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265 Cards in this Set
- Front
- Back
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Name possible non-GI causes of vomiting |
REMEMBER: ABCDEFGHI A > acidosis, Addisonian crisis B > brain injury, intracranial pressure C > cardiac infarction D > diabetic ketoacidosis (DKA) E > ear > labyrinth disease, Ménière's F > foreign substances (alcohol, drugs) G > gravidity > morning sickness H > hypercalcaemia, hyponatraemia I > infection > meningitis, UTI |
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What are the 3 most important anti-reflux mechanisms? |
1) intra-abdominal oesophagus 2) mucosal rosette of gastric fold 3) crura of the diaphragm |
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Hiatus hernia can be distinguished between sliding and rolling. |
sliding hiatus hernia - gastro-oesophageal junction + part of the stomach cardia slides through the hiatus - usually asymptomatic rolling hiatus hernia - part of the gastric fundus prolapses through the hiatus alonside the oesophagus - LOS remains below the diaphragm - strangulation or volvulus >>> symptomatic |
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What system is used for grading oesophagitis? |
LOS ANGELES CRITERIA > grades A >>> D |
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What investigation is used for diagnosis and assessment of oesophagitis and hiatus hernia? |
Endoscopy |
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What test is used to assess reflux if both oesophagitis and the Barrett's oesophagus are absent? |
24hr intraluminal pH monitoring > used for assessing: • pH monitoring • impedance (resistance to flow) • manometry (pressures in oesophagus) |
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Treatment of GORD > name two different classes with two different drug examples |
Alginate-containing antacids > magnesium antacids (SE: diarrhoea) > aluminium antacids (SE: constipation) H2-receptor antagonists > cimetidine, ranitidine > gastric acid suppressants PPI (proton pump inhibitors > H+/K+-ATPase) > omeprazole > lansoprazole |
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In someone with symptoms of heartburn but normal oesophageal mucosa on endoscopy and minor pH changes on the 24hr intraluminal pH monitor, we would suspect _____ ? |
hypersensitive oesophagus > pH monitoring negative (no drop below pH 4) > heartburn stimulated by minor pH changes > some PPI response |
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In someone with symptoms of heartburn but normal oesophageal mucosa on endoscopy and absolutely no pH changes on the 24hr intraluminal pH monitor, we would suspect ___ ? |
Functional heartburn > there is no acid stimulus causing the pain > there is low PPI-treatment response :( |
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Name 2 complications of GORD |
Peptic stricture - narrowing of the oesphagus, older patients - intermittent dysphagia for solids - endoscopic dilatation and long term PPIs might be needed Barrett's oesophagus |
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Define Barrett's oesophagus |
a replacement of the normal oesophageal squamous epithelium by metaplastic columnar glandular mucosa (resembling gastric histology) |
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How do you diagnose Barrett's oesophagus? |
ENDOSCOPY > proximal displacement of the gastro-oesophageal junction |
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How do you classify the extent of Barrett's oesophagus? |
Prague classification > recording the endoscopic distribution > circumferential extent (C) > maximal proximal extent (M) |
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What risk increases with Barrett's oesophagus? |
higher risk of oesophageal adenocarcinoma columnar metaplasia low grade > high grade dysplasia adenocarcinoma in situ invasive adenocarcinoma |
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Name 5 risk factors for gastro-oesophageal reflux: |
- pregnancy - obesity - fat, chocolate, coffee, alcohol ingestion - large meals - cigarette smokers - drugs > antimuscarinics (tiotropium, mebeverine) - hiatus hernia |
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Define achalasia |
oesophageal aperistalsis with impaired relaxation of the LOS |
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Patient presents with long history of intermittent dysphagia to both liquids & solids from the start. What is your first differential? |
ACHALASIA |
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What investigation do you do to diagnose achalasia? |
Barium swallow test |
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What would you seen on the barium swallow test in someone who has been diagnosed with achalasia? |
- dilated oesophagus - lack of peristalsis - "bird's beak" sign (narrowing at the LOS) - fluid level behind the heart |
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What investigation would you use to confirm aperistalsis? |
intraluminal manometry |
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What is the treatment for achalasia? |
> only palliative > endoscopic LOS dilatation (risk of perforation) > botulinum toxin (intrasphincterically) > Heller's operation (surgical division of LOS) |
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Achalasia increases risk of.... |
SQUAMOUS OESOPHAGEAL CARCINOMA |
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SYSTEMIC SCLERODERMA > what two major types are there? |
Limited cutaneous systemic scleroderma (LcSS) - ACA: anti-centromere antibody Diffuse cutaneous systemic scleroderma (DcSS) - anti-Scl70 antibody/ anti-topoisomerase |
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Which drug is known to cause cutaneous systemic scleroderma? |
bleomycin |
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What does the CREST syndrome comprise of? What antibody is it associated with? |
C = calcinosis R = Raynaud's E = oesophagus S = splenomegaly T = telangiectasia >>> ACA+ (anti-centromere-antibody) |
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Oesophagus and systemic sclerosis > what happens to the oesophagus (histologically) ? |
- smooth muscle replacement by fibrous tissue - fall in LOS pressure > continuous acid reflux - mucosal damage and inflammation - strictures and fibrotic changes develop |
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What causes bizarre "corkscrew" appearance of the oesophagus on barium swallow? |
DIFFUSE OESOPHAGEAL SPASM > e.g. nutcracker oesophagus > high amplitude peristalsis or aperistalsis > chest pain more common than heartburn > give antispasmodics, PPIs, GABA-agonists |
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What other non-GI conditions can cause oesophageal dysmotility? |
- MND - stroke - Bulbar palsy - DM - myasthenia gravis - myotonic dystrophy |
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What does Zenker's diverticulum, a common site of bolus impaction, arise from? |
Killian's dehiscence |
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Where does traction diverticulum form? |
near the middle of the oesophagus |
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What is the most common site of a benign oesophageal stricture? |
peptic stricture > at the gastrooesophageal junction > due to reflux |
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What are the potential causes of benign oesophageal stricture, besides reflux? |
- ingestion of corrosives - radiotherapy - sclerosis of varices - prolonged NG-intubation |
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What are the most common structural abnormalities of the oesophagus? |
webs & rings |
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Where in the oesophagus would you find a web? |
WEB - proximal oesophagus > esp. postcricoid region |
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Where in the oesophagus would you find a ring? |
RING - distal oesophagus > A ring (proximal to the sq/columnar junction) > B ring (at the sq/columnar junction) |
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What is the difference between A and B ring? > position > structures involved |
A ring (muscular) > proximal to the epithelial junction > made up of all 3 layers of the oesophageal wall > quite uncommon, rarely symptomatic B ring (mucosal) > aka Schatzki's ring > at the epithelial junction > composed of mucosa and submucosa only > characteristic history of intermittent bolus obstruction |
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define: Mallory-Weiss tear |
- a linear mucosal tear occurring at the gastro-oesophageal junction - rupture of the oesophageal mucosa only - seen in alcoholics common causes: > repeated retching, forceful vomiting, bout of coughing |
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define: Boerhaave's syndrome |
- a complete tear of the oesophageal wall at the gastro-oesophageal junction - commonly associated with violent vomiting |
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Clinical presentation of Boerhaave's syndrome. |
- haematemesis - severe retrosternal chest pain - hydropneumothorax (fluid level seen on CXR) THE MOST LETHAL PERFORATION OF THE GI TRACT (31% MORTALITY) |
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DEFINE: PLUMMER-VINSON SYNDROME - 3 features |
1) chronic microcytic iron deficiency anaemia 2) angular stomatitis, glossitis 3) oesophageal web |
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What is the most common cause of acute gastritis? |
> chemical injury > drugs, alcohol |
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What is the most common cause of chronic gastritis? |
helicobacter pylori infection |
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What is the most common cause of chemical gastritis? |
- biliary regurgitation - drug-induced - excess acid (Zollinger-Ellison) |
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List possible causes of acute gastritis |
- ischaemia - drugs - alcohol - infection |
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What infective agents can cause acute gastritis? |
- H. pylori - CMV - HSV |
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What antibodies are associated with chronic autoimmune gastritis? |
anti-parietal cell antibodies (in 90%) anti-intrinsic factor antibodies (in 50%) |
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What are the histological features of chronic autoimmune gastritis with regards to the: > the antrum |
fundus & body • chronic inflammation, pangastritis • intestinal metaplasia antrum • usually not inflamed, G-cell hyperplasia • increased gastrin production (compensating for the loss of parietal cells) • high gastrin stimulates ECL-cells > high histamine • ECL-cell hyperplasia can lead to gastrinoma production |
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PERNICIOUS ANAEMIA - which antibody is diagnostic? - what is the treatment? - what is its' effect on the stomach? |
antibody: anti-intrinsic factor antibody nutrient: B-12 (can't bind to the intrinsic factor treatment: hydroxycobalamine, i.m. consequence > loss of parietal cells & |
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What is the commonest bacterial pathogen in the world? |
helicobacter pylori (70% of adult population in developing countries affected) |
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Describe Helicobacter pylori > where does it reside in the body? > how does it protect itself? |
- gram negative flagellated curved rod - in the gastric pits > urease enzyme neutralising H+ by urease >> forming ammonia |
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What is the difference between: and body gastritis? |
antral gastritis >> duodenal ulceration, HCl production maintained body gastritis >>> gastric ulceration, parietal cell loss |
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What is the diagnostic test for H. pylori |
13^C urea breath test (more common) CLOT > done on biopsy (less common) |
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What malignancies is H. pylori associated with? |
- gastric adenocarcinoma - MALT lymphoma (NHL) |
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What non-GI conditions is HP associated with |
- coronary artery disease - iron deficiency - B12 deficiency |
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What is the eradication regimen for HP? |
PAC500 - PPI (lansoprazole) - amoxicillin - clarithromycin 500mg PMC250 - PPI (lansoprazole) - metronidazole - clarithromycin 250mg > diurnally, for 1 week |
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Name 3 possible infectious causes of granulomatous gastritis |
- TB - histoplasmosis - parasites (helminths) |
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Name 2 possible non-infective causes of granulomatous gastritis: |
- Crohn's disease - Sarcoidosis |
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What antigen does helicobacter pylori bind to? |
Lewis antigen |
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What is Curling ulcer? |
- an acute peptic ulcer of the duodenum > usually a complication of severe burn or reduced plasma volume (trauma > haemorrhage) - ischaemic ulcer |
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Where do stress ulcers most commonly arise? |
in the fundus |
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Where do peptic ulcers commonly arise? |
in the antrum or duodenum |
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What is Ménétrier's disease? |
- hypertrophic gastropathy - giant gastric folds, premalignant - mainly in the fundus - gastric pit hyperplasia - gastric gland atrophy (less HCl) - folveolar hyperplasia (more mucus) - impaired absorption, epigastric pain - hypoalbuminaemia (leaky mucosa) > oedema |
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define peptic ulcer |
A localised break in the superficial epithelium, penetrating down to the muscularis mucosa of either stomach or duodenum. Caused by acid and pepsin attack. |
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Where do the peptic ulcers most commonly arise from (generally)? |
From the site of epithelial junction > first part of duodenum > junction of antral & body mucosa > distal oesophagus > gastro-enterostomy site |
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What are the main causes of gastric ulcers? (list 3) |
- hyperacidity (e.g. Zollinger-Ellison syndrome) - HP gastritis - biliary reflux - NSAIDs - Smoking |
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What are the complications of peptic ulcers? |
- haemorrhage - penetration, erosion into another structure - rupture (peritonitis, sepsis) - stricture formation (obstruction) - anaemia - malignancy |
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GASTRIC & DUODENAL ULCER COMPARISON Which is more common in the UK? |
Duodenal ulcer (3x more common) |
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GASTRIC & DUODENAL ULCER COMPARISON Which is associated with lower socio-economic status? |
Gastric ulcer |
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GASTRIC & DUODENAL ULCER COMPARISON Which is more common in blood group A population? |
GASTRIC ULCER |
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GASTRIC & DUODENAL ULCER COMPARISON Which one is more common in blood group 0 population? |
DUODENAL ULCER |
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GASTRIC & DUODENAL ULCER COMPARISON Which one is more commonly associated with helicobacter pylori infection and elevated HCl production (lower pH)? |
DUODENAL ULCER |
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GASTRIC & DUODENAL ULCER COMPARISON Which one is characterised by the following: > pain related to meals > exacerbated with food/drink > haematemesis/ malaena > weight loss |
GASTRIC ULCER |
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GASTRIC & DUODENAL ULCER COMPARISON Which one is characterised by the following: > pain relieved with food or drink > no haematemesis > no weight loss > waking up at night because of severe pain > pain on hunger |
DUODENAL ULCER |
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GASTRIC & DUODENAL ULCER COMPARISON Which one of the two is more likely to perforate? |
DUODENAL ULCER |
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Where in the stomach does the gastric ulcer commonly occur? |
antral-body mucosa, at the lesser curvature |
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What is cicatrisation and what does it lead to? |
Shrinkage of the fibrous tissue > can lead to pyloric stenosis or central narrowin |
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What is dumping syndrome? |
Dumping = rapid fluid shift from plasma into the interstitium due to high osmotic gradient = reduction of blood volume > shock - nausea, sweating, faintness, palpitations |
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Where would the gastric adenocarcinoma occur in the stomach, it the cause was to be HP infection? |
DISTALLY |
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Patient comes with: |
if ≤55 yrs + no alarms > 13^C urea breath test if >55 yrs | ≤55 yrs + alarms > urgent upper GI endoscopy |
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What are the "ALARMS" signs for urgent endoscopy referral? |
A = anorexia L = loss of weight A = anaemia R = recent onset M = malaena S = swallowing difficulty (dysphagia) |
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Lack of which vitamin can cause xerophthalmia (night blindness) ? |
vitamin A (retinol) |
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Lack of which vitamin is the main cause of rickets and osteomalacia? |
vitamin D > produced in the skin (UV-B) > cholecalciferol > converted into 25-hydroxyvitamin D in the liver > converted by 1-alpha-hydroxylase into 1-25-dihydroxyvitamin D in the kidneys > regulated by PTH and FGF23 |
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B1 vitamin (Thiamin) deficiency has serious impact on both peripheral and central nervous system. |
PNS > Beri-beri (polyneuropathy) CNS > Wernicke-Korsakoff's syndrome |
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Which vitamin deficiency causes pellagra? |
B3 (Niacin) |
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The lack of folate will result in... |
> megaloblastic anaemia > neural tube defects in the foetus |
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Vitamin C deficiency (ascorbic acid) will result in a syndrome of "scurvy" characterised by bleeding gums, corkscrew hair and perifollicular haemorrhage. |
Ascorbic acid is needed for collagen synthesis |
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How do you treat B12 deficiency? |
Hydroxycobalamine, i.m. |
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List 3 features of Kwashiorkor. |
- hepatomegaly - generalised oedema - hypoalbuminaemia - skin thickening - apathy >> due to low protein & high carbohydrate diet >> impaired antioxidant defences probably |
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List 3 features of marasmus What is the cause? |
- cachexia, severe wasting - body fat loss, emaciation - no oedema - frequent diarrhoea >> childhood form of prolonged starvation |
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What is the moiety causing the damage in coeliac disease? |
Gluten > high glutamine & proline content > resistant to digestion by chymotrypsin |
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How do we diagnose coeliac disease? |
1) blood test > serology looking for tTG-antibody and EMA 2) tissue biopsy > taken on endoscopy > histopathological assessment to confirm the diagnosis |
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What are the three main histological features of the coeliac disease? |
1) villous atrophy 2) crypt hyperplasia 3) lymphocyte infiltrate in the lamina propria |
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Which virus infection in pregnancy is associated with higher risk of coeliac disease development? |
Rotavirus |
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State 3 symptoms of coeliac disease: |
- tiredness - bloating - painful mouth ulcers - unformed, liquidy stool - abdominal pain |
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State 3 signs of coeliac disease |
- IBS-like presentation - peristent diarrhoea, steatorrhoea - weight loss - mouth ulcers - angular stomatitis - folate and iron deficiency - family history of atopy |
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Which inborn immunity feature is commonly seen in coeliac disease? What does it predispose to? |
IgA deficiency Infections with encapsulated bacteria > staphylococcus aureus > Haemophilus influenzae |
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List 3 haematological complications of coeliac disease |
- iron deficiency aneamia (microcytic) - folate deficiency anaemia (macrocytic) - splenic atrophy (hyposplenism seen in most patients with coeliac disease) |
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Coeliac disease is associated with splenic atrophy due to chronic folate deficiency. |
- hypersegmented polymorphonuclear leucocytes (hypermature cells, lack of replacement) - Howell-Jolly bodies (basophilic nuclear remnants) other signs of hyposplenism: > target cells |
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What else should be monitored regularly in people with coeliac disease? |
Osteoporosis > due to gluten-free diet DXA > dual energy X-ray absortiometry |
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Which condition can cause partial villous atrophy in the jejunum? (as opposed to complete one in coeliac d.) |
Tropical sprue Giardia intestinalis infection |
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Name 3 main features of the tropical sprue |
- chronic diarrhoea - malabsorption - occurring in the residents of tropical areas |
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Which parasite causes the typical syndrome of: - malabsorption - steatorrhoea |
Giardia intestinalis > Rx: metronidazole |
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What bacteria causes the ill-famous Whipple's disease? |
TROPHERYMA WHIPPLEI |
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What is the typical presentation of Whipple's disease? |
- arthritis - diarrhoea, abdominal pain (progressive) - peripheral lymphadenopathy - heart, lung joint and brain involvement |
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What can we see on biopsy in Whipple's disease? |
PAS+ Mø > containing PAS positive granules Mø are infested by tropheryma whipplei >> seeno only on electron microscopy as trilaminar cell-walled bacteria Rx.: trimetophrim (for 1 year) |
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What increases the absorption of oxalate in the colon? |
Unreabsorbed bile salts (as it happens in distal ileum resection >>> no active bile salt reabsorption can take place) |
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If too damaged, distal ileum is sometimes resected (seen in Crohn's disease). |
> folate & B12 deficiency (macrocytic anaemia) > bile salt induced diarrhoea > bile salt induced amplification of oxalate uptake >> oxaluria >> calcium oxalate stones > steatorrhoea & gallstone formation (more bile salts lost > greater bile production > more lithogenic bile) |
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Which drug is commonly used in cases of intestinal resection and malabsorption to prevent diarrhoea and amplified oxalate absorption? |
cholestyramine > binds and mops up bile salts passing through the colon |
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How does diabetes causes malabsorption? |
autonomic neuropathy >> loss of motility > bowel stasis > bacteria overgrowth |
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What scoring system is used for assessment of severity of the ulcerative colitis? |
Truelove & Witt's Criteria > mild • <4 motions/day • apyrexial • Hb >110 g/L > moderate • 4-6 motions/day • mild pyrexia • Hb 105-110 g/L > severe • >6 motions • >37.8ºC • Hb <105g/L |
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Episodic or chronic diarrhoea with blood and mucus is strongly suggestive of... |
Ulcerative colitis |
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Severe, offensively smelling, hard to flush diarrhoea with urgency and tenesmus even at night is strongly suggestive of... |
Crohn's disaese |
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Frequently, ulcerative colitis is associated with one another autoimmune disease. Which condition is it? |
> PSC > Primary sclerosing cholangitis > autoimmune condition yet more frequent in men > increases a risk of cholangiocarcinoma (this is added on top of the initial risk of colorectal cancer) |
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Which GI condition is associated with HLA-B27 ankylosing spondylitis? |
Crohn's disease |
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What antibody can be seen in Crohn's disease? |
ASCA+ anti-saccharomyces cerevisiae antibody |
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Which conditions are associated with ASCA+ antibodies? |
Crohn's disease Behcet's disease Coeliac disease ± Ulcerative colitis |
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What antibody is associated with ulcerative colitis? |
pANCA |
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What markers are elevated in colonic inflammation and what test do we use to look for them? |
> calprotectin > lactoferrin >> identified on the stool test |
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When one of the IBDs is suspected, what is the important differential we should always consider and test for? |
Clostridium difficile infection > stool > CDT (C. difficile toxin > PCR and ELISA) |
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What drug therapy would you offer to a patient presenting with IBS? |
antimuscarinic > mebeverine tricyclic antidepressant > amitriptyline (low dose > subtherapeutical for depression) |
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INTESTINAL ISCHAEMIA What is the prognosis of mucosal infarction? |
> complete regeneration > mucosal integrity restored > excess of subsequent inflammation might lead to progression of transmural ischaemia |
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INTESTINAL ISCHAEMIA What is the prognosis of mural infarction? |
> repair and regeneration by fibrous stricture > reaches but does not cross the muscularis propria |
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INTESTINAL ISCHAEMIA What is the prognosis of transmural ischaemia? |
> gangrene > death of the segment > necrosis spreading if not resected > dilatation, flaccidity > loss of bowel sounds |
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Which part of the colon is most susceptible to ischaemic damage? |
Splenic flexure > a water-shed area between middle colic artery (from SMA) and left colic artery (from IMA) |
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What is the best investigation for ischaemic colitis? |
flexible sigmoidoscopy |
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In large bowel ischaemia, what characteristic feature can be seen on the abdominal X ray? |
"thumb-printing" > a sign of ischaemia at splenic flexure |
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Which infective agent is commonly responsible for production of power beta toxin? This toxin leads to coagulative necrosis, gas gangrene formation and the development of paralytic ileus, leading to sepsis and shock. |
clostridium perfringens |
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A patient with pulsatile abdominal mass was brought to A&E. He is very unwell, going to a shock. 1) What is the likely undergoing diagnosis? |
A patient with pulsatile abdominal mass was brought to A&E. He is very unwell, going to a shock. On examination, you notice his feet have acquired a grey tinge. 2) "THRASH FEET" >> microemboli released from the site of the aneurysm and impacted within the small capillaries of the man's feet > remember > UK NHS AAA Screening > everyone ≥65 yo > abdominal US |
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A dark crescent right below the diaphragm is a sign of... ______ ? |
....a ruptured viscus (air below the diaphragm) |
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Define McBurney's point |
2/3 of the way from the umbilicus to the ASIS (anterior superior iliac spine) |
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What imaging method is used for confirming the diagnosis of acute appendicitis? |
a CT scan |
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What is the differential diagnosis for acute appendicitis? > nausea, vomiting > raised inflammatory markers (e.g. CRP) |
> acute appendicitis > acute terminal ileitis (Yersinia, Crohn's) > inflamed Meckel's diverticulum |
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Name a few gynaecological causes of right/left iliac fossa pain |
> ruptured ectopic pregnancy > mittelschmerz > rupture of ovarian cyst > acute salpingitis > Fitz-Hugh-Curtis syndrome |
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What are the presenting features of acute salpingitis? |
> bilateral low abdominal pain > fever > vaginal discharge >> mostly STIs > gonococcus, chlamydia |
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Fitz-Hugh-Curtis syndrome > ... is associated with chlamydial infection. What happens and what is the typical presentation? |
1) Vaginal infection with chlamydia > thinning of the cervical mucus 2) bacteria from the vagina reach the uterus and oviducts 3) Bacteria travel up in the right paracolic gutter, reaching the liver and infecting the Glisson's capsule. PRESENTATION: |
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NAME THE CHARCOT'S TRIAD FOR |
1) fever 2) Right upper quadrant pain 3) jaundice |
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NAME REYNOLD'S PENTAD FOR ASCENDING CHOLANGITIS: |
1) FEVER 2) RUQ pain 3) jaundice 4) confusion 5) hypotension |
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What is the value for serum amylase, strongly suggestive of acute pancreatitis? |
when serum amylase = 5x normal |
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Where does the bowel obstruction most commonly occur? |
In the small intestine (75%) > 25% of obstructions occur in large bowel |
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What are the most common causes of large bowel obstruction in children? |
> unperforated anus (atresia) > Hirschprung's disease |
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What is the most common cause of large bowel obstruction in adults? |
In the western world > 90% due to volvulus (5%) strictures (3%) hernias (rare) In the developing world > 50% due to volvulus (due to high fibre diet??) |
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What is the most common cause of small bowel obstruction in children? |
> intussusception (small, thin walled, soft > easy to telescope in) > atresia (developmental failure) |
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What is the most common cause of small bowel obstruction in adults? |
> adhesions >>> inflammation & fibrosis > Crohn's disease > hernias > malignancies (not as common as in large bowel) |
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Where do the colorectal tumours most commonly arise from? |
about 70% of colorectal tumours arise distal to the transverse colon > in black females the most common site is the ascending colon on the right |
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What are the key facts about large bowel obstruction (LBO): > when does it present? > what imaging is used? |
> present later than small bowel tumours > vomiting appears only in more advanced stages > serum lactate is of less relevance than in > contrast enema X-ray (finding the obstruction) |
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Characterise the bowel sounds on obstruction |
initially increased sounds > increased secretions later decreased sounds > ischaemia develops > paralytic ileus > the failure of peristalsis |
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What is the pain pattern in intestinal obstruction? |
colicky >> diffuse >> constant |
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Pain >>>> vomiting |
obstruction |
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Vomiting >>>> pain ∆ most likely? |
infection |
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What is a useful marker of ischaemia in the small bowel obstruction? |
serum lactate |
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What is the most important biomarker elevated in pancreatitis? |
amylase |
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What are the serum amylase levels in acute pancreatitis? |
They are grossly elevated, 4-6x, and stay high until the acute pancreatitis resolves |
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What are the serum amylase levels in chronic pancreatitis? |
They are elevated at first but then fall back down. It is more useful to measure urine amylase, as the levels remain elevated for longer. |
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Besides serum amylase, what other enzyme is elevated? Why don't we use it for monitoring pancreatitis? |
> serum lipase |
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Besides pancreatitis, what are the other causes of elevated serum amylase? |
> upper GI perforation > biliary peritonitis > intestinal infarction (serum lactate more used though) |
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What are the causes of pancreatitis? |
G > gallstones E > ethanol (alcohol) T > trauma S > steroids M > mumps S > scorpion, spider bites H > hypercalcaemia E > ERCP D > drugs (azathioprine, oestrogens) |
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What is the underlying mechanism of the inflammatory reaction in acute pancreatitis? |
> enzymatic autolysis of the pancreas > elevated levels of activated trypsin can be precipitated by acute rise in intracellular Ca2+. |
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What are the causes of sudden Ca2+ elevation precipitating acute pancreatitis? |
> gallstone impaction and blockage of the pancreatic juice outflow > ductular hypertension >>> more free ionised cytosolic calcium (Ca2+) > alcohol binge >> acute rise in cytosolic free calcium (Ca2+) precipitating excess trypsinogen activation |
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What are the causes of long-term Ca2+ elevation causing chronic pancreatitis? |
> alcohol >>> impairing calcium regulation long-term, leading to persistent Ca2+ elevation > mutations in chymotrypsin C >> chymotrypsin C is normally mopping up excess trypsin > CFTR mutation > CYSTIC FIRBOSIS > impairs the mechanism of enzyme secretion >> pancreatic exocrine failure |
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What can we see on contrast enhanced CT of someone with chronic pancreatitis? |
pancreas calcification |
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What are the clinical features of chronic pancreatitis? |
> epigastric pain > anorexia, weight loss > exocrine & endocrine pancreatic failure > steatorrhoea & malabsorption > jaundice > fibrosed head of the pancreas |
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Should you reduce the fat intake in the treatment of pancreatitis? |
No. It would only exacerbate the malnutrition. |
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Should you reduce reduce the fat intake in the treatment of Crohn's disease? |
Yes |
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Name 3 different means of pancreatitis management |
abdominal pain > NSAIDs or opiates (tramadol) gallstones > ESWL (extracorporeal shock wave lithotripsy) steatorrhoea > H2 antagonist (ranitidine) diabetes > endocrine insufficiency > insulin s.c. |
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Which pathogen is known to cause HUS and TTP in children? |
EHEC: Escherichia coli O157 |
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What is the most common cause of food poisoning in the UK? |
Campylobacter jejuni |
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What is the causative agent of cholera and how does it cause the explosive watery diarrhoea? |
Vibrio cholerae > gram negative, curved bacillus > treat with tetracycline!!! |
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What two bacteria are famous for causing immediate (in <2hr) vomiting? |
Staphylococcus aureus Bacillus cereus |
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Which bacteria is the most common cause of traveller's diarrhoea worldwide? What is the usual treatment? |
ETEC > enterotoxic Escherichia Coli > Rx.: usually no antibiotics needed > ORS: oral rehydration solutions |
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Name 5 bacteria causing dysentery |
> Shigella > Salmonella > EHEC (entero-haemorrhagic) > EIEC (entero-invasive) > Campylobacter > Clostridium difficile > Yersinia enterocolica |
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Name 5 bacteria causing watery diarrhoea |
> ETEC (entero-toxic) > EPEC (entero-pathogenic) > Bacillus cereus > Staphylococcus aureus > vibrio cholerae (the most lethal cause of diarrhoea) |
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What is the main empirical treatment for diarrhoeal diseases? |
CIPROFLOXACIN (quinolone) but: > campylobacter spp > azithromycin (macrolide) > c. difficile > metronidazole > v. cholerae > doxycyclin (tetracycline) |
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Write down the sequence of events in development of oesophageal adenocarcinoma |
sq. epithelium >>> long-term GORD <<< metaplastic columnar epithelium >>> Barrett's oesophagus <<< dysplastic columnar epithelium neoplastic adenocarcinoma in situ >>> basement membrane breach <<<< neoplastic invasive adenocarcinoma |
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Where do oesophageal adenocarcinomas most usually occur in the oesophagus? What are the main causes? |
Adenocarcinoma > distal oesophagus > high incidence in the UK > due to GORD, obesity, hyperacidity > dysphagia, weight loss |
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Where do oesophageal squamous cell carcinomas most usually occur in the oesophagus? What is the epidemiology? What are the main causes? Presentation? |
Squamous cell carcinoma > proximal oesophagus > low incidence in UK, common in China, SEA > smoking, alcohol, hot drinks |
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What is the prognosis of gastric cancer? |
>> gloomy :( ... <10% of patients make it to the 5-year survival |
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Risk factors for gastric cancer. Name 5. |
> Helicobacter pylori > Diet (salt, pickling, smoked stuff) > Smoking > Pernicious anaemia |
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What is the most common treatment regimen for colorectal cancer? |
FOLFOX > folinic acid > 5-FU > 5-fluorouracil > Oxaliplatin TARGETED BIOLOGICALS (anti-VEGFR) > Bevacizumab |
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What types of polyps can be found in the GI tract (3 types) |
> Inflammatory polyps (Crohn's, UC) > Hamartomatous polyps >>> juvenile polyps >>> Peutz-Jehgers syndrome > Neoplastic polyps >>> tubular | villous adenoma |
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WHAT IS PEUTZ-JEHGERS SYNDROME? > mode of inheritance? > features? |
> autosomal dominant mutation in tumour suppressor gene (STK11) > dark freckles on acral & mucosal surfaces > multiple polyps (hamartomas) |
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What is the tumour marker in colorectal cancer? When can it be falsely elevated? |
CEA > carcinoma-embryonic antigen elevated in: |
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What is the main tumour marker for hepatocellular carcinoma? |
alpha-Feto-protein elevated in: > pregnancy > cirrhosis |
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What system is used specifically for staging of colorectal cancer? |
DUKES' STAGING A > limited to muscularis propria B > penetrated through muscularis propria C > breached the whole of m. propria + LN D > distant metastases |
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FAP (Familial Adenomatous Polyposis) > what gene has mutated? > mode of inheritance? > prophylaxis? |
> APC gene mutation, AD pattern > beta-catenin enters the nucleus and amplifies the expression of epithelial proliferation > multiple polyps form > confined to the colon > can be resected |
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LYNCH SYNDROME (HNPCC) (hereditary non-polyposis colorectal cancer) > what gene has mutated? > mode of inheritance? > prophylaxis? |
> loss of DNA mismatch-repair gene, AD > no proper apoptosis in response to damaged DNA > risk of cancer in: >>> uterus, ovary, stomach, small bowel |
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Which gene mutation is typically associated with pancreatic cancer? |
k-RAS2 > oncogene amplification (in 95% cases) |
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Which drug, when given at low dose, can prevent the formation of GI adenomas? |
aspirin |
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What are the risk factors for anal cancer? |
> syphilis (treponema pallidum) > anal warts (HPV 16/18/6/11) > MSM (anoreceptive) |
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What is the histology of anal cancer? |
Squamous cell carcinoma (85%) |
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ANAL TUMOUR OCCURRING AT THE ANAL MARGIN (above dentate line) > differentiation > histology |
> usually well-differentiated > squamous cell, keratinising (skin-like) > inguinal lymph nodes |
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ANAL TUMOUR OCCURRING IN THE ANAL CANAL (above dentate line) > differentiation > histology > LN drainage |
> poorly-differentiated > squamous cell, non-keratinising (mucosa-like) > pelvic lymph nodes |
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UK NHS BOWEL CANCER SCREEN > what test? > how often? |
> faecal occult blood > every 2yrs |
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What are the risk factors for pancreatic cancer? Name 3 |
> smoking > alcohol > chronic pancreatitis (alcohol, CF) > obesity, meaty diet |
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Which part of the pancreas does the pancreatic tumour most commonly arise from? |
the head of the pancreas (60%) >> painless obstructive jaundice >>> tumour of the head |
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What is the most common liver malignancy? |
Secondary metastatic tumour from elsewhere (usually stomach, lung, breast or colon) |
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What is the most common primary hepatic neoplasia? |
hepatocellular carcinoma (90%) |
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Name possible causes/ risk factors for HEPATOCELLULAR CARCINOMA? |
> HBV, HCV > cirrhosis (alcohol, haemochromatosis, PBC) > NAFLD > aflatoxins (aspergillus flavus) |
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What are the main causes/ risk factors for CHOLANGIOCARCINOMA? |
> flukes (clonorchis) > Caroli's disease > HBV, HCV |
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What would you expect to be elevated in cholangiocarcinoma? |
> ALP (alkaline phosphatase) > bilirubin (jaundice) |
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What are the signs consistent with HCC? |
> loss of appetite, weight loss > RUQ pain > jaundice, haemobilia > ascites > bruisin > irregular liver surface on palpation |
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What are the two famous surface signs of acute pancreatitis? |
Cullen's sign (peri-umbillical bruising) Grey-Turner's sign (flank bruising) |
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Name 4 causes of cirrhosis: |
> excess alcohol intake > hepatitis B, C > autoimmune hapatitis > hereditary haemochromatosis (HFE mut.) > Wilson's disease > NAFLD |
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What are the complications of liver failure? |
> ascites > oesophageal varices (haematemesis) > hepatic encephalopathy (ammonium) > hepatorenal syndrome (tubular necrosis) > SBP (spontaneous bacterial peritonitis) > HCC (hepatocellular carcinoma) |
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What is FETOR HEPATICUS? |
- usually a presentation of hepatic failure - lost ability to detoxify substances in the liver - volatile aromatic substances (sweet smelling) are exhaled in breath > faecal smell |
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What is Reye's disease? |
- encephalopathy + hepatic failure in children - occurs when a child takes aspirin after a viral infection (esp. with VZV) - leads to mitochondrial damage inside hepatocytes > liver damage > more ammonia |
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List 4 hepatotoxic drugs: |
analgesics (paracetamol > NAPQI) monoamine oxidase inhibitors (MAO-i) > selegiline (PD), hydracarbazine (atypical depression) TB drugs (isoniazid, rifampicin) Anti-convulsants (valproate) Social drugs (ecstasy) |
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Name 3 histological features of chronic hepatitis: |
> plasma cell infiltration > confluent necrosis > bridging fibrosis |
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Weil's disease > infective agent? |
> leptospira icterohaemorrhagiae (gram negative spirochaete) > acute hepatitis > meningitis |
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INTERFACE HEPATITIS = loss of definition of the portal-periportal limiting plate WHERE CAN WE SEE IT? |
> in chronic viral hepatitis (hep B, hep C) > in autoimmune hepatitis (AIH) |
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What antibodies are associated with chronic hepatitis? |
> ANA+ (anti-nuclear) > ASMA+ (anti-smooth-muscle) |
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Which antibody is asssociated with PBC? |
AMA+ |
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Which antibody is associated with PSC? |
pANCA |
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What is the difference in the pattern of liver fatty infiltration between NAFLD and ALD? |
NAFLD >> fatty change diffuse ALD >> fatty change confined to ZONE 3 mainly |
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What marker can we use for monitoring alcohol consumption in abstaining alcoholics? |
gamma-GT >> gamma glutamyl transferase |
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What is the preferred imaging method used in diagnosis of liver fatty change? |
diagnosis >> abdominal US scan degree of fibrosis >> elastography |
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What are the most common causes of hepatic cirrhosis? |
in the Western world >> alcohol Worldwide >> Hep B and C viruses |
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What are the genetic causes of liver cirrhosis? |
> alpha-1-antitrypsin deficiency (Ch.14) > cystic fibrosis (Ch.7 ∆F508) > Wilson's disease (Ch.13 ATP7B) |
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Which cells are mainly responsible for activation of the liver fibrosis? |
Stellate cells (aka Ito cells) Located in the space of Disse (between bile canaliculi & blood sinusoids) TGF-ß (transforming growth factor beta) |
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Micronodular cirrhosis occurs in ... (state the condition) |
ALCOHOL LIVER DAMAGE |
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Macronodular cirrhosis occurs in ... |
CHRONIC VIRAL HEPATITIS WILSON'S DISEASE |
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Which ion will be deficient in a severe cirrhotic disease? |
Sodium (Na+) |
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DEFINE PORTAL HYPERTENSION |
Portal vein pressure >12 mmHg |
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NAME POSSIBLE CAUSES FOR EACH: > HEPATIC PORTAL HTN >>> pre-sinusoidal >>> post-sinusoidal > POSTHEPATIC PORTAL HTN |
PREHEPATIC > portal vein thrombosis HEPATIC > presinusoidal > Schistosomiasis > postsinusoidal > Cirrhosis POSTHEPATIC > Budd-Chiari (hepatic vein obstruction) > Right heart failure > constrictive pericarditis |
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Pipe-stem cirrhosis is characteristic of... |
SCHISTOSOMIASIS |
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When percussing patient with ascites, what are we expected to find? |
Shifting dullness (at least 1-2L of ascitic fluid needed to demonstrate this) |
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What surgical intervention would you offer to a patient with portal hypertension? |
TIPS > trans-jugular intrahepatic portosystemic shunt complication? PSE > PORTO-SYSTEMIC ENCEPHALITIS |
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Name 3 bacteria commonly causing SBP What antibiotic would you give? |
> Escherichia coli (Gram- bacillus) > Klebsiella spp. (Gram- bacillus) > Enterococci (Gram+ coccus) > 3rd generation cephalosporin (cefotaxime) |
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State 3 signs of hepato-pulmonary syndrome |
> spider naevi > finger clubbing > cyanosis |
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List the main features of PBC > "female CIA agent" |
female CIA agent C = cholesterol high >> xanthelasmata C = cancer risk >>> HCC C = intralobular canaliculi affected I = icterus (jaundice) I = irreversible fibrosis (aka cirrhosis) A = AMA+ antibodies A = ADEK vitamin deficiency A = ALP elevated (alkaline phosphatase) |
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List the main histological features of PSC What is seen on the ERCP? |
> onion-skin appearance of lesions > periductally |
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List the main histological features of PBC |
> plasma cell infiltrate > granulomas > ZONE 1 affected mostly (cf. ALD > zone 3, NAFLD > diffuse) |
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TREATMENT OF PBC |
PBC > pruritus >>> cholastyramine | rifampicin > fix bilirubin & ALT/AST levels >>> PBC > biliary > bear = urso |
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TREATMENT OF PSC |
PSC > Liver Tx is the only proven treatment |
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HEREDITARY HAEMOCHROMATOSIS > what gene is responsible? > at what chromosome? |
> HFE gene (High Fe) > chromosome 6 > hepcidin > mostly AR, but can be AD as well |
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What organs are affected by excess Fe deposition in the HEREDITARY HAEMOCHROMATOSIS? |
liver > hepatomegaly, Fe-deposition in hepatocytes pancreas > impaired insulin secretion > often diabetes >>> BRONZE DIABETES skin > bronze pigmentation (high melanin) heart > restrictive cardiomyopathy > arrhythmias |
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What is characteristic of an MRI image in someone suffering from HEREDITARY HAEMOCHROMATOSIS? |
> reduced signal density of the liver & pancreas due to paramagnetic effect of ferritin & haemosiderin |
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What is the most effective treatment for HEREDITARY HAEMOCHROMATOSIS? |
venesection > regular excess iron removal > O.5L/ 2x weekly > reversal of tissue damage |
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WILSON'S DISEASE What is the mutation in Wilson's disease? |
> ATP7B gene > chromosome 13 > impaired binding of Cu onto caeruloplasmin > AR |
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WILSON'S DISEASE > an autosomal recessive disorder characterised by copper deposition into various tissues. |
LIVER > chronic hepatitis > macronodular cirrhosis (cf. ALD > micronodular) BASAL GANGLIA > tremor, involuntary movements, dementia CORNEY > Kayser-Fleischer Rings > copper deposits within the Descemet's membrane |
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At which chromosome could we find the locus for alpha-1-antitrypsin gene? |
chromosome 14 |
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List 3 histological features common in ALCOHOL LIVER DISEASE |
1) steatosis >> hepatocytes swollen with fat 2) Mallory bodies > denaturated intermediate filaments within hepatocytes) 3) centrilobular necrosis (around zone 3) 4) micronodular necrosis |
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BIOCHEMICALLY SPEAKING, WHAT IS THE EFFECT OF ALCOHOL ON THE LIVER METABOLISM? |
> altered REDOX potential > upregulation of MEOS (microsomal E(OH) oxidizing system) > increased fatty acid synthesis > decreased fatty acid oxidation ∆ deposition of fatty acids (esp. ZONE 3) |
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Where else, besides ALD, could we find Mallory bodies? |
in Wilson's disease |
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BUDD-CHIARI = posthepatic portal hypertension = occlusion of the hepatic vein LIST 3 POSSIBLE CAUSES: |
- extraluminal occlusion by mass effect of sarcoma - hepatocellular carcinoma - hydatid cyst - radiotherapy - hypercoagulability states: >>> polycythaemia rubra vera >>> paroxysmal nocturnal haemoglobinuria (Marchiafava-Micheli) |
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LIVER ABSCESS > IDENTIFY THE ORGANISM: • multiple microabscesses • history of foreign travel • swinging fever • abscess fluid ~ anchovy sauce |
ENTAMOEBA HISTOLYTICA > METRONIDAZOLE |
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LIVER ABSCESS > IDENTIFY THE ORGANISM: • granulomas • fibrosis with no cirrhosis • elevated ALP • presinusoidal portal hypertension |
SCHISTOSOMA MANSONI > the ova reach the liver and obstuct the portal branches |
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LIVER ABSCESS > IDENTIFY THE ORGANISM: • large cyst seen on the CT scan • daughter cysts within the original cyst • dull ache and hepatomegaly • peripheral oesinophilia |
HYDATID CYST > BY Echinococcus granulosus > PAIRS: puncture > aspirate > inject > re-aspirate > Abx: albendazole |
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WHAT ARE THE MAIN RISK FACTORS FOR CHOLANGIOCARCINOMA? List two. |
PSC > Primary sclerosing cholangitis Clonorchis sinensis > Chinese liver fluke |
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List at least 6 signs of liver disease |
- spider naevi, palmar erythema, xanthomas - clubbing, Dupuytren's contracture - hepatomegaly, splenomegaly, ascites - gynaecomastia, testicular atrophy - asterixis (hepatic flap) - jaundice (icterus) - caput medussae (portal HTN) - ecchymosis (bruising) - leukonychia (also seen in nephrotic syndrome) - fetor hepaticus (sweet breath smell) |
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List 4 different conditions where we could find finger clubbing: |
- lung cancer (esp. NSCLC), mesothelioma - interstitial lung disease (IPF, COP,...) - TB - empyema, bronchiectasis, CF - congenital heart disease (tetralogy of Fallot) - IBD (Crohn's and ulcerative colitis) - hepato-pulmonary syndrome - Grave's disease (thyroid acropachy) - primary biliary cirrhosis - loss of body hair - malabsorption |
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What other similar disease is Dupuytren's associated with? |
Peyronie's disease |
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JAUNDICE > definition + correct value (micro-mol/L) |
Icterus = yellowing of the skin, sclerae and mucosae due to elevated plasma bilirubin Visible when bilirum levels ≥50 micromol/L |
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What are the inherited forms of congenital jaundice? |
Unconjugated: > Crigler-Najjar syndrome (AD, homozygote) Conjugated > Rotor syndrome (AR) > Dubin-Johnson syndrome (AR) |
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Which congenital diseases are characterised by impaired conjugation? |
Gilbert's syndrome Crigler-Najjar syndrome > thus uncojugated jaundice (hepatic) > lack of UDP-GT |
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Which congenital diseases are characterised by impaired conjugated bilirubin secretion? |
Dubin-Johnson's syndrome Rotor syndrome > conjucated jaundice |
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What are the main differences between: Rotor syndrome & Dubin-Johnson syndrome |
(1) > Rotor syndrome presents with non-itching jaundice > Dubin-Johnson syndrome usually asymptomatic (2) > Dubin-Johnson syndrome = BLACK LIVER on biopsy (not seen in Rotor's syndrome) |
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DEFINE: KERNICTERUS |
Bilirubin induced brain dysfunction > unbound (unconjucated) bilirubin deposited in infant BG |
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CAROLI'S DISEASE > What? |
> What? Multiple saccular dilatations of intrahepatic bile ducts. Congenital hepatic cirrhosis > Who? > young adults > Recurrent cholangitis/ gallstones |
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MIRIZZI'S SYNDROME |
> obstructive jaundice from CBD compression > gallstone impacted in the cystic duct > cholangitis very common |
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WHAT IS THE CAUSE OF THE FOLLOWING: 2) big rise in ALP, small rise in ALT|AST 3) high PT, low albumin 4) high unconjugated bilirubin, high reticulocytes 5) abnormal mononuclear cells 6) rural areas, sewage workers 7) rigors? 8) liver symptoms + cold sores |
1) hepatitis 2) extrahepatic obstruction, biliary tree disease 3) chronic liver disease 4) haemolytic jaundice 5) glandular fever > EBV > monospot test 6) leptospirosis, Hep A 7) cholangitis, gallstones, liver abscess 8) herpes simplex virus hepatitis |
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WHAT ARE THE 3 MAIN TYPES OF GALLSTONES? WHICH ONE IS MOST COMMON? MORE COMMON IN MALES OR FEMALES? |
1) CHOLESTEROL STONES 2) PIGMENT STONES >>> brown pigment stones (calcium salts + fatty acids) >>> black pigment stones (calcium bilirubinate + some salts) 3) MORE COMMON IN FEMALES |
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WHAT IS EACH STONE'S MOST LIKELY AETIOLOGY? > CHOLESTEROL STONE > BLACK PIGMENT STONE > BROWN PIGMENT STONE |
CHOLESTEROL STONE > Western diet, diabetes mellitus, pregnancy > leptin, deoxycholic acid BROWN STONE > chronic parasite infection > bile stasis, Caroli's syndrome, PSC BLACK PIGMENT STONE > 60% from haemolytic patients > subclinical bacterial infection |
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LIST 4 FEATURES OF BILIARY COLIC |
- constant, crescendo pain - pain can radiate into R shoulder - nausea + vomiting - fever & rigors (suggesting cholecystitis or cholangitis) |
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What is the best investigation for detection of gallstones? |
abdominal US scan |
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What is the cardinal feature of the ADENOMYOMATOSIS OF THE GALLBLADDER? |
ROKITANSKY-ASCHOFF SINUSES > multiple intramural diverticula form > hyperplasia of the mucosa > thickening of the gallbladder wall |
