby organs (bowel, bladder)
- Venous thromboembolism
Pathophysiology of bowel obstruction
- Peristalsis against a mechanical obstruction causes a “colicky, central abdominal pain” as well as distension and vomiting
- Leads to dilation of the bowel proximal to blockage
- This compresses mesenteric vessels and mucosal oedema, causing increased secretion of fluid into the distended bowel. (third spacing) This causes dehydration, tachycardia and hypotension (and can lead to ischaemia, infarction or perforation)
- Bowel ischaemia leads to perforation and peritonitis, which is life threatening and can cause sepsis, shock and death.
Causes of small bowel obstruction
Previous surgery (main cause)
- Previous abdominal surgery leads to formation of adhesions (abdominal strictures stuck by fibrous tissue)
Hernias
Malignancy
Gallstone ileus
Paralytic ileus
Crohns
Signs and symptoms of small bowel obstruction
Signs
- Colicky central abdominal pain with mild distension (higher than LBO)
- Nausea/vomiting early and constipation late
- Abdominal mass indicates hernia
- Hyperresonance on percussion (tenderness indicates peritonitis)
- Tinkling bowel sounds
Causes of large bowel obstruction
Colorectal cancer most common
Volvulus (twisting of stomach or intestine)
Stricture secondary to diverticulitis
Risk factors for large bowel obstruction
Increasing age
Colorectal cancer
Strictures (Diverticulitis, IBD, post surgical bowel resection)
Volvulus
Diabetes
Family history
Signs and symptoms of large bowel obstruction
- Onset of symptoms is much slower in LBO than SBO
- More constant abdominal pain with lower, larger distention.
- Constipation happens early and vomiting/nausea occurs late.
- Hyperactive Tinkling bowel sounds early, followed by absent bowel sounds later
Investigations in bowel obstruction
1 - X Ray (first line imaging) - Will show dilated bowel loops in affected bowel. Volvuluses possible also. Free air under diaphragm suggests perforation EMERGENCY SURGERY
2- CT abdomen and pelvis with contrast is GOLD. Identify bowel loops, areas of ischaemia and perforation and underlying cause.
Management of bowel obstruction
“Drip and suck” (Fluid and NG)
- IV fluid resuscitation (correct dehydration and hypovolaemia caused by third spacing)
- NG Tube - Abdominal decompression
- Antiemetics and Nil By Mouth (bowel rest)
- Surgery last resort
> Endoscopic Decompression using flexible sigmoidoscope (untwist volvulus)
Define pseudo obstruction of the bowel, with some causes, investigation and treatment
Clinical picture mimicking colonic obstruction, but with no mechanical cause
- Postoperative stress
- Intraabdominal trauma/sepsis
- Drugs (opioids and antidepressants)
- Pelvic, spinal, femoral fracture
X ray shows Gas-filled large bowel
Treat underlying condition, neostigmine may help motility
Causes of upper GI bleeds (7)
- Peptic ulcers
- Mallory-Weiss tears
- Oesophageal varices
- Oesophagitis
- Boerhaave’s syndrome: spontaneous perforation of oesophagus, usually due to vomiting, which ruptures all the layers of the oesophageal wall (transmural).
- Oesophagus cancer
- Stomach cancer
Causes of lower GI bleeds
- Diverticulitis
- IBD, both
- Tumours
- Haemorrhoids
- Anal fissures
- Proctitis
- Perforated appendicitis
What is the Glasgow Blatchford score
Identifies if patients with an upper GI bleed need emergency intervention such as blood transfusion or endoscopic intervention. Helps to identify patients who are low risk too.
Takes into account urea, BP (low worse), haemoglobin and features such as malaena, tachycardia, syncope etc.
0-1 outpatient treatment
5+ risk of 30day mortality
7+ endoscopic intervention
Variceal vs non variceal bleeding history factors
Variceal - Liver disease / alcohol excess
Treated with antibiotics and terlipressin
Endoscopy in 12 hours
Non- variceal - History of peptic ulcers, NSAID, anticoagulation
Treated with PPI, endoscopy in 24 hrs
Define Mallory-Weiss tear
Longitudinal lacerations to mucosa and submucosa at border of Gastro-oesophageal junction
Causes of mallory-weiss tear
Due to conditions that cause retching or vomiting
- Alcohol weakens gastric mucus membrane
- Chronic cough
- GORD
- Chest trauma
- Heavy lifting/straining
- Gastroenteritis
Signs and symptoms of mallory weiss tear
Patient with alcohol background having episodes of violent retching or vomiting. Can vomit blood but blood in faeces is rare
Investigations in mallory weiss tear (2)
Glasgow blatchford - assess if patient needs inpatient or outpatient care
1st - Upper GI endoscopy shows longitudinal tear(s) in mucosa at gastro-oesophageal junction
FBC may be appropriate to assess bleed risk/anaemia
What score is conducted to risk stratify endoscopic treatment of Upper GI bleeds
Rockall score
- Calculated after endoscopy to risk stratify patients for adverse outcomes following endoscopic treatment of upper GI bleed.
Management of mallory weiss tear
MWT usually self limiting but can be fixed in endoscopy
- Clipping with adrenaline
- Thermal coagulation with adrenaline
- Variceal band litigation
- High dose PPI, give after endoscopy
Define oesophageal varices
Abnormal, dilated veins at the lower end of oesophagus, usually as result of portal hypertension. Present in half of patients with cirrhosis.
Risk factors for oesophageal varices
Portal hypertension
Cirrhosis
Alcoholism
Schistosomiasis infection
Large varices and decompensated cirrhosis are risk factors for bleeding
Signs/symptoms of oesophageal varices
Asymptomatic if no bleeding,
otherwise can have shock symptoms
Otherwise symptoms of liver failure
- Spider angioma
- Palmar erythema
- Leukonychia
- Encephalopathy
- Jaundice
- Ascites
Investigations of oesophageal varices
Upper GI endoscopy
2 scores important to conduct in an upper GI bleed
Rockall
Glasgow blatchford
Management of oesophageal varices
no bleeding- endoscopic surveillance + beta blocker
Bleeding- fluid resuscitation until haemodynamically stable
Stop bleed
- IV terlipressin (causes splanchic vasoconstriction)
- Variceal banding on endoscopy
- TIPS (transjugular intrahepatic portosystemic shunt) if banding fails
Prophylaxis
Beta blocker
Endoscopic variceal band litigation
What are the two bowel ischaemia conditions?
Ischaemic colitis - Ischaemia of the large bowel causing inflammation, usually due to pathology of the inferior mesenteric artery
Mesenteric ischaemia - Ischaemia of small bowel, usually due to pathology of the superior mesenteric artery
Causes of mesenteric ischaemia
Thrombosis
Emboli
AF
affecting the SMA (Superior Mesenteric Artery)
Causes of Ischaemic Colitis
Thrombosis
Emboli
AF
Hypoperfusion
Watershed areas most affected
- Splenic flexure
- Sigmoid colon/caecum
Signs/symptoms of mesenteric ischaemia
Triad:
- Central/RIF Acute severe abdominal pain
- No abdominal signs on exam
- Rapid hypovolaemic shock
- Epigastric bruit if chronic
Signs/Symptoms of ischaemic colitis
- LLQ pain and bright bloody stools (May have hypovolaemic shock)
Investigations of bowel ischaemia
Mesenteric ischaemia - CT Angiogram
Ischaemic colitis - Colonoscopy + biopsy (after recovery - prevent stricture formation, done to rule out other causes.
Treatment of bowel ischaemia
Mesenteric ischaemia - Fluid resuscitation, IV Heparin, bowel rest
- Laparotomy
Ischaemic colitis - IV fluid and prophylactic Antibiotics
- Surgery if infarcted/gangrenous
Define anal fissure with causes
Painful tear in squamous lining of lower anal canal, distal to dentate lining resulting in pain on defection
Causes:
- Hard faeces
- Enemes
- Endoscope
- IBD
Signs/symptoms of anal fissure, investigation and treatment
Extreme pain, especially on defecation
Bleeding
Faecal impact and constipation due to avoidance of toileting
Perianal inspection and rectal exam sufficient
Increase fibre + fluids
Lidocaine ointment + GTN ointment
Define anal fistula with causes
Abnormal connection between epithelial surface of anal canal and skin. (Abnormal “Tracks”)
Causes
- Progression from abscess
- Perianal sepsis
- Crohn’s
- Rectal carcinoma
Signs and symptoms of anal fistula. Investigations and treatment
Pain
Malodorous, mucusy discharge
Pruritus ani
Secondary to abscess
MRI to exclude sepsis
Endoanal ultrasound
Treated surgically
Define anal abscess with symptoms, investigation and treatment
- Superficial infection, appearing as a tender red lump under skin near anus, usually caused by gut organisms.
- Painful swelling with pus in stools
- Investigation physical exam
- Managed with surgical excision and drainage (resistant to antibiotics as walled off)
Define pilonidal sinus/abscess with symptoms and treatment
Hair follicles stuck in natal cleft (ass crack), forming small tracks (sinuses) and get infected forming abscesses.
Causes a swollen, pus filled, smelly abscess on cleft.
Surgical removal
Define haemorrhoids/ piles
Haemorrhoids are normally spongy vascular structures in anal canal that act as cushions for stool as it passes through.
Haemorrhoidal disease (haemorrhoids) is when they get swollen and inflamed
Classifications of haemorrhoids
Internal - above dentate line
External - below dentate line
Internals graded
1 - No protrusion out of anal canal
2 - Protrusion during stool passage but retract
3 - Protrude, dont retract but can be pushed in
4 - Prolapsed haemorrhoids that cannot be pushed in
Causes of haemorrhoids
Recurrent increased abdominal pressures
- Straining during bowel movements
- Chronic diarrhoea, constipation
- Congestion from pelvic tumour
Signs/symptoms of haemorrhoids and investigations
Internal: Usually asymptomatic, can be slightly uncomfortable, and have fresh red blood
External: Very painful, patients cant sit. Have discharge, swelling and itching.
Rectal exam and proctoscopy for internal
Management of haemorrhoids
1 - Increase fibre/fluids
- Stool softeners
- Topical analgesia or steroids
2/3/4 - Rubber band litigation, sclerotherapy or surgical treatment
2 main types of oesophageal cancer
Adenocarcinoma (lower 1/3 of oesophagus, associated with Barrett’s oesophagus)
Squamous cell carcinoma (Upper 2/3 oesophagus, smoking and alcohol)
Risk factors for oesophageal cancers
Adenocarcinoma
- Barrett’s oesophagus
- Obesity
- Male
- Smoking
SCC
- Achalasia
- Alcohol
- Smoking
- Hot beverages
Signs/symptoms in Oesophageal cancer
Usually detected LATE so prognosis bad
ALARMS
A - Anaemia
L - Loss of weight
A - Anorexia
R - Recent sudden worsening of symptoms
M - Malaena/ Haematemesis
S - Swallowing with progressive difficulty
What does non progress dysphagia suggest
Achalasia
Investigations in oesophageal cancer
Upper GI endoscopy and biopsy, with barium swallow
CT/PET for staging
What system used for cancer staging
TNM
Management of oesophageal cancer
Adenocarcinoma: Chemotherapy/ radiotherapy + surgical (oesophagectomy)
SSC - Only chemo/radio
Main test for blood in stools
FIT test (Faecal immunochemical testing)
What type of cancer are gastric carcinomas, with the two types
Mostly adenocarcinomas (lymphoma, leiomyosarcoma, carcinoid tumour also possible)
Divided into
Intestinal (type 1) - Well differentiated (resemble normal cells), better prognosis
Diffuse (type 2) - Poorly differentiated
Causes of gastric carcinoma
Male
CDH-1 mutation
H Pylori (especially intestinal)
Lynch syndrome
Gastritis (autoimmune)
Pernicious anaemia
Signs/symptoms and investigation of gastric cancer
Severe epigastric pain with classic cancer symptoms
Progressive dysphagia
Iron deficiency anaemia
Polyarteritis nodosa
Upper GI endoscopy + biopsy
Management of gastric cancer
Gastrectomy (oesophageogastrectomy if oesophagus involved)
Chemotherapy
Complications of gastric cancer
Polyarteritis nodosa
Anaemia
Metastasis (lung, liver, peritoneum, ovary, virchows node)
Bleeding
Gastric outlet obstruction
Hereditary causes of large bowel cancer
- Autosomal dominant
familial adenomatous polyposis (FAP) - Autosomal dominant condition causing polyp formation - Hereditary non polyposis colon cancer (HNPCC-Lynch syndrome) - MSH1 mutation, rapidly increasing progression from adenoma to adenocarcinoma
Common metastases of large bowel cancer
Liver and lung
What are polyps
Abnormal growth of tissue projecting from colonic mucosa, increase with age. Polyps with APC mutation more likely to become neoplastic. Removed in colonoscopy
How is large bowel cancer staged
TNM and Dukes’ used for large bowel carcinoma
Signs symptoms of large bowel cancer
Left sided
- Rectal mass with LLQ pain and abdominal dysfunction, rectal bleeding, tenesmus
Right sided
- Iron deficiency anaemia
- Progressive bowel habit change
- Symptoms of large bowel obstruction
How is large bowel cancer investigated
Colonoscopy and biopsy
CT colonography if patient old, unstable
CT CAP (colon abdomen pelvis) for staging and metastases
Faecal occult blood and faecal immunochemical tests used for blood in stools
Management of large bowel cancer
Iron replacement
Chemo/radiotherapy
Colon resection
Hartmann’s procedure, in sigmoid colon
Define pseudomembranous colitis
Swelling of large intestine due to C. diff overgrowth, usually due to gut flora being wiped out by antibiotics.
Treated with vancomycin or metronidazole
Treatment of C diff
Oral metronidazole
What electrolyte is increased in upper GI bleed?
Urea
