Gastroenterology Flashcards
GI, Pancreas
What is Achalasia?
Disorder of motility of the lower oesophageal sphincter = functional stenosis
What is the common presentation of Achalasia?
Dysphagia worse on eating solid foods
What imaging would you do?
Barium swallow
What would the barium swallow show for achalasia ? (specific sign)
Bird beak sign
What is eosinophilic oesophagitis?
Abundance of eosinophils in the oesophageal lining
What are the causes of EO?
Genetic makeup and bodys response to the environment
What makes someone more likely to have EO?
A history of allergies
What are the symptoms of EO?
Dysphagia and the feeling that food will stick in the throat. (in teens they may also have nausea and not want to eat)
What is a Schatzki ring?
Extension of normal oesophageal tissue containing mucosa and submucosa
Who is this typically found in?
50+ population
Common presentation of Schatzki ring ?
Can be asymptomatic or can present with dysphagia
3 weeks of diarrhoea. He describes it as non-bloody, very loose and foul-smelling. He has also had some mild abdominal pain and a slight fever. He eats takeaways frequently and returned one month ago from a holiday in India. He has no signs of dehydration. The GP requests a stool sample which demonstrates an infective cause of his symptoms.
Giardisis
What is the first line antibiotic treatment for Giardisis?
Metronidazole
What tests would you want to carry out on a person with potential IBD?
Bloods - FBC, U&Es, G&S, coagulation, CRP/ESR
Stool test - calprotectin (raised in IBD not IBS) and microscopy - possible infection
Imaging - colonoscopy/endoscopy
MRI/CT if think complications could be present
What are the main pathological differences between UC and Crohn’s disease?
Crohn’s is more patchy and is from mouth to anus including ulcers. The inflammation is in skip patches and is transmural with strictures and fistulas more common with deep fissures and ulceration (cobblestone). As well as non-caseating granulomas and increased macrophages.
UC is confined to the mucosal level and in the colon rectum area primarily. Goblet cells are reduced and their are increased crypt abscesses as well as ulceration and pseudopolyps.
What is the general presentation of IBD?
Diarrhoea (with blood or mucous), abdominal pain and tenderness - lower in UC and general in Crohn’s. In Crohn’s abdominal masses may also be present .
Malaise, anorexia, fever, weight loss.
Extra - eye inflammation, Osteoarthritis, erythema nodosum/pyoderma gangrenosum, clubbing, anaemia
What are the 4 possible medical treatments for IBD - pros and cons?
Amino salicylates (mesalazine 5-ASA) - induction and maintenance. First line for mild/moderate.
Corticosteroids - prednisolone (increase GC). Induction only as can’t be used long term due to S/E’s
Biologics - Infliximab (Anti-TNF⍺), (anti-IL-12/23), (anti A⁴B⁷). Work well especially for progressive disease however do come with lots of side effects. Induce and maintain.
Thiopurines (azathioprine) - induce and maintain. Used to reduce steroid use. TPMT must be nil/reduced prior to starting to reduce risk of myelosuppression.
What are some possible complications of IBD?
Toxic megacolon and perforation Obstruction and strictures (Crohn's) Bleeding/anaemia folate, iron and B12 anaemia in Crohn's (TI) Malabsorption/nutrition Colorectal cancer (UC)
What test is used to determine whether H.Pylori is present?
Carbon-13 breath test
A patient comes into the GP suffering from dyspepsia. What symptoms would you expect as part of this and what would your list of differential diagnoses look like?
Epigastic/retrograde pain and discomfort Reflux Nausea and vomiting GI disease: GORD Peptic ulcer gastric cancer/oesophageal cancer Hiatus hernia
What are the risk factors for GORD and why do these make it more likely?
Hiatus hernia - moving of the Z line making reflux more likely
Obesity/pregnancy = increased intraabdominal pressure
Diet/smoking/alcohol = relaxation of lower oesophageal sphincter
Lower oesophageal dysfunction
H.pylori - increases pepsin
A 40 yr old patient come into the GP with dyspepsia that is worse after eating and when they go to bed. They’ve noticed some regurgitation of food and a bitter taste in their mouth as well as feeling they are belching more than often.No red flags were noted. What is your next step based on the most likely diagnosis and what would be the treatment?
GORD
Lifestyle advice - lose weight, diet, exercise, sleeping with more pillows, smoking or alcohol cessation
Symptom relief - antacids, pepto-bismol, prostaglandins.
Gastric protection and treatment - PPI (omeprazole) or H2 antagonist (Cimetidine)
What possible complication/consequence of GORD do you want to rule out/avoid and what does this mean?
Barretts oesophagus.
Pre-cancerous metaplasia due to acid on the oesophagus causing it to become gastric mucosa. This can then become adenocarcinoma.
How is Barrett’s oesophagus treated?
Local mucosal removal if small. If more general then have ablation which is a cure. If disease is very advanced than surgical resection although this is a big surgery.
What does a patient need to have done before having a H.Pylori C13 breath test?
2 weeks of PPIs
In a serious untreatable by medication case of GORD what would the treatment be? And what are some complications?
Surgery - Nissens Fundoplication (laparoscopic)
- Reduce and repair a hiatus hernia
- wrap the fundus of stomach around the OG junction so that when the stomach contracts the OGJ remains closed preventing reflux.
COmplications = dysphagia, scarring, hernia, achlasia
How would you describe H.pylori?
Spiral shaped gram negative urease secreting bacteria. Causes 90% of ulcers (more DU than GU).
What is the eradication treatment for H.pylori?
How would you alter this if they were penicillin allergic?
7 day triple therapy:
PPI 2 times per day (lansoprazole 20mg)
and Amoxicillin 1g 2 times per day and Clarithromycin (500mg) or Metronidazole (400mg) 2 times per day.
If penicillin allergic then take clarithromycin and metronidazole instead of the amoxicillin.
What are risk factors for Peptic Ulcers?
Smoking, NSAIDs, stress, H.pylori
A patient comes in with a query peptic ulcer, their symptoms include epigastric retrosternal pain that is relieved when they eat due to this they have put on weight. Which ulcer is this most likely to be and what is the pathophysiology behind it?
Duodenal ulcer (duodenal cap)
H.Pylori –> increased pepsin –> abrasions in duodenum –> abnormal healing.
A patient comes in with a query peptic ulcer, their symptoms include epigastric retrosternal pain after eating causing them to have a decreased appetite and weight loss. Which ulcer is this most likely to be and what is the pathophysiology behind it?
Gastric ulcer (antrum/lesser curve)
H.pylori –> pangastritis –> decreased mucosal repair mechanism.
Which peptic ulcer is more common and which peptic ulcer is more likely to be/become cancerous?
Duodenal = common Gastric = Cancerous
A patient comes in with dyspepsia what are the red flag signs that would warrant a 2 week wait OGD?
Weight loss Fever Worsening dysphagia Recurrent dyspepsia despite treatment Mass Vomiting Iron deficient anaemia
What is the main treatment of peptic ulcers?
Eradication of H.pylori
In which cases would surgery be undertaken on a patient with a peptic ulcer?
Bleeding - normally does resolve spontaneously but if it doesn’t
Perforation - omental patch
Obstruction - uncommon but would resect/bypass
Which genetic condition would make a peptic ulcer more likely regardless of H.pylori and why is this?
Zollinger-Ellison syndrome - Men-2 can cause a gastrin producing tumour. Increasing the acid.
What is a side effect of magnesium tricilitate and what type of drug is it?
Diarrhoea
Antacid
What is a side effect of Aluminium hydroxide and what type of drug is it?
COnstipation
Antacid
What does the major pancreatic duct feed into and then what does that feed into?
Common bile duct –> Major duodenal papilla
What does the exocrine part of the pancreas produce?
Secretions - amylase and lipase
What does the endocrine part of the pancreas produce?
Hormones
There are 4 cell types in the pancreas what are they and what is their function?
Alpha = glucagon
Beta = Insulin
Delta = somatostatin
C cells = no function
Which factors increase the risk of getting pancreatic cancer?
Increased age Blood group A Tobacco, alcohol, obesity Diabetes mellitus Chronic pancreatitis
A patient has pancreatic cancer where and what type of cancer is it most likely to be?
Exocrine - Ductal adenocarcinoma of the head of the pancreas
A patient has a functional endocrine tumour what are the possibilities of which type of tumour it could be?
Insulinoma
Glucagonoma
Gastrinoma
VIPoma
Where could a peripancreatic tumour be?
Ampulla, bile duct, duodenum
A 55yr old patient comes into the GP saying her husband has noticed her getting more yellow recently she is now also noticing it and is concerned. When questioning her she has not had any pain however she has noticed that her urine has been getting darker and that her stools are more pale and hard to flush from the toilet. She has generally not been feeling herself and has noticed her clothes getting baggier. On examination she has cervical lymphadenopathy and a palpable mass in her abdomen. Based on this history and examination what is the most likely diagnosis and what would be the management plan?
Pancreatic cancer.
Bloods - LFTs, Ca19-9, CRP
Ultrasound
CT - if confirms diagnosis then stent or surgery
Otherwise EUS/laparoscopy
Whipple resection –> remove 30% stomach, head of pancreas and duodenum.
However most are inoperable due to mets or blood vessel involvement so chemo/radiotherapy.
What is the I GET SMASHED acronym?
Idiopathic Gallstones Ethanol Trauma Steroids Mumps/Malignancy Autoimmune IgG4 Scorpion sting Hypertriglyceridemia/Hypercalcaemia ERCP Drugs - Azathioprine
What is the pathophysiology of acute pancreatitis?
Hypersecretion and/or back flow obstruction causing enzyme induced autodigestion
A 60 yr old man presents to A&E with sudden onset epigastric pain which is tender. This pain is alleviated if he leans forwards but otherwise is worse on movement. O/E he has a distended abdomen with bruising around the umbilicus and on his flanks. What would be your next steps and treatment and the most likely diagnosis in this case?
Most likely acute pancreatitis
Bloods - FBC, CRP (over 150), U&Es, LFTs, Lipase and Amylase (3x normal)
Ultrasound –> MRI –> CT
Analgesia - monitoring hourly urine, EWS, oxygen and fluids
Then dependent on the cause surgery or other medical management.
What is the atlanta criteria used for?
Grading acute pancreatitis.
Mild = no organ dysfunction and self resolving
Moderate = organ failure improved in 48 hours
Severe = persistent organ failure and local/systemic complications
Which 2 signs are seen on the abdomen in acute pancreatitis?
Grey turners sign - flank bruising
Cullens sign - periumbilical bruising
What is the difference between cholethiasis and choledocholithiasis?
Cholethiasis = gallstones in the gallbladder Choledocholithiasis = gallstones in the common bile duct.
What forms the common bile duct?
The cystic duct from the GB and the hepatic ducts
What causes the Gall bladder to contract and what causes it to relax?
Contract = PNS (rest/digest) Relax = SNS (fight/flight)
What increases the risk of gallstones?
5 F’s
Fat Female Fertile (oestrogen) Forty Family history \+ diabetes, drugs, diet
What are the 3 types of gallstones that you can get and in who is most likely to get each and what are they made of?
Cholesterol (western world) - white, large and calcium
Pigment - developing world - black/brown (bile pigments)
Mixed - irregular shape
A 45 year old female presents with RUQ pain thats worse after they eat a takeaway. She has also suffered with some nausea and vomiting and a metallic taste in her mouth. Her LFTs are normal except raised bilirubin and ALP. What is the most likely diagnosis and pathophysiology behind the pain. As well as the management going forward?
Biliary colic
Due to the gallstones becoming lodged in the biliary duct.
Would want a Ultrasound to confirm.
Then give IV morphine, an anti-emetic. Then a elective cholecystectomy (within 6 weeks) as recurrence is high.
A patient has been diagnosed with choledocholithiasis what is the gold standard and the treatment option?
MRCP is gold standard testing. Then do a ERCP.
What are the possible complications of ERCP?
Acute pancreatitis
Acute cholangitis
Perforation - due to endoscopy
What is the pathophysiology of acute cholecystitis?
Gallstones cause an obstruction –> Increased gall bladder pressure –> oedema and inflammation –> venous ischaemia –> empyema, necrosis, perforation or fistula of GB.
A patient has a positive murphy’s sign what does this involve and what is the most likely diagnosis?
Palpating RUQ while patient breathes in = pain and stops breathing. = Acute cholecystitis
A 35 yr old female presents with persistent epigastric and RUQ pain. She has had a loss of appetite and n+v as well as having a fever. O/E she has a positive murphy’s sign. Based on the most likely diagnosis what would be your next investigations and what would could be the causative agents for this?
What would be the DDx?
Bacteria = E.Coli or pseudomonas.
Bloods - Raised CRP and WCC. Deranged LFTs.
Do a USS then a CT/MRCP.
DDx
- Pancreatitis - Mi - Appendicitis - renal stones
- Peptic ulcer - Pneumonia - Gastritis
- hiatus hernia - Hepatitis
What is the management for asymptomatic gallstones?
Lifestyle modifications and a preventative cholecystectomy for high risk patients
What is the management for symptomatic cholecystis?
Cholecystectomy - within 1 week (72 hrs) of presentation
Antibiotics (ciprofloxacin/co-amoxiclav and metronidazole)
Cholecystomy (incision into GB to remove infection)
What is cholangitis and what is the management of it?
Acute inflammation of the biliary tree.
Fluid resuscitation and antibiotics (+/- ERCP)
What makes up Charcot’s triad and what is it indicative of?
Jaundice + RUQ pain + fever/rigors = Ascending cholangitis.
What makes up Reynolds pentad and what is it indicative of?
Charcot’s triad + altered mental state + hypotension = Obstructive ascending cholangitis
What is the difference between ERCP and MRCP?
MRCP = non-invasive imaging ERCP = invasive imaging and therapeutic intervention. Using a endoscopy and fluoroscopy to view the biliary system.
What are common complications of coeliac disease?
Iron and vitamin D deficiency
Anaemia
Osteomalacia/osteoporosis
what is Zenker’s diverticulum and what is the gold standard diagnosis tool?
Outpouching of the hypopharynx.
Tool = barium swallow
A patient presents with progressive dysphagia, a cough, regurgitation of food/drink and bad breath. O/E they have a lump on the left side of their neck what is the most likely diagnosis?
Zenker’s diverticulum.
What is Bouveret syndrome?
gastric outlet obstruction by a large gallstone in the pylorus or first part of the duodenum.
Which IBD would have granulomata on histopathology?
Crohn’s
What is the MELD score used to determine the severity of?
Cirrhosis
A 40 year old male comes into the GP with chronic pain in their back and epigastrium that is sometimes accompanied by nausea and vomiting. He drinks 5 beers a night 7 days a week and has done for a long time. O/E he is cachexia and appears malabsorbed having lose significant weight. You order a faecal elastase which is low. What is the most likely diagnosis and what management would you suggest for this man?
Chronic pancreatitis - exocrine insufficiency
Alcohol cessation
Adequate pain relief
- NSAID –> Opioid –> neuropathic analgesia
Nutritional help - CREON (enzyme replacement) and monitor vitamins (ADEK)
What are risk factors for chronic pancreatitis - environmental and genetic?
Chronic alcohol use Hypercalcaemia or hyperlipidaemia Infection - HIV Mumps Coxsacchic Echinococcus CF Auto immune pancreatitis SLE Malignancy Stricture Congenital
Which form of cancer is most common in the mid and upper 1/3rd of oesophagus, and what are risk factors?
Squamous cell carcinoma
Smoking and excess alcohol
Which form of oesophageal cancer is most common and occurs in the lower 1/3rd of the oesophagus? And what are the risk factors?
Adenocarcinoma
Chronic GORD
Obesity
High fat diet
A patient presents with progressive dysphagia. What is the main diagnosis you should want to rule out and how would you do that?
Oesophageal cancer
Ask about weight loss, check lymph nodes
2WW OGD - all patients with dysphagia
In oesophageal cancer what imaging modalities can be used to check for mets?
CT - chest, abdomen and pelvis
PET-CT
A patient has Adenocarcinoma oesophageal cancer what is the most likely management options?
Neo-adjuvant chemotherapy
Chemotherapy and radiotherapy and surgery.
Surgery = deflate 1 lung for 2 hrs during surgery. Remove tumour, oesophagus, top of stomach and lymph nodes. Then use remaining stomach as a conduit and put it in place of the oesophagus
What are the main complications of oesophageal cancer surgery?
Anastomotic leak (8%)
Pneumonia (30%)
Death (4%)
What is the main treatment for squamous cell carcinoma oesophageal cancer?
Chemoradiotherapy.
What is the surgical treatment for achalasia and what is it?
Heller’s cardiomyotomy
Cut a length incision into the lower oesophageal oesophagus. A common complication is reflux therefore a total or partial fundoplication is also carried out to prevent this.
What type of disease is IBS?
A functional disease of exclusion.
A patient comes in with suspected IBS what tests would you do to diagnose this?
Rule out things
- FBC, Coeliac (tTG), CRP/ESR
Stool MC+S (infection)
Faecal calprotectin (IBD)
What is the ROME criteria?
Different symptoms of IBS are put into different categories to determine the best treatments.
What is the management of IBS?
Lifestyle - stress, anxiety or depression management. Regular exercise and diet (FODMAPS or lactose free)
Diarrhoea = loperamide
Constipation = movicol or lactulose (osmotic)
–> avoid fibre and stimulant laxatives.
Analgesia = anti-spasmodics (buscopan/mebeverine) or peppermint oil.
–> avoid NSAIDs and Paracetamol as they are ineffective.
What symptoms may occur in IBS/functional gastro disease?
abdominal pain (RIF) and discomfort Bloating Nausea Vomiting Increased bowel frequency and urgency Gynae - dysmenorrhea or dyspareunia Urinary - frequent, urgent, nocturia, incomplete emptying Headache Fatigue Bad breath/bad taste in mouth
What is the pathophysiology behind coeliac disease?
Gliadin in gluten is not broken down. This then crosses the intestinal mucosa and binds to HLA DQ2/DQ8 which activates T cells causing chronic inflammation and epithelial damage leading to malnutrition.
What are the risks/associated conditions for Coeliac disease? (IDTAITO)
IgA deficiency Downs syndrome Turners syndrome Autoimmune - thyroid/hepatitis IgA nephropathy Type 1 diabetes mellitus Other autoimmune conditions (e.g Sjogren's , addisons)
How would coeliac presentation in a child differ to that in a adult?
Child = failure to thrive, abdominal pain and bloating, diarrhoea and constipation, irritable, anaemia, muscle wasting
Adult = chronic diarrhoea, Nausea and vomiting, fatigue, weight loss, joint pain, anaemia, anxiety.
What extraintestinal coeliac symptoms are there?
Arthritis Dermatitis Herpetiformis Osteoporosis Infertility Ataxia Anxiety Depression Epilepsy
what investigations would be carried out for potential coeliac disease?
Anti-tTG antibody test
Total IgA –> if this low then want to do EMA, DGP and IgG tTG
HLA-DQ2/DQ8 screen
Biopsy (only in adults or unsure kids) - 4 changes
- loss of Villous atrophy = flat mucosa
- crypt cell hyperplasia
- Intraepithelial lymphocytosis
- lamina propria are infiltrated by inflammatory cells
What is the management of Coeliac disease?
Life long gluten free diet
Immunisations - 5yr pneumococcal and sometimes the influenza.
What are some of the possible complications of coeliac disease?
Hypersplenism
Osteoporosis
B12, folate, Iron deficiency = anaemia
small bowel T-cell lymphoma
What is the difference between diverticulosis, diverticular disease, diverticulitis and diverticular bleed?
Diverticulosis = presence of diverticular
Diverticular disease = symptoms due to diverticula
Diverticulitis = inflammation of the diverticula
Diverticular bleed = diverticular erodes into a large vessel causing large painless bleeding.
What is the pathophysiology of diverticulosis and diverticulitis?
Weaker bowel –> increased luminal pressure –> outpouching of mucosa through weak bowel wall.
Diverticulitis = overgrowth of bacteria in these outpouchings
Risk factors for diverticular disease?
FH Age Low fibre - constipation obesity smoking NSAIDs
How do the presentations of diverticular disease and diverticulitis differ?
DD = intermittent lower abdo pain that can be relieved by defecating. Altered bowel habits, nausea and flatulence Ditis = acute abdominal pain in the LIF that is sharp and worse on movement. Decreased appetite, pyrexia and nausea.
What investigations and treatment would you do for diverticular disease?
FBC, CRP, U+Es
Faecal calprotectin (if unsure)
Flexible sigmoidoscopy - if not available then CT colograph.
Simple analgesia and increased fluids.
If bleeds and not self resolving = embolisation or surgical resection.
What investigations and treatment would you do for diverticulitis?
What would occur on any scans?
FBC, CRP, U+E’s
Group and save
Urinary dipstick
VBG
CT abdomen-pelvis = thickened colonic wall, pericolonic fat stranding, abscesses, free air or air bubbles.
Antibiotics + IV fluid + analgesia (should work in 2-3 days)
What is the Hinchey classification used for?
Severity of acute diverticulitis
What are the possible complications of diverticular disease?
Diverticular stricture due to scarring and fibrosis. This can lead to a large bowel obstruction –> sigmoid colectomy.
Fistulas - colovesical or colovaginal
When would a hartmanns procedure be carried out in the means of diverticular disease?
Perforation with faecal peritonitis or in sepsis.
