Gastrointestinal Flashcards
What is inflammatory bowel disease?
- umbrella term for disease causing inflammation of the GI tract
- associated with periods of remission and exacerbation
- crohn’s and ulcerative colitis
Crohn’s vs UC: Crohn’s
NESTS
- no blood or mucous (less common)
- entire GI tract
- skip lesions on endoscopy
- terminal ileum most affected and transmural (full thickness) inflammation
- smoking is a risk factor
also associated with weight loss, strictures and fistulas
Crohn’s vs UC: UC
CLOSEUP
- continuous inflammation
- limited to colon and rectum
- only superficial mucosa affected
- smoking is protective
- excrete blood and mucus
- use aminosalicyclates
- primary sclerosing cholangitis
Presentation of inflammatory bowel disease
- diarrhoea
- abdominal pain
- passing blood
- weight loss
Testing for inflammatory bowel disease
- routine bloods
- CRP → inflammation and active disease
- faecal calprotectin
- DIAGNOSTIC = endoscopy (OGD/colonoscopy) with biopsy
- imaging → complications
What is faecal calprotectin?
- released by intestines when inflamed
- >90% sensitive and specific to IBD in adults
What does management of IBD involve?
- inducing remission
- maintaining remission
- surgery
Inducing remission in Crohn’s
- steroids → oral prednisolone, IV hydrocortisone
- consider adding immunosuppressants
What immunosuppressants can be used in Crohn’s
- azathioprine
- mercaptopurine
- methotrexate
- infliximab
- adalimumab
Maintaining remission in Crohn’s
based on risks, side effects, nature of the disease, patient’s wishes
- azathioprine, mercaptopurine
alternatives = rest of the immunosuppressants
Surgery in Crohn’s
- if only distal ileum affected → surgical resection of area to prevent further flare ups
- treat stricture and fistulas
Inducing remission in UC
mild to moderate
- aminosalicylates eg mesalazine
- corticosteroids eg prednisolone
severe
- IV corticosteroids eg hydrocortisone
- IV ciclosporin
Maintaining remission in UC
- aminosalicylates
- azathioprine
- mercaptopurine
Surgery in UC
- removal of colon and rectum → panproctocolectomy
- patient left with permanent ileostomy or ileo-anal anastomosis
What is IBS?
- functional bowel disorder
- no identifiable organic disease underlying symptoms
- result of abnormal functioning of normal bowel
- very common, more common if young/female
Symptoms of IBS
ABCDEF
- abdominal pain
- bloating
- constipation
- diarrhoea
- eating makes it worse
- fluctuating bowel habit
- improved by opening bowels
Diagnostic criteria of IBS
diagnosis of exclusion
- normal bloods
- faecal calprotectin -ve
- coeliac disease serology -ve
- cancer not suspected/excluded
Management of IBS
- general healthy diet and exercise advice
- loperamide for diarrhoea, linaclotide for constipation, antispasmodics for cramps
- tricyclic antidepressants
- SSRIs
can also offer CBT
What is coeliac disease?
- exposure to gluten = autoimmune reaction that causes inflammation in small bowel
- usually develops in early childhood
Pathophysiology of coeliac disease
- auto-antibodies created in response to gluten
- target epithelial cells of the intestine → inflammation
- affects small bowel esp jejunum
- causes atrophy of intestinal villi and crypt hypertrophy
- malabsorption of nutrients → symptoms
Presentation of coeliac disease
- often asymptomatic
- failure to thrive in children
- diarrhoea
- fatigue
- weight loss
- mouth ulcers
- anaemia secondary to iron, B12, folate deficiency
- dermatitis herpetiformis
- neurological symptoms (rare)
What is dermatitis herpetiformis?
itchy blistering skin rash that typically appears on the abdomen
Diagnosis of coeliac
- raised anti-TTG
- raised anti-EMA
- total IgA levels → exclude IgA deficiency first
- endoscopy and intestinal biopsy → crypt hypertrophy and villous atrophy
What auto-antibodies are created in response to gluten?
- anti-tissue transglutaminase (anti-TTG)
- anti-endomysial (anti-EMA)
What conditions are associated with coeliac disease?
- T1DM
- thyroid disease
- autoimmune hepatitis
- PBC
- PSC
- Down’s syndrome
Complications of coeliac disease
- vitamin deficiency
- anaemia
- osteoporosis
- ulcerative jejunitis
- non-hodgkin’s lymphoma
Treatment for coeliac diease
lifelong gluten free diet
What is GORD?
- gastro-oesophageal reflux disease
- acid from stomach refluxes through the lower oesophageal sphincter and irritates lining of oesophagus
Why is the oesophagus more sensitive to stomach acid?
the epithelial lining is squamous
Presentation of GORD
- dyspepsia
- heartburn
- acid regurgitation
- retrosternal/epigastric pain
- bloating
- nocturnal cough
- hoarse voice
Diagnosis of GORD
- clinical diagnosis
- refer for endoscopy if red flags
When would you refer for an endoscopy?
- dysphagia
- > 55yrs
- weight loss
- upper abdominal pain/reflux
- treatment resistant dyspepsia
- N&V
- anaemia
- raised platelets
Management for GORD
- lifestyle advice
- acid neutralising medications → gaviscon, rennies
- PPIs → reduce stomach acid eg omeprazole, lansoprazole
- ranitidine = alternative to PPIs
surgery = laparascopic fundoplication → tie fundus of stomach around lower oesophagus → narrows lower oesophageal sphincter
What lifestyle advice would you suggest for GI problems?
- reduce tea, coffee, alcohol
- weight loss
- avoid smoking
- smaller, lighter meals
- avoid heavy meals before bed time
- stay upright after meals
What is a peptic ulcer?
ulceration of the mucosa of the stomach (gastric) or duodenum (duodenal)
duodenal are more common
Risk factors of peptic ulcers
- h.pylori
- NSAIDs/SSRIs/steroids
- smoking
gastric → stress
duodenal → alcohol
Presentation of peptic ulcers
epigastric pain
- gastric = worse on eating, relieved by antacids
- duodenal = before meals and at night, relieved by eating/milk
- N&V
- dyspepsia
- bleeding causing haematemesis, coffee ground vomiting, maelaena
- iron deficiency anaemia
Diagnosis of peptic ulcers
- h.pylori test → urease breath test
- endoscopy if red flags
Treatment for peptic ulcers
- lifestyle modification
- treat cause
- high dose PPIs
Complications of peptic ulcer
- haemorrhage
- perforation
- gastric outflow obstruction
- malignancy
What is appendicitis?
- inflammation of the appendix
- peak incidence = 10-20
- less common in young children and adults over 50
Pathophysiology of appendicitis
- pathogens can get trapped due to obstruction at the point where appendix meets bowel
- infection and inflammation
- may proceed to gangrene and rupture
- faecal contents and infective material are released into peritoneal cavity
- peritonitis → inflammation of peritoneal lining
Signs and symptoms of appendicitis
KEY FEATURE = abdominal pain
- loss of appetite
- N&V
- low-grade fever
- Rovsing’s sign → palpation of LIF causes pain in RIF
- guarding on palpation
- rebound tenderness in RIF
- percussion tenderness
Describe abdominal pain in appendicitis
- starts as central
- moves down to RIF within first 24hrs
- eventually becomes localised in RIF
- on palpation → tenderness at McBurney’s point
What is McBurney’s point
1/3 of the distance from the anterior superior iliac spine to the umbilicus
Diagnosis of appendicitis
- based on clinical presentation and raised inflammatory markers
- GOLD STANDARD = CT → confirms diagnosis
- US to exclude female pathology
Differential diagnoses for appendicitis
- ectopic pregnancy
- ovarian cysts
- Meckel’s diverticulum = malformation of distal ileum
- mesenteric adenitis
Management of appendicitis
- appendicectomy
- laparoscopic preferred → less risks and faster recovery
Complications of appendidectomy
- damage to other organs eg bowel, bladder
- removal of normal appendix
What is a diverticulum?
- a pouch/pocket in the bowel wall
- 0.5-1cm
- diverticulosis = diverticula without inflammation or infection
- diverticular disease = if patients have symptoms
- diverticulitis = inflammation and infection of diverticula
Pathophysiology of diverticula
- wall of LI contains a layer of circular muscle
- weaker in areas penetrated by blood vessels
- increased pressure can cause a gap to form
- mucus herniates through muscle layer and forms diveritcula
do not form in the rectum
Diverticulosis
- wear and tear of bowel
- most commonly in sigmoid colon
- diagnosis = colonoscopy or CT
- treatment not needed if asymptomatic
- high fibre diet, bulk-forming laxatives
Presentation of diverticulitis
- pain and tenderness in LIF
- fever
- D,N&V
- rectal bleeding
- palpable abdominal mass
- rasied inflammatory markers
Management of diverticulitis
- oral co-amoxiclav (5 days)
- analgesia (not NSAIDs or opiates)
- clear liquids until symptoms improve
severe
- manage like acute abdomen/sepsis
Complications of diverticulitis
- perforation
- peritonitis
- peridiverticular disease
- large haemorrhage
- fistula
What is acute gastritis?
acute inflammation of the stomach mucosa due to imbalance between mucus defence and acid
Pathophysiology of acute gastritis
- stomach usually lined by HCO3, prostaglandins and mucus barrier → protects against stomach acid
- acid damage → superficial inflammation and can given erosions
- loss of superficial layer
- progression to ulcer
- loss of mucosal layer
Risk factors for acute gastritis
- alcohol
- drugs → NSAIDs, steroids
- hiatus hernia
Symptoms of acute gastritis
- epigastric pain/discomfort
- vomiting
- heartburn
Management of acute gastritis
- PPIs/H2 blockers
- decrease alcohol and tobacco
What is chronic infective gastritis?
- most common form of gastritis
- caused by H.pylori → makes a urease enzyme
- breaks down mucus defence
- destroys protective layer
- leads to chronic inflammation
What can chronic inflammation lead to in gastritis?
increases risk of
- gastric adenocarcinoma
- MALT lymphoma
Symptoms of chronic infective gastritis
- epigastric pain
- peptic ulcer disease
Tests for chronic infective gastritis
- breath test
- stool antigen, serology
- histology from biopsy, CLO test → pH
Management for chronic infective gastritis
tripe therapy to kill H.pylori
- PPI → lansoprazole
- amoxicillin
- clarithromycin
What is chronic autoimmune gastritis?
- occurs due to autoimmune destruction of gastric parietal cells
- T cells make antibodies against parietal cells and/or IFs → stomach atrophy
main problem = lack of IF → B12 deficiency
Symptoms of chronic autoimmune gastritis
- megaloblastic/pernicious anaemia (lack of IF)
- mild jaundice
- diarrhoea
- sore tongue
Management of chronic autoimmune gastritis
- B12 injections
- folic acid supplements
What are oesophageal varices?
- dilated veins at sites of portosystemic anastomosis
- left gastric and inferior oesophageal veins
Causes of oesophageal varices
pre-hepatic
- portal vein thrombosis
- portal vein obstruction
hepatic
- cirrhosis
- schistosomiasis
post hepatic
- Budd Chiari
- RHS HF
- constructive pericarditis
- compression
Presentation of oesophageal varices
- haematemesis and/or melena
- epigastric discomfort
- sudden collapse → haemodynamic instability
Investigations for oesophageal varices
- urgent endoscopy
- FBC, U&E, clotting (INR) LFTs
- chest xray/ascitic tap
Management of oesophageal varices
- ABCDE
- Rockall score
bleeding varices
- terlipressin
- prophylactic Abs → ciprofloaxcin
- balloon tamponade
- endoscopic banding
- TIPS
bleeding prevention
- beta blocker
- endoscopic banding
- cirrhosis = screening endoscopy
What is a Rockall score?
prediction of rebleeding and mortality
What is Barrett’s oesophagus?
- metaplasia of lower oesophagus mucosa
- stratified squamous to columnar epithelium with goblet cells
Risk factors for Barrett’s oesophagus
- GORD
- male
- caucasian
- family history
- hiatus hernia
- obesity
- smoking
- alcohol
Presentation of Barrett’s oesophagus
classic history = middle aged caucasian male with long history GORD and dysphagia
Investigations for Barrett’s oesophagus
- oesophago-gastro-duodenoscopy
- biopsy
Management of Barrett’s oesophagus
- lifestyle changes
- endoscopic surveillance with biopsies
- high dose PPIs
- dysplasia → endoscopic mucosal resection, radiofrequency ablation
- severe = oesophagectomy
What lifestyle changes are needed in Barrett’s oesophagus?
- weight loss
- smoking cessation
- reduce alcohol
- small regular meals
- avoid hot drinks/alcohol/eating <3hrs before bed
- avoid nitrates, anticholinergics, TCAs, NSAIDs, K+ salts, alendronate
What is a Mallory Weiss tear?
haematemesis from tear in oesophageal mucosa
Risk factors for Mallory Weiss tear
- alcoholism
- hyperemesis gravidarum
- gastroenteritis
- bulimia
- chronic cough
Presentation of Mallory Weiss tear
- haematemesis
- melena
- symptoms of hypovolaemic shock
Investigations for Mallory Weiss tear
- Rockall score
- FBC, U&E, coagulation studies
- ECG, cardiac enzymes
Management of Mallory Weiss tear
most resolve spontaneously
- ABCDE
- terlipressin and urgent endoscopy
- Rockall score
- inpatient observation
- banding/clipping
- adrenaline
- thermocoagulation
What is Boerhaave syndrome?
- oesophageal rupture
Mackler triad
- vomiting
- chest pain
- subcutaneous emphysema
What are the two types of oesophageal cancer?
adenocarcinoma
- more common in developed world
- lower 1/3 → near GO junction
squamous
- more common in developing world
- upper 2/3
Risk factors of adenocarcinoma
- GORD
- Barrett’s oesophagus
- smoking
- achalasia
- obesity
Risk factors for squamous oesophageal cancer
- smoking
- alcohol
- achalasia
- obesity
- low fruit/veg/fibre/vitA,C
- hot drinks
- Plummer-Vinson syndrome
Symptoms of oesophageal cancer
- vomiting
- progressive dysphagia
- anorexia and weight loss
- odynophagia
- hoarseness
- malaena
- cough
Typical presentation of oesophageal cancer
ALARMS
- anaemia
- loss of weight
- anorexia
- recent onset progressive symptoms
- malaena/haematemesis
- swallowing difficulties eg dysphagia
Investigations for oesophageal cancer
- upper GI endoscopy and biopsy
- CT scan/endoscopic US → staging
Management of oesophageal cancer
- operable disease → surgical resection, adjuvant chemo
- palliation
What are the two types of gastric cancer?
- intestinal/differentiated → more common
2. diffuse/undifferentiated
Risk factors of intestinal gastric cancer
- male
- h.pylori
- chronic gastritis
- atrophic gastritis
- older age
Features of intestinal gastric cancer
- histology → glandular
- appearance →large, irregular
- locations → antrum, lesser curvature
Risk factors of diffuse gastric cancer
- blood type A
- genetic
- younger age
Features of diffuse gastric cancer
histology
- poorly differentiated
- signet ring cells
appearance
- gastric linitis → submucosa invasion
- no movement on barium swallow = progressed
location = anywhere esp cardia
Red flags for upper GI cancer
upper abdominal mass consistent with stomach cancer and: - dysphagia of any age - age 55+ and weight loss with: upper abdominal pain or reflux or dyspepsia
2 week wait for endoscopy
What symptoms qualify for non-urgent endoscopy?
- haematemesis
- treatment resistant dyspepsia
- upper abdominal pain
- anaemia
Presentation of gastric cancer
- often late presentation
- anorexia
- weight loss
- anaemia
- dysphagia
- N&V
- epigastric pain → better with antacids
- paraneoplastic syndromes
- metaplastic signs
Investigations for gastric cancer
- gastroscopy → 8-10 biopsies
- endoscopic US → depth of invasion
- CT/MRI/PET
Management of gastric cancer
- nutritional support → fruit/veg/folate/fibre
- surgical resection
- chemo
Risk factors for colon cancer
- family history
- hereditary conditions → FAP
- IBD
- diet → high fat/red meat, low fibre/folate/Ca2+
- DM
- lifestyle
- history of bowel/endometrial/breast/ovarian cancer
- later first pregnancy/early menopause
Symptoms of colon cancer
depends on location
- pain
- palpable mass
- bleeding
- change in bowel habit
- weight loss
- vomiting
- obstruction
Diagnosis of colon cancer
faecal occult blood test
- > 50 and bowel habit change/iron deficient anaemia
- > 60 and anaemia
colonoscopy and biopsy
flexible sigmoidoscopy/barium enema/CT colonoscopy
Management of colon cancer
- surgical resection
- depends on site of cancer
- normally anastomosis required
What are the key hereditary causes of colon cancer?
- familial adenomatous polyposis
- hereditary nonpolyposis colorectal cancer
- Lynch syndrome
What are bowel obstructions?
an arrest on the onward propulsion of intestinal contents
What are the types of bowel obstructions?
- small bowel → most common
- large bowel
- psudeo
Causes of SBO
- adhesions → previous abdominal/pelvic surgery or previous abdominal infections
- hernias
- malignancy
- Crohn’s
Pathophysiology of SBO
- obstruction of bowel
- distention above blockage due to buildup of fluid and contents
- increased pressure → pushes on blood vessels in bowel wall
- vessels become compressed
- vessels cannot supply blood
- ischaemia, necrosis, perforation
Clinical presentation of SBO
- pain → initially colicky then diffuse, high in abdomen
- profuse vomiting following pain (earlier than LBO)
- less abdominal distention than LBO
- tenderness = strangulation/risk of perforation
- constipation = late in SBO
- increased bowel sounds → tinkling
Diagnosis of SBO
- abdominal xray → central gas shadows, distended loops, fluid levels
- examination of hernia orifices and rectum
- FBC
GOLD STANDARD = non-contrast CT → locates obstruction
Management of SBO
- aggressive fluid resuscitation
- decompression of bowel
- analgesia and anti-emetics
- Abs
- surgery to remove obstruction → laparotomy
What is involved in decompression of the bowel?
- IV fluids with nasogastric tube
- always try before surgery
Causes of LBO
- malignancy
- volvulus
- diverticulitis
- Crohn’s
- intussusception
What is volvulus?
- rotation/twisting of bowel on mesenteric axis
- commonly in sigmoid colon
What is intussusception
- bowel roles inside of itself
- almost only in neonates/infants → softer bowels
Clinical presentation of LBO
- abdominal pain → more constant and diffuse than SBO, lower abdomen
- more abdominal distention than SBO
- palpable mass eg hernia
- vomiting → later than SBO
- constipation → earlier than SBO
- normal bowel sounds then louder then silent
Diagnosis of LBO
- abdominal xray
- FBC
- digital rectal exam → empty rectum, hard/compacted stools, blood
GOLD STANDARD = CT
What can be seen on an abdominal xray in LBO?
- peripheral gas shadows proximal to blockage
- caecum and ascending colon distended
Management of LBO
same as SBO
What are psuedo-bowel obstructions?
- identical presentation to SBO or LBO → depends on location
- entire bowel can be obstructed → both presentations
Causes of psuedo-bowel obstructions
- intra-abdominal trauma-
- post-op states eg paralytic ileus
- intra-abdominal sepsis
- drugs eg opiates, antidepressants
- electrolyte imbalances
Treatment of pseudo-bowel obstructions
treat underlying cause
What are the two types of diarrhoea?
- acute → <2 weeks
- chronic → >2 weeks
Causes of diarrhoea
viral → majority
- children = rotavirus
- adults = norovirus
bacterial
- campylobacter jejuni
- bloody diarrhoea
- e.coli
- salmonella
- shigella
parasitic
- giardia lamblia
Management of diarrhoea
- treat underlying cause → bacterial = metronidazole
- oral rehydration therapy
- anti-emetics agents eg metoclopramide
- anti-motility agents eg loperamide
self-limiting
What are the 3 main types of ischaemic bowel disease?
- acute mesenteric ischaemia → SB
- chronic mesenteric ischaemia → SB
- ischaemic colitis → LB
What areas are most susceptible to ischaemia?
watershed areas
- splenic flexure
- caecum
Causes of AMI
- SMA thrombosis
- SMA embolism due to AF
- mesenteric vein thrombosis
- non-occlusive disease → poor blood flow/CO
Presentation of AMI
classic triad
- acute, severe abdominal pain → constant, central
- no abdominal signs on exam
- rapid hypovolaemia → shock
AF and sever abdominal pain = AMI
Diagnosis of AMI
blood
- high Hb
- metabolic acidosis
abdominal xray → rule out obstruction
laparoscopy → visualise necrosis
CT/MRI angiography → visualise blockages in arteries
Management of AMI
- fluid resuscitation
- Abs → metronidazole, gentamicin
- IV heparin
- surgery → remove necrotic bowel
Complications of AMI
- sepsis
- peritonitis
Chronic mesenteric ischaemia
- very similar to AMI
- symptoms on a lower level, persist for much longer
- abdominal angina
Causes of IC
- thrombosis, emboli
- low flow states → low CO, arrhythmias
- surgery
- vasculitis
- coagulation disorders
- the pill
- idiopathic
Presentation of IC
- sudden onset LIF pain
- passage of bright red blood
- signs of hypovolaemic shock
Diagnosis of IC
- urgent CT → rule out perforation
- flexible sigmoidoscopy with biopsy
- barium enema
GOLD STANDARD = colonoscopy with biopsy
- after recovery
- exclude strictures at site, confirm mucosal healing
Management of IC
- most patients fine with symptomatic treatment
- fluid replacement
- Abs
Gangrenous IC
- peritonitis and hypovolaemic shock
- surgery
