Gastroenterology Flashcards
inWhat is the anatomical critera for an upper GI bleed classification?
If it occurs above the ligament of treitz.
Aetiology of an upper GI bleed
Peptic ulcers
Oesophageal varices
Mallory-Weiss tear
Clinical presentation of an upper GI bleed
Melaenia (black stools).
Haematemesis - looks like coffee grounds
Abdominal pain
What score can be used to assess a patients condition in a suspected upper GI bleed?
Glasgow-Blatchford score
Acute management of upper GI bleed
ABCDE
Fluid resuscitation
Blood transfusion
Keep patient nil by mouth
What are the 2 types of upper GI bleeds?
Variceal and non-variceal bleed.
What features of a patient’s history would indicate an non-variceal bleed?
Peptic ulcers
NSAID use
Anticoagulants, antiplatelets
What features of a patient’s history would indicate an variceal bleed?
Alcoholism
PMH of liver disease
Management of non-variceal bleed
Blood transfusion
Stop NSAIDs, anticoagulants
Endoscopy within 24 hours
Management of oesophageal variceal bleed
ABCDE
Terlipressin (ADH analogue)
Antibiotics
Endoscopy within 12 hours.
Oesophageal band ligation surgery.
Define small bowel obstruction
SBO is a form of Intestinal failure
Inability of the gut to absorb necessary water, nutrients and electrolytes sufficient to sustain life, requiring intravenous supplementation or replacement.
Aetiology of small bowel obstruction
Intestinal adhesions
Hernias
Cancerous tumours
What are the 3 types of intestinal obstruction that can occur?
Intraluminal
Intramural
Extraluminal
Aetiology of intraluminal small bowel obstruction
Gastrointestinal tumour
Diaphragm disease
Meconium ileus
Gallstone ileus
Aetiology of intramural small bowel obstruction
Inflammatory- Crohn’s disease, diverticulitis
GI Tumours
Hirschsprung’s disease
Clinical presentation of small bowel obstruction
Abdominal colic
Bilious vomiting - green color
Constipation follows vomiting
Abdominal distension
Examination of small bowel obstruction
PR exam - bloating = gas is getting through so not likely to be obstructed.
Tinkling bowel sounds upon auscultation
Investigation of small bowel obstruction
FBC - to check for anaemia, infection
CRP to assess for inflammation.
U + E
Serum lactate - marker of anaerobic respiration.
CT abdomen and pelvis with contrast - gold standard
Gastrografin challenge: Administration of oral X ray contrast, perform AXR to see how far contrast has got.
General management of small bowel obstruction
Supportive Management
Pain: analgesia (usually opiates, IV since vomiting).
Assess fluid balance: Nasogastric tube, urinary catheter.
Resusciate: IV fluids
Alleviate nausea: Antiemetics
Nutrition: If >5 days without intake, may need parenteral feed.
Surgical removal of obstruction for unstable patients.
Management of small bowel obstruction due to adhesions
Signs of ischaemia/shock = resuscitate, operate.
If non-ischaemic, non-operative management for up to 3 days.
Complications of small bowel obstruction surgeries
Renal failure
Sepsis
Arrythmias
What medication is contraindicated for bowel obstructions?
Laxatives
Aetiology/risk factors for Barret’s oesophagus
GORD
Hiatus hernia
Obesity
Pathophysiology of Barret’s oesophagus
Metaplasia of the oesophageal epithelium from squamous epithelium to columnar epithelium in lower third of oesophagu
Caused by acid reflux which kills the squamous cells.
Regenerated columnar cells have a layer of mucous that protects from further acidic damage.
Complications of Barrett’s oesophagus
Oesophageal cancer
How would normal oesophageal squamous epithelium appear on endoscopy?
White tissue due to light reflection.
How would columnar epithelium due to Barret’s oesophagus appear on endoscopy?
Red tissue
Risk factors for gastic carcinoma
Dietary nitrosamines
H.pylori infection
Tobacco smoking
E.cadherin protein mutation
Clinical presentation of gastric cancer
ALARM symptoms +/-
Epigastric pain
Nausea/vomiting
Anaemia
Dysphagia if pressing on pyloric sphincter.
Virchow’s node - supraclavicular node enlargement.
Where can gastric cancer commonly metastasize to?
Ovaries - Krukenburg tumour
Liver- jaundice
Management of oesophageal, gastric and bowel cancer
Surgical resction of tumour + chemotherapy.
Aetiology of familial adenomatous polyposis
Genetic mutation in APC gene.
Pathophysiology of familial adenomatous polyposis
Causes formation of several adenomatous polyps in the colon
Complication of familial adneomatous polyposis
Can become malignant and turn into colon cancer.
Aetiology of lynch syndrome (hereditary non polyposis colorectal cancer)
Mutation in DNA protein repair genes
Pathophysiology of lynch syndrome
Can result in non-responsiveness to chemotherapy due to inactivation of apoptosis.
What type of cancer is gastric, small, and large bowel cancer?
Adenocarcinomas.
Aetiology of extraluminal small bowel obstruction
Bowel adhesions
Volvulus - twisting of the bowel.
Peritoneal tumour
How do normal gut flora prevent infection?
Inhibiting overgrowth of endogenous pathogens
Preventing colonisation by exogenous pathogens.
Bacterial aetiology of diarrhoea
Shigella
Salmonella
E.coli
C.difficile, C.perfringens
Campylobacter jejuni
V.cholerae
Bacillus cereus
Non-infective aetiology of diarrhoea
IBD - Crohn’s/ulcerative colitis
Bowel cancer
Hyperthyroidism
Pancreatitis
Which bacteria can cause secretory diarrhoea?
Vibrio cholerae
ETEC E.coli
Clostridium perfringens
Bacillus cereus
Which bacteria can cause dysentery?
Shigella
Salmonella
E.coli (EIEC, EHEC)
C.difficile
Campylobacter jejuni
Viral aetiology of diarrheoa
Norovirus
Rotavirus
Parasitic aetiology of diarrhoea
Giardia lamblia
Cryptosporidium
Entamoeba histolytica
What organism can cause diarrhoea from re-heated food/takeaways, etc?
C.perfringens
Bacillus cereus
What organisms can cause diarrhoea from petting zoos?
E.coli
Cryptosporidum
Salmonella
What is traveller’s diarrhoea?
Occurs a few days after arrival in a new country.
Aetiology of traveller’s diarrhoea
ETEC
Campylobacter
Cholera
Aetiology of clostridium difficile infection
Broad spectrum antibiotic use:
Co-amoxiclav
Cephalosporins
Clindamycin
Ciprofloxacin
Pathophysiology of clostridium difficile infection
Contains endospores which can survive stomach acidity.
BSA use kills normal gut flora which allows C.diff flourishing.
Releases toxin A + B causing mucosal damage and dysentery
Clinical presentation of clostridium difficile infection
Fever
Dystentery
Abdominal pain
Management of clostridium difficile infection
Oral Metronidazole + oral vancomycin
Complication of clostridium difficile infection
Pseudomembraneous colitis.
Aetiology of vibrio cholerae infection
Shellfish, saline environments (floods, etc)
Pathophysiology of vibrio cholerae infection
Release of cholera toxin which causes intestinal Cl- secretion and fluid loss through diarrhoea.
Clinical presentation of vibio cholerae infection
Profuse, rice-water diarrhoea
Vomiting
Dehydration
What is the most common cause for diarrhoea in children?
Rotavirus
Medical management of diarrhoea in children
Fluid Replacement/oral rehydration salts to prevent dehydration
What goes out must come in - e.g 1 l a day excretion means administer same amount gradually over the day (sips).
Zinc treatment
Preventative management of diarrhoea in children
Rotavirus and measles vaccinations
Promote breastfeeding + Vitamin A supplementation
Promote hand washing with soap
Water treatment & safe household storage
Why can formula feeding in LEDCs cause an increased risk of diarrhoea?
Water used to mix the formula with may not be sanitary.
What are some red-flag signs to point towards gastrointestinal cancer?
Anaemia
Loss of weight
Anorexia (loss of appetite)
Recent onset of progressive symptoms
Melena/masses
Swallowing difficulties.
What is gastritis?
Inflammation of the stomach mucosa.
Aetiology of acute gastritis
Helicobacter pylori infection
Alcohol abuse
Stress (critically ill, major surgery)
NSAIDs (COX inhibitor → inhibits prostaglandin synthesis→ less alkaline mucus secretion)
Aetiology of chronic gastritis
H.pylori infection
Autoimmune gastritis
Pathophysiology of autoimmune gastritis
Anti-parietal cell antibodies cause destruction resulting in loss of intrinsic factor and HCl production.
Complications of autoimmune gastritis
Can lead to decreased vitamin B12 absorption and pernicious anaemia.
Clinical presentation of gastritis
Dyspepsia (indigestion)
Epigastric pain
Anorexia
Nausea & vomiting
Bloating
Investigation of gastritis
For H.pylori infection:
Urea breath test
Stool antigen test
Endoscopy
Management of gastritis
Omit causative agent, e.g NSAID use, alcohol
H.pylori infection:
First line - triple therapy of PPI + amoxicillin 1g + clarithromycin 500mg
If penicillin allergy, replace amoxicillin with metronidazole 400mg.
Management of autoimmune gastritis
IM Hydroxycobalamin (vit.B12 replacement for pernicious anaemia)
Complications of chronic gastritis
Increased risk of peptic ulcers (H.pylori infection) and pernicious anaemia (autoimmune gastritis)
What are the types of peptic ulcers
Gastric and duodenal ulcers.
Aetiology of peptic ulcers
NSAIDs
H.pylori infection
Gastritis
Clinical presentation of peptic ulcers
Localised burning epigastric pain.
Dyspepsia
Anorexia/weight loss
Can prevent with haematemesis/weight loss of artery perforation.
How is the nature of the pain in a gastric ulcer?
Worsens after eating due to increased HCL production to digest food.
How is the nature of the pain in a duodenal ulcer?
Better right after eating due to closure of pyloric sphincter to prevent acid from entering duodenum during gastric digestion.
Gets worse a while after eating due to food and acid entering duodenum.
What arteries can be perforated with peptic ulcers?
Gastric ulcer: Left gastric artery
Duodenal ulcer:Gastroduodenal artery
Investigation of peptic ulcers
Gold standard - endoscopy
H.pylori tests - urea breath test and stool antigen test.
Complication of gastric ulcers
Increased risk of gastric carcinoma
Aetiology of malabsorption
Defective intraluminal digestion - cystic fibrosis, biliary obstruction.
Insufficient absorptive area - - coeliac disease, giardia lamblia infection
Defective epithelial transport - Abetalipoproteinaemia
Lack of digestive enzymes - disaccharide deficiency
Lymphatic obstruction - lymphoma, TB
Clinical presentation of malabsorption
Unexpected weight loss
Steatorrhea - fat is not getting digested/absorbed
Diarrhoea
Anaemia - iron deficiency
Aetiology of coeliac disease
Associated with HLADQ 2 and HLADQ 8
Associated with other autoimmune conditions - T1DM, hashimoto’s, dermatitis herpetiformis.
Associated with IgA deficiency
Pathophysiology of coeliac disease (gluten sensitive enteropathy)
T4 hypersensitivity reaction.
Prolamins (gliadin protein in wheat) pass through intestinal epithelium and are deaminated by tissue transglutaminase.
APCs present the peptides to T-cells through HLADQ 2 and HLADQ 8.
Result in inflammatory response and synthesis of
anti-tissue transglutaminase (anti-tTG) and anti-endomysial (anti-EMA) antibodies.
Causes villous atrophy and malabsorption.
Clinical presentation of coeliac disease
Symptoms of malabsorption -
Anaemia
Steatorrhoea
Diarrhoea
Weight loss
Dermatitis herpetiformis - itchy bumps
Angular stomatitis - ulcers on the corners of mouth.
Investigation of coeliac disease
First line - serology - Raised anti-tTG Ab
Second line - serology - Raised anti-EMA Ab
Gold standard - endoscopic duodenal biopsy
Management of coeliac disease
Lifelong gluten-free diet
May require vitamin and mineral supplements.
Recommend regular immunisation as coeliac disesae can cause hyposplenism.
What could be seen histologically for coeliac disease?
Villous atrophy, crypt hyperplasia.
What conditions comprise inflammatory bowel disease (IBD)?
Crohn’s disease
Ulcerative colitis
Aetiology/risk factors of IBD
Family history
NSAID use
Smoking - increases risk of CD but not UC
Where can IBD occur?
CD: From mouth to anus, can be rectal sparing.
UC: Colon, always with rectal involvement, does not go more proximal than ileocaecal valve.
What is the nature of the lesions in IBD?
CD: Skip lesions, areas of inflammation with gaps of normal tissue in between.
UC: Continuous lesions.
What is the macroscopic morphology of the inflammation in IBD?
CD: Transmural inflammation with cobblestone-like appearance
UC: Only superficial (mucosal and submucosal) inflammation.
Friable (easily bleeding) mucosa.
What is the microscopic morphology of the inflammation in IBD?
CD: Can have non-caseating granulotamous inflammation, presence of goblet cells.
UC: Can have crypt abscesses, no goblet cells or granulomas.
What are some gastrointestinal presentations of IBD?
CD: Diarrhoea
Lower right quadrant pain usually.
UC: Dysentery
Lower left quadrant pain
Both: Symptoms of malabsorption - anaemia, weight loss, steatorrhoea
What are some extra-intestinal presentations of IBD?
Ankylosing spondylitis (HLA B27)
Aphthous ulcers / amyloidosis
Clubbing
Pyoderma gangrenosum
Iritis (aka anterior uveitis)
Erythema nodosum
Sclerosing cholangitis
Investigation of IBD
FBC - Anaemia, neutrophilia, thrombophilia
ESR and CRP - elevated
Serology - pANCA (Perinuclear Anti-Neutrophil Cytoplasmic Antibodies)
Stool samples - faecal calprotectin
Gold standard - colonoscopy (or endoscopy for CD) with biopsy
Abdominal imaging - barium swallow and AXR.
What would serology reveal for IBD?
CD - negative pANCA
UC - positive pANCA
What would abdominal imaging reveal for IBD?
CD: String sign upon barium X-ray
UC: Lead-pipe appearance for UC on AXR.
What are some complications of IBD?
CD: Fistula formation, amyloidosis, malabsorption
UC: Toxic megacolon, colorectal cancer, sclerosing cholangitis.
What is the age distribution of clinical presentation like for IBD?
CD: Bimodal distribution with peaks from ages 15-30 and ages > 60.
UC: Risk increases with age, mainly presents in15-30 y/o.
Medical management of Crohn’s disease
First line - steroids e.g prednisolone/hydrocortisone/budesonide.
Second line - add DMARDs such as azathioprine or methotrexate
If still severe - infliximab (anti-TNF monoclonal antibody)
Maintaining remission - azathioprine + methotrexate
Medical management of Ulcerative Colitis
Mild:
First line - mesalazine (aminosalicylate)
Second line - add prednisolone (steroid)
Severe:
IV fluid resuscitation
IV hydrocortisone
Prophylaxis with LMWH to prevent clot formation.
If still unresponsive, infliximab (anti-TNF monoclonal antibody)
Surgical management of IBD
Subtotal colectomy with end ileostomy.
What are functional gut disorders/disorders of gut-brain interaction?
Symptoms occur in the absence of any structural abnormalities and can affect the gut-brain axis to cause issues such as:
Visceral hypersensitivity
GI dysmotility
Alteration of gut microbiome
What are examples of compose functional gut disorders/disorders of gut brain interaction?
Irritable bowel syndrome (IBS)
Functional dyspepsia
Aetiology/risk factors for IBS
Mood disorders - depression
Anxiety/stress
Clinical presentation of IBS
Recurrent abdominal pain that eases with defacaetion
Bloating
Changes in stool habits (diarrhoea/constipation)
Symptoms worse after eating.
Can have urinary and gynaecological symptoms
Differential diagnosis for IBS
Coeliac disease, lactose intolerance, bile acid malabsorption, IBD, colorectal cancer.
Investigation of IBS
Rule out differentials
FBC - check for anaemia
ESR & CRP - check for inflammation
Stool sample - IBS has negative faecal calprotectin
Serology - endomysial antibody and tissue transglutaminase antibody negative = not coeliac
Colonoscopy - rule out colorectal cancer.
Management of IBS
Low FODMAP diet
Diarrhoea - anti-motility agents (Loperamide)
Constipation - laxatives (prucalopride)
Aetiology of dyspepsia
Functional (idiopathic) dyspepsia
H.pylori infection
Peptic ulcers
Gastritis
Clinical presentation of dyspepsia
Posprandial fullness
Early satiety
Epigastric pain/burning sensation
Bloating
Acid reflux, can be when lying down
What are the ALARMS symptoms?
Anaemia
Loss of weight
Anorexia (loss of appetite)
Recent onset of progressive symptoms
Masses / Melena (black stools) → or bleeding from any part of GI tract
Swallowing difficulties
What do the ALARMS symptoms indicate?
Gastrointestinal cancer.
Aetiology of a Mallory-Weiss tear
Heavy coughing
Vomiting - alcoholic dry heaving.
Weight lifting
Hiatus hernia
Pathophysiology of a Mallory-Weiss tear
Sudden increase in intra-abdominal pressure can cause mucosal tear in near gastro-oesophageal junction.
Clinical presentation of Mallory-Weiss tear
Haematemesis
Abdominal pain
Postural hypotension
Dizziness
Investigation of Mallory Weiss tear
Endoscopy
Management of Mallory-Weiss tear
Endoscopic injection therapy
Aetiology of Achalasia
Mainly idiopathic
Chagas disease
Pathophysiology of Achalasia
Ganglionic degeneration in auerbach’s plexus causes lack of contraction of lower oesophageal sphincter and lack of peristalsis.
Clinical presentation of Achalasia
Dysphagia of solids and liquids
Food regurgitation - can cause aspiration pneumonia
Spontaneous chest pain due to oesophageal spasm.
Investigation of Achalasia
CXR - dilated oesophagus
Endoscopy
Barium swallow fluoroscopy - bird’s beak sign
GS: Manometry (oesophageal motility study) = gold
Management of Achalasia
Lifestyle - Smaller, more frequent meals.
Medical - Nitrates/CCBs to relax LOS such as isosorbide dinitrate/nifedipine
Interventional - Endoscopic pneumatic dilation, laporoscopic cardiomyotomy
Complications of Achalasia
Aspiration pneuomonia during sleep
Increased risk of oesophageal squamous cell carcinoma
Aetiology of GORD
Obesity
Pregnancy
Hiatus hernias
Smoking
NSAIDs, Caffeine, Alcohol
Male gender (2x more likely)
Hypersecretion of acid
Pathophysiology of GORD
Reduced tone of LOS causes gastric acid reflux into oesophagus.
Clinical Presentation of GORD
Heartburn - burning chest pain aggravated by bending, stooping or lying down.
Pain becomes worse with spicy food/hot drinks.
Cough
Increased belching
Epigastric pain
Regurgitation of stomach contents - worse when lying down.
Hoarse voice due to laryngopharyngeal reflux
Investigation of GORD
Endoscopy - presence of Barret’s or oesophagitis is diagnostic.
Intraluminal pH monitoring.
Management of GORD
Lifestyle:
Smoking cessation
Reduced alcohol intake
Eating smaller meals
Avoiding eating 3-4 hours before sleeping.
Medical:
FL: PPI e.g omeprazole
Can also use:
Alginate containing antacids - magnesium trisilicate
H2 receptor antagonists - cimetidine, ranitidine.
Interventional - Nissen fundoplication
Where is the appendix located?
McBurney’s point - 1/3 of the way between ASIS and umbilicus.
Aetiology of appendicitis
Faecoliths (hardened stool)
Lymphoid hyperplasia
Intestinal worms
Pathophysiology of appendicitis
Luminal obstruction causes stasis of faecal matter and overgrowth of bacteria causing infection and inflammation.
Examination of Appendicitis
Rovsing’s sign - palpation of LIF causes pain in RIF
Psoas sign - RIF pain upon right hip extension.
Obturator sign - RIF upon right hip flexion and internal rotation.
Guarding - reflect contraction of abdo muscles upon palpation.
Rebound tenderness - pain when pressure is removed during palpation.
Investigation of Appendicitis
FBC: Leukocytosis
Raised ESR, CRP
Abdominal US (in children and pregnant women)
Abdominal CT with contrast - gold standard
Urinalysis (exclude UTI)
Pregnancy test
Management of Appendicitis
Antibiotics: Cefuroxime + Metronidazole
Surgical appendectomy
What are the 3 types of bowel ischaemias?
Acute mesenteric ischaemia
Chronic mesenteric ischaemia (AKA intestinal angina)
Ischaemic colitis (AKA chronic colonic ischaemia)
What areas of the bowel are most susceptible to ischaemia?
Splenic flexure and caecum due to them being watershed regions.
Aetiology of acute mesenteric ischaemia
SMA atheroma/embolism causing thrombosis.
Embolus from heart in a patient with AF is most common.
Mesenteric vein thrombosis - more common in younger patients
Hypotension, shock, decreased cardiac output.
Clinical presentation of acute mesenteric ischaemia and ischaemic colitis
Severe diffuse abdominal pain (left sided for ischaemic colitis)
Pallor, weak rapid pulse due to shock (rapid hypovolemia)
Nausea/vomiting.
Absence of bowel sounds.
Haematochezia
Investigation of acute mesenteric ischaemiaand ischaemic colitis
1st line: CT abdomen with contrast or angiography
ABG: Metabolic acidosis
Gold standard: colonoscopy
Management of acute mesenteric ischaemia and ischaemic colitis
IV gentamicin and metronidazole
IV heparin
Surgery - bowel resection.
Complications of bowel ischaemia and appendicitis
Bowel necrosis and appendix rupture can result in bacterial spreading leading to:
Sepsis
Peritonitis
Risk factors/aetiology of pseudomembraneous colitis
C.difficile infection
Recent antibiotic usage
CMV infection & immunocompromisation
Stay in a healthcare center/nursing home.
Pathophysiology of pseudomembraneous colitis
C.diff infection causes colonic mucosa to become inflamed, ulcerated, and covered by an adherent membrane-like material.
Investigation of pseudomembranous colitis
FBC - leukocytosis
Stool sample - C.diff infection
Colonoscopy - raised yellow plaques
Histology - owl eyes inclusion bodies for CMV
Management of pseudomembranous colitis
Stop original antibiotic - replace with oral metronidazole + vancomycin.
Maybe need faecal microbiota transplant.
Aetiology of large bowel obstruction
Malignancy (90%)
Sigmoid volvulus (5%) (coffee bean appearance on abdo X-Ray)
Diverticulitis
Intussusception (more common in children) is when the bowel fold within itself
Clinical presentation of large bowel obstruction
Continuous abdominal pain
Severe abdominal distension
Constipation first, followed by vomiting (initially bilious, then faecal vomiting)
Absent bowel sounds
Investigation of large bowel obstruction
1st line: Abdo XRay
Dilation of the large bowel >6cm
Dilation of the caecum >9cm
Gold standard: CT of the abdomen and pelvis with contrast
Management of large bowel obstruction
ain: analgesia (usually opiates, IV since vomiting).
Assess fluid balance: Nasogastric tube, urinary catheter.
Resusciate: IV fluids
Alleviate nausea: Antiemetics
Nutrition: If >5 days without intake, may need parenteral feed.
What can be caused by an H.pylori infection?
Gastritis - usually antral.
Peptic ulcers
Gastric cancer
Pathophysiology of h.pylori inection
Secretion of urease which convertes CO2 to ammonia.
Ammonia combines with stomach H+ to form ammonium which is toxic to the alkaline gastric mucus.
Investigation of h.pylori infection
Urea breath test - screening.
Stool antigen test - monoclonal antibodies to detect antigen.
Endoscopy - histoligical sampling and culturing.
Management of h.pylori infection
Triple therapy - 2 antibiotics (clarithromycin and amoxicicillin/metronidazole if allergic) + PPI (omeprazole/lanzoprazole)
What is a diverticulum?
Outpouchings of the gastrointestinal tract wall.
What is diverticulosis?
The presence of diverticula
What is diverticulitis and where does it mainly occur?
The presence of inflamed diverticula
Most comonly occurs in sigmoid colon, espesially in regions with perforating arteries.
Aetiology/risk factors of colonic diverticulosis
Constipation (low fiber diet)
Obesity
NSAIDs
Smoking
Pathophysiology of colonic diverticulosis
High colonic pressures causes regions of mucosa to outpouch and extrude through the mucosal wall.
Often has muscle thickening.
Pathophysiology of colonic diverticulitis
When faecal obstruction due to the diverticulum causes stagnation and bacterial overgrowth.
Can lead to infection and infection of the diverticula.
Clinical presentation of colonic diverticulitis
Bowel habits changed
Bloating / flatulence
Left illiac fossa pain
Nausea/vomiting
Haematochezia
Fever
Examination of colonic diverticulitis
Tenderness + guarding
Tympanic to percussion - gas/bloating.
Diminished bowel sounds.
Investigation of colonic diverticulitis
FBC - Leukocytosis
Raised ESR and CRP
Gold standard - CT colonography
Management of colonic diverticulitis
If uncomplicated:
High fiber diet
Analgaesia (paracetmol)/antispasmodics (mebeverine)
Complicated:
- Antibioitics - co-amoxiclav.
What is a hernia?
The profusion of a viscus (organ) or part of a viscus through a defect of the walls of its cavity into an abnormal position.
What are some examples of hernias?
Inguinal hernia (direct and indirect)
Femoral hernia
Hiatal hernia
Pathophysiology of Zencker’s diverticulum
Esophageal dysmotility causes herniation of mucosal tissue in Killians triangle - area between cricopharyngeus and thyropharyngeus muscle.
Can cause food to get stuck there.
Clinical presentation of Zencker’s diverticulum
Bad breath, dysphagia, choking.
What is the most common congenital gastrointestinal disorder?
Meckel’s diverticulum.
Pathophysiology of Meckel’s diverticulum
Persistence of vitelline duct, can cause intussusception, volvulus, or obstruction near terminal ileum
What is malrotation?
Anomaly of midgut rotation during fetal
development can cause improper positioning of bowel.
What is intussusception?
Telescoping of a proximal bowel segment into
a distal segment, most commonly at ileocecal
junction.
Example of intussusception in children
Meckel’s diverticulum.
What is a volvulus?
Twisting of portion of bowel around its
mesentery.
What type of volvulus is more common in infants/children?
Midgut volvulus
What type of volvulus is more common in adults?
Sigmoid volvulus.
Pathophysiology of Hirschprung disease
Congenital megacolon characterized by lack of innervation from enteric plexuses, leading to lack of motility.
What are haemorrhoids?
Disrupted and dilated anal cushions - masses of spongy vascular tissue due to swollen veins around the anus
Aetiology/risk factors of haemorrhoids
Constipation
Chronic coughing
Heavy lifting
Pregnancy
Clinical presentation of haemorrhoids
Bright red bleeding (on wiping. Not mixed in stool
Pruritus ani (anal itching)
Constipation
Lump around or inside the anus
Investigation of haemorrhoids
Digital rectal exam
Proctoscopy - see internal haemorrhoids
What are the classifications of haemorrhoids?
1st degree - internal, no bleeding
2nd degree - prolapsed but spontaenously reduces
3rd degree - prolapsed but requires manual reduction
4th degree - prolapsed but does not reduce
Management of haemorrhoids
Increased fluid and fiber intake
Laxatives
1st and 2nd degree - rubber band ligation, sclerosant injection
3rd & 4th degree - haemorrhoidectomy, haemhorroidal artery ligation operation (HALO)
What is an anal fistula?
Abnormal open connection between the anal canal and the skin of the gluteus maximus.
Aetiology of anal fistula
Anorectal abscess (70%)
Crohn’s ulcerations (30%)
TB
Clinical presentation of anal fistula
Throbbing pain, worse when sitting
Blood/mucus in stool
Pruritus ani
Investigation of anal fistula
Digital rectal exam
Endoanal ultrasound
Management of anal fistula
Surgical fistulotomy
What is an anal fissure?
Painful tear in the sensitive skin-lined lower anal canal, distal to the dentate line.
Aetiology of anal fissure
Constipation
Anal trauma
Associated with IBD.
Clinical presentation of anal fissure
Extreme pain on passing stools
Blood in stool / on wiping
Management of anal fissure
Increase dietary fiber and fluid intake
Lidocaine + GTN
Clinical presentation of anal abscess
Anal discharge/pus
Pain
Possible fever
Investigation of anal abscess
Endoanal ultrasound
Management of anal abscess
Surgical drainage and antibiotics
Aetiology of anal abscess
IBD
Anal trauma
Anal fistula
Aetiology of pilonidal sinus/abscess
Ingrown hairs
Pathophysiology of pilonidal sinus/abscess
Hair follicles get stuck under the skin in the natal cleft (butt crack) resulting in irritation and inflammation leading to small tracts which can become infected
Clinical presentation of pilonidal sinus/abscess
Painful swelling
Systemic infectin symptoms - fever, etc
Foul smelling discharge/pus.
Management of pilonidal abscess
Sinus excision and antibiotics.
What enteric pathogens can be identified by light microscopy?
Protozoans like cryptosporidium, entamoeba histioloitica and giardia lambila.
What is the purpose of XLD agar?
Can be used to differentiate between shigella and salmonella.
How would salmonella appear on an XLD agar?
Black spots
How would shigella appear on an XLD agar?
Red spots
Investigation of oesophageal and gastric cancer
Endoscopy (gastroscopy) + biopsy
CT chest/abdomen for metastasis
What are the 2 types of gastric cancer
T1 - intestinal type
T2 - diffuse type
Risk factors for t1 (intestinal) gastric cancer
Males, older age
Risk factors for t2 (diffuse) gastric cancer
Females, younger age
What regions of the stomach is affected by t1 gastric cancer?
Antrum + lesser curvature
What regions of the stomach can be affected by t2 gastric cancer?
Any region
Which type of gastric cancer is more metastatic?
T2 (diffuse) so has worse prognosis.
What is the histological distinction between t1 and t2 gastric cancer
T1: well formed tubules
T2: poorly differentiated signet ring cells
Clinical presentation of oesophageal cancer
Progressive dysphagia (solids followed by liquid)
Weight loss
Anorexia
Hoarse voice (pressing on recurrent laryngeal nerve)
Odynophagia (painful swallowing)
Red flags (ALARMS)
What are the 2 types of oespophageal cancer
Adenocarcinoma (lower 1/3)
Squamous cell carcinoma (upper 2/3)
Risk factors/aetiology of oesophageal adenocarcinoma
GORD
Barret’s oesophagus
Obesity
Male gender
Caucasian
Risk factors/aetiology of oesophageal squamous cell carcinoma
Smoking
Alcohol
BAME ethnicity
Achalasia
Investigation of bowel cancer
Gold standard = colonoscopy + biopsy
CT chest abdo pelvis for staging.
What screening tests is used to check for bowel cancer?
Faecal immunochemical test (FIT) test.
What bacteria are associated with causing peritonitis?
Gram negative: E.coli, kleibsiella pneumoniae
Gram positive: S.aureus, Mycobacterium tuberculosis,
Aetiology/risk factors of peritonitis
Appendicitis, ascites, liver failure, cirrhosis, surgery, TB infection
Pathophysiology of spontaneous bacterial peritonitis
Bacteria infects ascitic fluid
Presentation of peritonitis
Abdominal pain worse on movement (localised or spread)
Guarding
Pyrexia
Nausea/vomiting
Can have shoulder tip pain
Investigation of sponteneous bacterial peritonitis
Ascitic tap – raised ascitic fluid neutrophils
Ascitic fluid culture – shows causative organisms
ESR + CRP
Management of spontaenous bacterial peritonitis
ABCDE
IV antibiotics (cefotaxime)
Supportive therapy (IV fluids, analgesics, electrolytes)
Paracentesis
Examination of diverticulitis
Rebound tenderness
Guarding
