Gastroenterology Flashcards
What are the symptoms and signs suggestive of GI perforation?
Acute Abdomen pain worse on coughing/moving
Hx of alcohol/NSAIDs/ulcer/cancer/IBD
Tachcycardia +/- hypotension
Increased RR
Peritonism (abdo tender, guarding, rebound, rigidity)
Reduced/absent bowel sounds
What would your initial investigations be for someone presenting with peritonism?
Bedside- basic obs, ECG, urine dip + BhCG if female
Bloods- FBC, CRP, lactate, amylase, ABG (acidosis)
Imaging- Erect CXR (air under diaphragm), Abdomen XR if ? obstruction
What is the initial management of perforation?
Resuscitate with IV fluids
O2
IV access
Analgesia (IV morphine 5-10mg IV with cyclizine 50mg/8hr)
Cross match blood
IV abx
What are the causes of perforation?
Ulcer, appendicitis, IBD, diverticulitis, obstruction, GI cancer, gallbladder perforation
What are the main causes of bowel obstruction?
Small bowel- adhesions, hernia, IBD
Large bowel- malignancy, diverticulitis, volvulus, faeces
What are the symptoms and signs of bowel obstruction?
Vomiting, constipation (if no flatus = complete), colicky abdominal pain, bloating, anorexia
Small bowel= early vomiting, late constipation
Large bowel= early absolute constipation, late vomiting Tachycardia +/- hypotension
- Increased RR
- Abdo distension
- Absent/tinkling bowel sounds
- Peritonitis
- Surgical scars/hernia
How would a strangulated bowel present?
Constant severe pain
Ill patient
Peritonitis
What is the management of strangulated bowel?
Urgent surgery
What is the management of a small bowel obstruction?
Drip and suck- IV fluids, NG tube, NBM
Surgery if deteriorate
K often lost and needs replacing
What is the management of a large bowel obstruction?
IV fluids, NBM, surgical r/v If caecum >10cm on AXR need urgent surgery
Otherwise investigate cause with CT/colonoscopy Then surgery
What is paralytic ileus? What are the investigations and management?
Loss of bowel motility as a response to inflammation e.g. surgery, pancreatitis
Can mimic intestinal obstruction
Usually less abdo pain
Imaging to exclude obstruction
Management: conservative with IVT, NBM, NG tube until resolves. May need electrolyte replacement e.g. Mg and K.
What are the possible complications of bowel obstruction?
Perforation, bowel infarction, strangulation, hypokalaemia, hypovolaemia
What are the causes of acute pancreatitis?
- Gallstones
- Ethanol
- Trauma
- Steroids
- Mumps
- Autoimmune
- Scorpion venom
- Hypercalcaemia, hypertriglyceridaemia, hypothermia
- ERCP
- Drugs (azathioprine, bendroflumethiazide, furosemide, steroids, sodium valproate etc)
What are the risk factors for Barrett’s oesophagus?
GORD
Male
Smoking
Central obesity
Histology of Barrett’s oesophagus
lower oesophageal mucosa squamous epithelium replaced by columnar epithelium
Goblet cells
Brush border
What is the increased risk of oesophageal adenocarcinoma associated with Barrett’s?
50-100 fold
What is the management of Barrett’s oesophagus?
Endoscopic survelliance + biopsies
High dose PPI
Which biliary disease is associated with UC?
Primary sclerosing cholangitis
Features of PSC
Cholestasis- jaundice and pruritis
RUQ pain
Fatigue
Investigation to diagnose PSC
ERCP/MRCP
PSC is associated with an increased risk of…
Cholangiocarcinoma
Main autoAbs in PSC
ANCA
ANA
Beaded appearance of bile ducts suggests…
PSC
Features of Wilsons disease
Hepatitis
Cirrhosis
Speech, behavioural, psychiatric problems
Asterix, chorea, dementia
Kayser-Fleischer rings
Renal tubular acidosis
Haemolysis
Blue nails
Dx of Wilsons
Reduced serum caeruloplasmin
Reduced serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)
Increased 24hr urinary copper excretion
1st line treatment for Wilson s
Penicillamine
Inhertiuance of Wilsons disease
Autosomal recessive
Disease characterised by excess copper deposition
Wilson’s
H pylori is most associated with
Peptic ulcer disease
H pylori eradication
7 days of: PPI + amox + clarithromycin
or
PPI + metronidazole + clarithromycin
Definition of constipation
Infrequent stools
Difficulty passing stools
Sensation of incomplete emptying
Chronic constipation
Sx for at least 12 weeks in last 6 months
Functional constipation
Unknown cause
Secondary constipation
Due to drug/medical condition
Management of constipation (adults)
Manage underlying causes/drugs
Lifestyle- increase fibre, fluid intake, activity levels
If faecal loading/impaction manage this 1st
Laxatives (titrate to produce soft formed stool w/out straining at least 3x per week):
1) Bulk forming e.g. ispaghula
2) Osmotic e.g. macrogol (1st line)/lactulose/phosphate enema
3) Stimulant e.g. Senna, docusate, bisacodyl, sodium picosulfate
Management of opioid induced constipation
osmotic laxative + stimulant laxative
Features indicating constipation in children
Stool patterns:
- Fewer than three complete stools per week (unless exclusively breastfed, when stools may be infrequent).
- Hard, large stool.
- ‘Rabbit droppings’ stool.
- Overflow soiling in children older than 1 year of age (commonly very loose, smelly stools, which are passed without sensation or awareness)
Symptoms associated with defecation in a child at any age:
- Distress or pain on passing stool.
- Bleeding associated with hard stool.
- Straining.
Symptoms associated with defecation in a child older than 1 year of age:
- Poor appetite that improves with passage of large stool.
- Waxing and waning of abdominal pain with passage of stool.
- Evidence of ‘retentive posturing’ — typical posture is straight-legged, on tiptoes with an arched back.
- Anal pain.
Past history of constipation.
Previous or current anal fissure.
Management of constipation in children
- Offering reassurance that underlying causes of constipation have been excluded.
- Advising that idiopathic constipation is treatable with laxatives, although they may need to be taken for several months.
- Offering sources of information and support.
- Treating faecal impaction with a recommended disimpaction regimen.
- Starting maintenance laxative drug treatment if impaction is not present or has been successfully treated.
- Advising on behavioural interventions such as scheduled toileting, use of a bowel habit diary, and reward systems.
- Arranging regular follow-up to assess adherence and response to treatment.
- Considering the need for specialist referral if symptoms do not respond to optimal treatment in primary care, or if there is faecal impaction and the child is very distressed.
1st line treatment for feacal impaction in children
Movicol 1st line
If not working after 2 weeks add stimulant laxative e.g. Senna
Once disimpacted start maintenance laxatives
Choice of laxatives in children
Osmotic laxatives - increase fluid in large bowel, softening stool and stimulating peristalsis
e.g. Movicol, lactulose
Stimulant laxatives - cause peristalsis by stimulating colonic and rectal nerves
e.g. Senna, Docusate, Bisacodyl, Sodium picosulfate
Most common risk factors for peptic ulcer disease
H.pylori infection
NSAIDs
Complications of peptic ulcer disease
Haemorrhage
Perforation
Gastric outlet obstruction
Gastric malignancy (increased risk in H.pylori positive gastric ulcer disease)
Management of peptic ulcer disease
Lifestyle measures:
- Weight loss
- Avoid triggers e.g. coffee, chocolate, tomatoes, fatty, spicy foods
- Smaller meals
- Eat meals 3-4 hours before bed
- Stop smoking
- Reduce alcohol
Manage stress/anxiety/depression
Medication review:
- Stop NSAIDs
- Consider reducing or stopping (if possible and appropriate) any other potential ulcer-inducing drugs, such as:
Aspirin, bisphosphonates, corticosteroids, potassium supplements, selective serotonin reuptake inhibitors (SSRIs), or recreational drugs such as crack cocaine.
Test for H.pylori: carbon-13 urea breath test or stool antigen test (no PPI for 4 weeks, no abx for 2 weeks):
- If positive and not associated with NSAIDs, prescribe eradication therapy
- If positive and associated with NSAIDs, give full dose PPI for 2 months then eradication therapy
- If negative prescrive full dose PPI 4-8 weeks
Symptoms of infective gastroenteritis
- Rapid onset
- Recent vomiting/diarrhoea
- Feels unwell
- Crampy abdominal pain
- Flu-like symptoms
- Pyrexia
- Other household members/contacts affected
Causes of infectious diarrhoea
- Viral infection- norovirus, sapovirus, rotavirus
- Bacterial causes- Salmonella, Camylobacter, E.coli, Shigella, C.difficile.
- Parasitic- Cryptosporidium, Giardia, Entamoeba histolytica, and Cyclospora.
Causes of bloody diarrhoea
Bacterial: Campylobacter jejuni, Salmonella, Escherichia coli O157:H7, Vibrio parahaemolyticus, Shigella, Yersinia, Aeromonas, Clostridium difficile.
Viruses: cytomegalovirus.
Parasites: Entamoeba histolytica, schistosomiasis.
Features of E.coli infection
Common amongst travellers
Watery stools
Abdominal cramps and nausea
Giardiasis
Prolonged, non-bloody diarrhoea
Cholera
Profuse, watery diarrhoea
Severe dehydration resulting in weight loss
Not common amongst travellers
Shigella
Bloody diarrhoea
Vomiting and abdominal pain
Staphylococcus aureus
Severe vomiting
Short incubation period
Campylobacter
A flu-like prodrome is usually followed by crampy abdominal pains, fever and diarrhoea which may be bloody
May mimic appendicitis
Complications include Guillain-Barre syndrome
Bacillus cereus
Two types of illness are seen
- vomiting within 6 hours, stereotypically due to rice
- diarrhoeal illness occurring after 6 hours
Amoebiasis
Gradual onset bloody diarrhoea, abdominal pain and tenderness which may last for several weeks
Incubation period for gastroenteritis…
- 1-6 hrs:
- 12-48 hrs:
- 48-72 hrs:
- > 7 days:
Incubation period:
- 1-6 hrs: Staphylococcus aureus, Bacillus cereus*
- 12-48 hrs: Salmonella, Escherichia coli
- 48-72 hrs: Shigella, Campylobacter
- > 7 days: Giardiasis, Amoebiasis
Management of gastroenteritis
Fluid intake
Oral rehydration salts in children/adults with risk factors (>60yrs, frail, comorbidities)
Antidiarrhoeal drugs and anti-emetics are not usually necessary (anti-diarrhoeals may be used in adults for symptom control, loperamide is 1st line but do not use if blood/mucus, high fever, E.coli 0157 or Shigellosis. Can use metoclopramide if severe vomiting)
Treat cause
e.g. antibiotics for Entamoeba, Campylobacter (severe sx only), Giardia
Notify pubic health if…
Suspected:
- Cholera
- Bloody diarrhoea due to gastroenteritis
- Food poisoning
- Haemolytic uraemic syndrome
Treatment for amoebiasis (Entamoeba histolytica)
Metronidazole 400mg TDS 5-10d
Followed by diloxanide 500mg TDS 10d
Treatment for E.coli 0157
Supportive
Avoid anti-motility drugs
Advise against NSAIDs
Treatment of Giardiasis
Metronidazole
400mg TDS 5d or 500mg BD 7-10d or 2g OD 3d
Treatment of Salmonella gastroenteritis
Antibiotics not recommended for healthy people
Consider abx if >50yrs, immunocompromised or cardiac valve disease/endovascular abnormalities: ciprofloxacin 500mg BD 1d
Risk factors for haemorrhoids
- Constipation.
- Straining while trying to pass stools.
- Ageing.
- Heavy lifting.
- Chronic cough.
- Conditions that cause raised intra-abdominal pressure (such as pregnancy and childbirth).
Secondary care treatments for haemmorrhoids
Non-surgical treatments include rubber band ligation, injection sclerotherapy, infrared coagulation/photocoagulation, and bipolar diathermy and direct-current electrotherapy.
Surgical treatments include haemorrhoidectomy, stapled haemorrhoidectomy, and haemorrhoidal artery ligation.
Affects of poisoning
Impaired respiration
Respiratory depression
Hypotension
Hypertension (amphetamines, phencyclidine, cocaine)
Cardiac conduction defects/arrythmias (TCAs, anti-psychotics, some anti-histamines)
Hypothermia (esp. OD of barbiturates/phenothiazines)
Hyperthermia (CNS stimulants)
Convulsions
Methaemoglobinaemia
Repeated doses of activated charcoal are used for elimination of which drugs?
- Carbamazepine
- Dapsone
- Phenobarbital
- Quinine
- Theophylline
Features of acute alcohol intoxication
Ataxia
Nystagmus
Dysarthria
Drowsiness
Coma
Hypotension
Acidosis
Aspiration of vomit
Management of acute alcohol intoxication
Conservative management
Maintain airway
Reduce risk of aspiration
Measure blood glucose and give glucose if needed
Features of salicylate poisoning
Hyperventilation causing respiratory alkalosis
Tinnitus
Deafness
Vasodilation
Sweating
Coma (uncommon)
Acid-base disturbances- metabolic acidosis
Management of salicylate poisoning
Measure plama salicylate, pH and electrolytes
Activated charcoal if within 1hr on ingesting >125mg/kg aspirin
Replace fluid losses
IV sodium bicarbonate (after correcting K+)
Haemodialysis if severe (plasma-salicylate [>700mg/L] or severe metabolic acidosis)
Features of opioid poisoning
Coma
Respiratory depression
Pinpoint pupils
Hypotension
Hypothermia
Hyporeflexia
King’s College Hospital criteria for liver transplantation (paracetamol liver failure)
King’s College Hospital criteria for liver transplantation (paracetamol liver failure)
Arterial pH < 7.3, 24 hours after ingestion
or all of the following:
- prothrombin time > 100 seconds
- creatinine > 300 µmol/l
- grade III or IV encephalopathy
Management of benzodiazepine overdose
Flumazenil
The majority of overdoses are managed with supportive care only due to the risk of seizures with flumazenil. It is generally only used with severe or iatrogenic overdoses.
Management of TCA overdose
- IV bicarbonate may reduce the risk of seizures and arrhythmias in severe toxicity
- arrhythmias: class 1a (e.g. Quinidine) and class Ic antiarrhythmics (e.g. Flecainide) are contraindicated as they prolong depolarisation. Class III drugs such as amiodarone should also be avoided as they prolong the QT interval. Response to lignocaine is variable and it should be emphasized that correction of acidosis is the first line in management of tricyclic induced arrhythmias
- dialysis is ineffective in removing tricyclics
Features of TCA overdose
Early features relate to anticholinergic properties: dry mouth, dilated pupils, agitation, sinus tachycardia, blurred vision.
Features of severe poisoning include:
- arrhythmias
- seizures
- metabolic acidosis
- coma
ECG changes include:
- sinus tachycardia
- widening of QRS
- prolongation of QT interval
Widening of QRS > 100ms is associated with an increased risk of seizures whilst QRS > 160ms is associated with ventricular arrhythmias
Beta blocker overdose- management
Management
- if bradycardic then atropine
- in resistant cases glucagon may be used
Cause of oesophagitis
Acid reflux into oesophagus
Symptoms of oesophagitis
Heartburn
Acidic taste
Belching
Dysphagia
Uncommon: Hoarseness Persistent cough Asthma type symptoms
Complications of oesophagitis
Stricture
Barrett’s oesophagus
Oesophageal cancer (risk slightly increased)
Treatment of oesophagitis
Omeprazole/lansoprazole
Ranitidine
GORD definition
chronic condition reflux of gastric contents into oesophagus
Symptoms of GORD
Heartburn
Acid regurgitation
Risk factors for GORD
Obesity
Smoking
Alcohol
Coffee
Stress
Pregnancy
Drugs- Ca channel blockers, anticholinergics, theophylline, benzos, nitrates (all decrease lower oesophageal sphincter pressure)
Management of GORD
Lifestyle advice
Sleep with head of bead raised
Medication review
Full dose PPI for 4 weeks for proven GORD or 8 weeks if severe oesophagitis
Complications of GORD
Barrett’s oesophagus (10-15%)
Oesophageal Ca (1-10% of those above)
Oesophageal ulcers
Anaemia
Stricture
Aspiration pneumonia
Dose of omeprazole
20mg OD
Dose of lansoprazole
30mg OD
Dose of ranitidine
150mg BD
Definition of dyspepsia
UGI sx present for >4 weeks
- Upper abdo pain/discomfort
- Heartburn
- Acid reflux
- Nausea
- Vomiting
Common causes of dyspepsia
- GORD
- Peptic ulcer disease
- Functional dyspepsia (non-ulcer dyspepsia)
Management of dyspepsia
- Lifestyle modification- weight loss, smoking cessation, reducing alcohol, smaller meals, avoid triggers (coffee, chocolate, tomatoes, fatty, spicy foods)
- Manage anxiety/depression/stress
- Medication review
- If sx persist, full dose PPI for 4 weeks OR H.pylori testing (carbon-13 breath test)- if persist, try alternative strategy
Drugs which exacerbate dyspepsia
- NSAIDs
- alpha and beta blockers
- Aspirin
- Anti-cholinergics
- Benzos
- Bisphosphonates
- Steroids
- Nitrates
- Theophyllines
- TCAs
Assessing dyspepsia
- Alarm symptoms- weight loss, recurrent vomiting, dysphagia, evidence of GI bleed
- Frequency, duration and pattern of symptoms
- Family hx of UGI malignancy
- Lifestyle factors
- Assess for stress/anxiety/depression
- Review medication
- Check weight and BMI
- Check for signs of anaemia
- Check for abdominal masses/tenderness
- Check FBC for anaemia/raised platelets
2WW criteria for oesophageal Ca
Anyone with dysphagia
>55 with weight loss + upper abdominal pain/reflux/dyspepsia
Symptoms of gastritis/erosive gastritis
Epigastric discomfort
Gnawing/burning pain
Nausea, vomiting, loss of appetite, belching, and bloating.
Erosive gastritis= pain, bleeding or a stomach ulcer
Investigations for gastritis
H pylori test
Stool test
Endoscopy
Causes of gastritis
H. pylori
Excessive use of cocaine or alcohol
Regularly taking aspirin, ibuprofen or other NSAIDs
Stress
Autoimmune
Treatment of gastritis
Lifestyle modification- smaller meals, avoid spicy/acidic/fried foods, reduce alcohol, manage stress
Antacids
PPIs
H2 receptor antagonists
Complications of gastritis
Stomach ulcer
Stomach polyps
Stomach tumours
What is a Mallory-Weiss tear?
Haematemsis, usually after prolonged or forceful retching, coughing, straining or hiccupping
Management of a Mallory-Weiss tear
Resuscitation- maintain airway, O2, 2 wide bore cannulae, send bloods, IVT/blood
Most patients stop bleeding spontaneously
Some require endoscopic intervention
2WW criteria for oesophageal/gastric Ca
Dysphagia at any age
Age 55+ with weight loss and any one of:
- upper abdo pain
- reflux
- dyspepsia
Treatment of oesophageal Ca
Localised oesophageal adenocarcinoma- surgical resection with neoadjuvant chemoradiotherapy, or chemotherapy( before, or before and after surgery)
Resectable non-metastatic SCC- radical chemoradiotherapy or chemoradiotherapy then surgical resection
Non-metastatic Ca but unsuitable for surgery- chemoradiotherapy, chemotherapy, local tumour treatment (stenting) or supportive care.
Advanced Ca- palliative combination chemotherapy (5-fluorouracil or capecitabine + cisplatin1 or oxaliplatin)
Treatment of oesophageal stricture
Benign stricture- Endoscopic dilatation with baloon/bougie
Malignant stricture- Surgical excision (oescophagectomy) or stenting
Pathophysiology of oesophageal varices and their causes
Variceal haemorrhage occurs from dilated veins (varices) at the junction between the portal and systemic venous systems.
Occur due to portal hypertension - most common causes are alcoholic and viral liver cirrhosis.
Other causes:
- Prehepatic; protal vein thrombosis/obstruction, fistula
- Intrahepatic; acute hepatitis, schistosomiasis
- Posthepatic; Budd-Chiari, compression (e.g. from tumour), constrictive pericarditis
Management of variceal bleed
Risk assessment- Blatchford score
Resuscitation- assess airway, wide bore access x2, O2 if needed, fluids (crystalloid and colloid rapid infusion), transfuse blood ASAP, correct anaemia/coagulopathy
Terlipressin until haemostasis achieved or 5 days completed
Urgent endoscopy- band ligation, consider TIPS if bleeding not controlled
Baloon tube tamponade (Sengstaken-Blakemore tube) can be used as temporary treatment for uncontrolled haemorrhage
Antibiotic prophylaxis
Should have beta-blockers +/- nitrates and endoscopic screening and treatment long term
Major risk factors for gastric cancer
Increasing age
Male
H.pylori
Low vegetable/fruit consumption
Smoking
Familial risk
Management of gastric cancer
Nutritional support and symptom control
Surgery is treatment of choice with lymphadenectomy if curable
Perioperative combination chemo (5-fluoracil + epirubicin/cisplatin)
Palliative- chemotherapy, traztuzumab, stenting, gastrectomy if obstructing
What are diverticula?
Diverticula are sac-like protrusions of mucosa through the muscular wall of the colon, which occur in the sigmoid colon in about 85% of people over the age of 80.
Diverticulosis vs diverticulitis vs diverticular disease
Diverticulosis = diverticula present, no symptoms
Diverticular disease is a condition where diverticula cause symptoms, such as intermittent lower abdominal pain, without inflammation and infection.
Diverticulitis is a condition where diverticula become inflamed and infected, typically causing severe lower abdominal pain, fever, general malaise, change in bowel habit, and occasionally rectal bleeding.
Management of diverticular disease
High fibre diet and adequate fluid
Weight loss, quit smoking
Bulk forming laxatives
Simple analgesia
Symptoms of diverticular disease
- Intermittent abdominal pain in the left lower quadrant. Pain may be triggered by eating and may be relieved by the passage of stool or flatus.
- Constipation, diarrhoea, or occasional large rectal bleeds.
- Bloating and the passage of mucus rectally.
- Tenderness in the left lower quadrant on abdominal examination.
Symptoms suggestive of diverticulitis
- Constant abdominal pain, usually severe and starting in the hypogastrium before localizing in the left lower quadrant, with fever.
Note: in a minority of people and in people of Asian origin, pain may be localized in the right lower quadrant.
- Change in bowel habit, and possible significant rectal bleeding.
- Possible nausea, vomiting, dysuria, and urinary frequency.
- A previous history of diverticulosis or diverticulitis.
- Tenderness in the left lower quadrant, palpable abdominal mass or distention on abdominal examination.
Management of diverticulitis
If mild and uncomplicated- oral co-amox 1 week (if infection suspected) or analgesia, clear fluids, reintroduce solid food gradually as symptoms improve
If more severe/complicated- admit, IV antibiotics/fluids/analgesia, surgery if complicated
Symptoms/signs of appendicits
The classic symptoms are:
- Abdominal pain — this is the primary presenting complaint, and it is typically described as a peri-umbilical or epigastric pain that worsens during the first 24 hours (becoming constant and sharp) and migrates to the right iliac fossa (RIF). The pain is typically worsened by movement.
- Anorexia — almost always present.
- Nausea.
- Constipation.
- Vomiting (profuse vomiting may indicate development of peritonitis).
On examination, there may be:
- Tenderness on percussion, guarding, and rebound tenderness at the RIF — these are the most reliable clinical findings.
- Facial flushing, dry tongue, halitosis, low-grade fever (not more than 38°C), and/or tachycardia.
Investigations for ? appendicitis
Pregnancy test- rule out ectopic
Urine dip- exclude UTI (may be abnomral in 50% with appendicitis due to inflammation adjacent to bladder/UT)
Bloods- FBC (neutrophil predominant lecuocytosis in 80-90%), CRP
Imaging- US if dx doubtful, CT (more sensitive and specific)- enlarged appendix, wall thickening, fat stranding, wall enhancement.
