Blackboard Mock Exam 2018 Flashcards
A 65 year old obese man presents with gradual worsening dysphagia for solids, which had initially been intermittent. He has had GORD for many years but is poorly compliant with medication.
What is the diagnosis? A. Oesophageal cancer B. Benign oesophageal stricture C. Globus hystericus D. Candidal oesophagitis E. Parkinson’s disease F. Scleroderma G. Diffuse oesophageal spasm H. Eosinophilic oesophagitis I. Upper oesophageal web J. Oesophageal diverticulum K. Stroke L. Achalasia
B. Benign oesophageal stricture
Healing of oesophageal damage inflicted in GORD involves the deposition of collagen. This causes contraction of the distal oesophagus which causes the formation of strictures. This is often associated with dysphagia for solids. Other complications of GORD include oesophageal ulcer, haemorrhage or perforation, Barrett’s oesophagus and oesophageal adenocarcinoma.
A 30 year old woman presents with aspiration pnuemonia. She has a long history of intermittent mild dysphagia for both liquids & solids and often suffers from severe retrosternal chest pain. Occasionally she gets food stuck but overcomes this by drinking vast amounts of water.
What is the diagnosis? A. Oesophageal cancer B. Benign oesophageal stricture C. Globus hystericus D. Candidal oesophagitis E. Parkinson’s disease F. Scleroderma G. Diffuse oesophageal spasm H. Eosinophilic oesophagitis I. Upper oesophageal web J. Oesophageal diverticulum K. Stroke L. Achalasia
L. Achalasia
This is achalasia which is a motility disorder with loss of peristalsis in the distal oesophagus and failure of the LOS to relax in response to swallowing. This presents commonly with dysphagia to both liquids and solids, regurgitation and retrosternal chest pain, which can be slowly progressive over time. In structural obstruction such as cancer, dysphagia to liquids is uncommon unless the disease is very advanced. Retrosternal pressure experienced can be precipitated by drinking liquids but is eased by continuing to drink, and the pain may be relieved by cold water. This may wake the individual from sleep. A UGI endoscopy is needed to exclude malignancy as a cause of dysphagia. The diagnosis is established on manometry or barium studies. Treatment is symptomatic.
A 75 year old male smoker presents with a 3 month history of dysphagia for solids. He has lost 8kg in weight over the last 5 months. O/E he has lymphadenopathy.
What is the diagnosis? A. Oesophageal cancer B. Benign oesophageal stricture C. Globus hystericus D. Candidal oesophagitis E. Parkinson’s disease F. Scleroderma G. Diffuse oesophageal spasm H. Eosinophilic oesophagitis I. Upper oesophageal web J. Oesophageal diverticulum K. Stroke L. Achalasia
A. Oesophageal cancer
Dysphagia (normally in a progressive pattern) coupled with weight loss points to malignancy. Dysphagia occurs when there is obstruction of more than 2/3 of the lumen and presence indicates locally advanced disease. There may additionally be odynophagia. Lymphadenopathy is a sign of metastatic disease here. Men are twice as likely to develop oesophageal cancer. GORD, Barrett’s oesophagus, FH, tobacco and alcohol are all risk factors. The two main types are squamous cell carcinoma and adenocarcinoma. Tumours in the upper 2/3 of the oesophagus are SCC whereas those that lie in the lower 1/3 are adenocarcinomas. The main test to order is an OGD with biopsy. Treatment is either surgical resection or with chemo or radiotherapy alongside endoscopic ablation with or without stenting and brachytherapy.
A 33 year old presented with retrosternal discomfort on swallowing but without any real difficulty swallowing. O/E he was found to have creamy plaques in his mouth and later admitted to having AIDS.
What is the diagnosis? A. Oesophageal cancer B. Benign oesophageal stricture C. Globus hystericus D. Candidal oesophagitis E. Parkinson’s disease F. Scleroderma G. Diffuse oesophageal spasm H. Eosinophilic oesophagitis I. Upper oesophageal web J. Oesophageal diverticulum K. Stroke L. Achalasia
D. Candidal oesophagitis
This is really odynophagia rather than true dysphagia. Whenever a patient complains of ‘difficulty swallowing’, you should always take a good history and explain what the patient actually means by this. Does the patient mean that there is true difficulty swallowing, or just that it is painful to swallow, or is there a feeling of a lump in the throat (globus). The white plaques here give alongside discomfort away the diagnosis. The patient also has AIDS and is therefore immunocompromised. Candidiasis here is an opportunistic infection in an immunocompromised host and is a mucosal infection caused in most cases by Candida albicans (and occasionally by other species). Patients may present like this, or with oral or vaginal infection. Oral thrush may be seen (pseudomembranous candidiasis) with altered taste sensation or indeed dysphagia, as well as odynophagia in oesophageal disease. In vaginal infection, there is erythema with a white discharge and pruritis. This patient should be started on an empirical trial of antifungals. A systemic azole can be used such as fluconazole or itraconazole.
A 45 year old female with a history of psychological problems presented with difficulty swallowing which had been getting progressively worse over the last 6 months. She described a sensation of a lump in the throat but after examinations and an endoscopy, no cause could be found.
What is the diagnosis? A. Oesophageal cancer B. Benign oesophageal stricture C. Globus hystericus D. Candidal oesophagitis E. Parkinson’s disease F. Scleroderma G. Diffuse oesophageal spasm H. Eosinophilic oesophagitis I. Upper oesophageal web J. Oesophageal diverticulum K. Stroke L. Achalasia
C. Globus hystericus
Globus hystericus is a sensation of fullness or a lump in the neck or difficulty swallowing which is not a true case of dysphagia. Swallowing can be performed normally and there is no real lump or obstruction in the throat. In some cases the cause is unknown and is believed to be psychogenic in cause and is associated with anxiety disorders. In other cases throat inflammation can cause this sensation. The normal examination and endoscopy here in a patient with a psychiatric history is diagnostic.
An adult male with hypogonadism, small testicles and gynaecomastia is found to be infertile.
What is the diagnosis? A. DiGeorge syndrome B. Down's syndrome C. Edwards syndrome D. Klinefelter's syndrome E. William’s syndrome F. Tuberous sclerosis G. Turner's syndrome H. Fragile X syndrome I. Prader-Willi syndrome J. Patau's syndrome K. Angelman syndrome
D. Klinefelter’s syndrome
Klinefelter’s syndrome is the presence of an extra X chromosome in a male to give 47, XXY. Hypogonadism is a principle feature of this condition and there is reduced fertility. Hypogonadism itself does not mean ‘small testicles’ but XXY men do also have small testicles. They will also often have low testosterone levels but high LH and FSH levels due to primary hypogonadism. The only reliable method of diagnosis is with karyotype analysis and the degree to which XXY males are affected varies from person to person. Gynaecomastia is to some extent present in around a third of individuals affected by this condition. 1 in 10 will choose cosmetic surgery to fix this.
A child with severe learning difficulties, cleft lip & palate, polydactyly and multiple heart defects. Karyotype analysis shows trisomy 18.
What is the diagnosis? A. DiGeorge syndrome B. Down's syndrome C. Edwards syndrome D. Klinefelter's syndrome E. William’s syndrome F. Tuberous sclerosis G. Turner's syndrome H. Fragile X syndrome I. Prader-Willi syndrome J. Patau's syndrome K. Angelman syndrome
C. Edward’s syndrome
Edwards syndrome is trisomy 18 and is phenotypically similar to Patau’s. Most affected are females and most die before birth. The incidence, as with most trisomies, increases with advanced maternal age. The rate of survival is low due to cardiac abnormalities, renal malformations and other visceral disorders. Signs and symptoms include those mentioned and a whole host of other signs of this phenotype such as a small head, small jaw, widely spaced eyes and ptosis. The cardiac defects seen include VSD, ASD and PDA (all the lovely 3 letter acronyms). Classic EMQ signs include webbing of the second and third toes and the Rocker bottom feet characterised by calcaneal prominence and a convex rounded bottom to the foot, which is associated with both trisomy 13 and 18.
A male child is found to have moderate learning difficulties and behavioural problems. There is a family history of learning difficulties. On examination he has large testicles, epicanthic folds and large ears. DNA testing reveals trinucleotide repeat expansion (CGG).
What is the diagnosis? A. DiGeorge syndrome B. Down's syndrome C. Edwards syndrome D. Klinefelter's syndrome E. William’s syndrome F. Tuberous sclerosis G. Turner's syndrome H. Fragile X syndrome I. Prader-Willi syndrome J. Patau's syndrome K. Angelman syndrome
H. Fragile X syndrome
This is fragile X syndrome. History includes learning difficulties, which can range from mild to severe, social communication difficulties (patients may be autistic), hyperactivity and attention deficit and motor co-ordination difficulties. There may be a FH of learning difficulties too. Examination may reveal macrocephaly, low muscle tone, long face, high arched palate, prominent jaw, big testicles (macro-orchidism), large ears and strabismus. DNA testing is diagnostic and reveals a ragile site on Xp27.3 (FRM1 gene position). This is characterised by trinucleotide repeat expansion (CGG) to more than 200 copies.
A child with moderate learning difficulties, round face, small head, slanting eyes and a single palmar crease.
What is the diagnosis? A. DiGeorge syndrome B. Down's syndrome C. Edwards syndrome D. Klinefelter's syndrome E. William’s syndrome F. Tuberous sclerosis G. Turner's syndrome H. Fragile X syndrome I. Prader-Willi syndrome J. Patau's syndrome K. Angelman syndrome
B. Down’s syndrome
This is the one you need to be really aware of. Down’s syndrome is trisomy 21 and the diagnosis is one which is made antenatally or perinatally. You will never have a patient with Down’s who gets diagnosed as a child unless you are in a country which is very deprived of any medical personnel and your patient was born in a rural farm away from civilisation. The patient may have a history of delayed development, congenital cardiac anomalies, epilepsy as a child, atlanto-occipital instability, GI or hearing problems and there may also be associated autism. Examination may display dysmorphism, oblique palpebral fissures, epicanthic folds, low nasal bridge and low set ears, characteristic central iris Brushfield spots, short curved 5th finger, single palmar crease and may also have cardiac murmurs. Karyotype analysis will reveal trisomy 21, robertsonian translocation, or mosaicism.
Adult female with short stature, amenorrhoea, webbed neck and widely spaced nipples. She is found infertile although there is no cognitive impairment.
What is the diagnosis? A. DiGeorge syndrome B. Down's syndrome C. Edwards syndrome D. Klinefelter's syndrome E. William’s syndrome F. Tuberous sclerosis G. Turner's syndrome H. Fragile X syndrome I. Prader-Willi syndrome J. Patau's syndrome K. Angelman syndrome
G. Turner’s syndrome
Turner’s syndrome is characterised on diagnostic karyotype analysis by 45 XO (complete or partial absence of the second sex chromosome occuring in 1 in 2500 liver female births). This may be diagnosed antenatally by amniocentesis, which is an invasive test performed after 15 weeks gestation. The patient will be phenotypically female and may give a history of amenorrhoea, infertility, visual problems and hearing loss. Specific learning difficulties are normal but there is no cognitive impairment and intelligence is normal. Examination may reveal short stature, low-set ears, webbed neck, low hairline and cubitus valgus. Obvious stigmata though such as webbed neck only affects 20-30% of patients.
I wouldn’t worry too much about most of these syndromes. A brief overview of the rest for those who are interested: Prader-Willi is characterised by 15q11-13 deletion and patients can have a short stature, small hands and feet, and dysmorphism. The classic association is with hyperphagia and obesity from 3 years of age. Angelman’s is characterised by 15q11-12 deletion and there is severe general developmental delay and cognitive impairment. William’s is characterised by deletion of 7q11.23 and has classic phenotypic features. DiGeorge classically presents with a triad of cardiac abnormalities, hypoplastic thymus and hypocalcaemia but manifestations are highly variable. Tuberous sclerosis is characterised by seizures in infants and children, variable cognitive impairment and examination may reveal ash leaf patches of hypomelanotic macules. There is either mutation of TS1 or TS2 on DNA analysis.
A 31 year old woman is brought into A&E by her boyfriend who claimed she may have had too many ‘sleeping pills’ after he tried to break up with her. Prior to this she had drank two bottles of wine and consumed three chocolate cakes. She is ataxic with slurred speech with a GCS of 10. Her medical file shows she is taking medication for panic attacks.
What is the cause? A. Alcohol intoxication B. Carbon monoxide C. Anthrax D. Opiate analgesics E. Methanol F. Ecstasy G. Benzodiazepines H. Insulin I. Tricyclic antidepressants J. Ethylene glycol K. Sympathomimetics L. Salicylates M. Volatile solvents
G. Benzodiazepines
This woman here who is clearly distraught after her breakup has overdosed on benzodiazepines. The clue here is given when it says she is taking medication for panic attacks at the moment. BZDs are the most commonly prescribedmedication for anxiety disorders, sedation and sleep. Patients may present like this and may be intentional or accidental in nature, and may be in combination with other CNS depressants such as alcohol and opioids in older people. Occasionally overdose is due to medication error. The key feature of overdose is excessive sedation and anterograde amnesia. Vital signs are unremarkable. Larger doses can lead to coma and respiratory depression. Treatment is symptomatic and may include assisted ventilation and haemodynamic support and death is uncommon and often due to mixed overdoses with other depressants such as alcohol. Flumazenil is a BZD antagonist that can be used in first time or infrequent users to reverse CNS depression but it is contraindicated in those who are long-term of frequent users (like this patient) due to the risk of provoking seizures, which outweights the benefits.
A 29 year old man presents to A&E with agitation, tremor, dilated pupils, tachycardia, arrhythmias, convulsions after ingesting an overdose of an unknown substance.
What is the cause? A. Alcohol intoxication B. Carbon monoxide C. Anthrax D. Opiate analgesics E. Methanol F. Ecstasy G. Benzodiazepines H. Insulin I. Tricyclic antidepressants J. Ethylene glycol K. Sympathomimetics L. Salicylates M. Volatile solvents
K. Sympathomimetics
The symptoms described here are those of sympathetic activation and the overdose here is of sympathomimetics. This group of drugs mimic the effects of transmitter substances of the sympathetic nervous system such as adrenaline, dopamine and noradrenaline.
A 23 year old man who has taken an overdose of an unknown drug after getting dumped by his pregnant girlfriend (he is not the father) was admitted to A&E. He is slightly tachycardic, complains of tinnitus and has high blood pressure at first but 30 minutes later, starts seizing and is intubated. There is a wide anion-gap metabolic acidosis.
What is the cause? A. Alcohol intoxication B. Carbon monoxide C. Anthrax D. Opiate analgesics E. Methanol F. Ecstasy G. Benzodiazepines H. Insulin I. Tricyclic antidepressants J. Ethylene glycol K. Sympathomimetics L. Salicylates M. Volatile solvents
L. Salicylates
This is salicylate overdose which is potentially fatal and can present either acutely or indolently with more chronic exposure. It is a relatively common overdose so really with anyone presenting with an unknown overdose it should be considered along with paracetamol. The unexplained acid-base disturbance should make you suspicious of this diagnosis. Tinnitis is common in the early stages of acute salicylate poisoning and reflects CNS toxicity. There may also be deafness and both are reversible. Seizures are common especially in patients with salicylate levels >80mg/dL. An ABG is also indicated in this patient which during the course of salicylate poisoning would initiually show a respiratory alkalosis and later a concomitant metabolic acidosis, potentially with a wide anion gap. GIT decontamination should be considered as an adjunct on arrival to A&E and activated charcoal can be given. The mainstay of treatment is alkaline diuresis induced by an infusion of sodium bicarbonate. In cases of severe poisoning, it is still started as a bridge to haemodialysis.
Inebriation, coma, reduced reflexes, tachycardia, pulmonary oedema, shock, metabolic acidosis.
What is the cause? A. Alcohol intoxication B. Carbon monoxide C. Anthrax D. Opiate analgesics E. Methanol F. Ecstasy G. Benzodiazepines H. Insulin I. Tricyclic antidepressants J. Ethylene glycol K. Sympathomimetics L. Salicylates M. Volatile solvents
B. Carbon monoxide
This man who works in a petrol refinery is suffering from carbon monoxide poisoning and his co-worker who has found him lying on the ground is starting to suffer from similar symptoms due also to CO exposure. CO is a colourless and odourless gas so patients may not initially be aware of the poisoning which can cause hypoxia, cell damage and death (in approximately 1/3). CO can come from fire or non-fire sources and early symptoms are non-specific and include the symptoms seen here: headache, dizziness and nausea. Increasing exposure leads to cardiovascular effects like myocardial ischaemia, infarction and possible arrest. Neurological symptoms include the confusion seen here and may lead eventually to coma and syncope. Diagnosis is based on carboxyhaemoglobin levels and the clinical picture here is very suggestive. It is worth noting that in severe CO poisoning, pulse oximetry readings may be falsely raised. Key in treatment is the use of high-flow oxygen, hyperbaric oxygen and supportive care. Hyperbaric treatment entails complications such as barotrauma, oxygen toxicity and pulmonary oedema.
A pregnant 17 year old woman who has been recently abandoned by her boyfriend is brought into hospital with altered mental status by her mother, who reported that she had a brief seizure beforehand. She is tachycardic with low BP and appears flushed. She responds to pain only and her skin feels warm and dry. Pupils are poorly reactive to light and dilated. What is the cause? A. Alcohol intoxication B. Carbon monoxide C. Anthrax D. Opiate analgesics E. Methanol F. Ecstasy G. Benzodiazepines H. Insulin I. Tricyclic antidepressants J. Ethylene glycol K. Sympathomimetics L. Salicylates M. Volatile solvents
I. Tricyclic antidepressants
This is an overdose of tricyclic antidepressants which are a class of drugs with a narrow therapeutic index and therefore become potent toxins in moderate doses to both the CNS and cardiovascular system. This patient has reason to be depressed and is therefore on these pills. There is a sudden deterioration of mental status here and the diagnosis here is clinical. The main aim in treatment is to provide respiratory and cardiovascular support until the medicine has been fully metabolised and eliminated. The warm, dry and flushed skin is part of the anticholinergic effects (physostigmine should NOT be used to reverse this as it has been in rare cases been associated with asystole – would you rather have a patient who is flushed or flatlined?). Other anticholinergic effects include dilated pupils, urinary retention, decreased or absent bowel sounds and changes in mental status. Hypotension is common and is due to alpha 1 antagonism. Classic ECG changes are of sinus tachycardia progressing to wide complex tachycardia and ventricular arrhythmias (with increasing severity and intoxication). Condution problems and hypotension is improved with hypertonic sodium bicarbonate and if arrhythmias are present, treatment of these involves correcting the acidosis, hypoxia and electrolyte abnormalities. Anti-arrhythmics are generally avoided. If hypotension is refractory then a vasopressor can be used. BZDs can be used for any seizures.
A 66 year old woman admitted with diarrhoea and weight loss. O/E she has a fine tremor and has rapid atrial fibrillation. FBC, ESR and CRP are normal.
What is the diagnosis? A. Clostridium difficile B. Amoebic dysentery C. Crohn's disease D. Ulcerative colitis E. Malabsorption F. Thyrotoxicosis G. Cancer of the colon H. Cancer of the rectum I. Bacterial gastroenteritis J. Diverticular disease K. Drug induced L. Irritable bowel syndrome
F. Thyrotoxicosis
This woman has symptoms and signs of hyperthyroidism (diarrhoea, weight loss, AF and a fine tremor). In countries where sufficient iodine intake is not an issue, Graves’ disease is the most common cause of hyperthyroidism. Peripheral manifestations such as ophthalmopathy, pretibial myxoedema and hyperthyroid acropachy do not occur with other causes of hyperthyroidism. Acropachy manifests as clubbing with soft tissue swelling. Pretibial myxoedema is almost always associated with ophthalmopathy. Treatment aims to normalise thyroid function and is achieved by radioactive iodine, antithyroid medications or with surgery. They are all effective and relatively safe options. Symptomatic therapy is given with beta blockers such as propranolol.
A 30 year old city banker comes to the GP with symptoms of abdominal bloating, intermittent constipation and diarrhoea with occasional nausea. This started about 6 months ago but she has not lost any weight or found any blood in her stools.
What is the diagnosis? A. Clostridium difficile B. Amoebic dysentery C. Crohn's disease D. Ulcerative colitis E. Malabsorption F. Thyrotoxicosis G. Cancer of the colon H. Cancer of the rectum I. Bacterial gastroenteritis J. Diverticular disease K. Drug induced L. Irritable bowel syndrome
L. Irritable bowel syndrome
The intermittent diarrhoea and constipation, with bloating, without symptoms suggestive of IBD make IBS a more likely diagnosis. IBS is a chronic condition with abdominal pain associated with bowel dysfunction and is a diagnosis of exclusion. The pain or discomfort may be relieved by defecation. Examination is usually unremarkable and the diagnosis is based on the patient’s history in line with the Rome Criteria. If the patient presents with any worrying symptoms, then these will warrant a more thorough investigation. Treatment depends on the patient’s predominant symptoms. Antispasmodics relieve abdominal pain or discomfort but do not affect bowel habit. Examples include peppermint oil and dicycloverine. Laxatives can also be used such as lactulose. Lifestyle and dietary modifications combined with reassurance remain the 1st line intervention for functional bowel disease. IBS is linked with stressful jobs such as working as a banker in the city and there is a female/male ratio of 2:1.
An 18 year old student attends A&E at 2am with acute onset of vomiting, diarrhoea and abdominal cramps. There is some blood in the stool and he has a high fever. He hasn’t been abroad recently. His FBC had a normal Hb but raised neutrophils.
What is the diagnosis? A. Clostridium difficile B. Amoebic dysentery C. Crohn's disease D. Ulcerative colitis E. Malabsorption F. Thyrotoxicosis G. Cancer of the colon H. Cancer of the rectum I. Bacterial gastroenteritis J. Diverticular disease K. Drug induced L. Irritable bowel syndrome
I. Bacterial gastroenteritis
This acute presentation in a previous fit and healthy individual and the raised neutrophils on FBCand a fever indicate an infective cause for his GI symptoms. It is self-limiting and diagnosis is on isolating the organism from a stool culture (if needed). Blood in the stool allows you to narrow down the list of potential causative organisms. Treatment is supportive with fluid and electrolyte replacement and antibiotics are generally used only for patients with risk factors for severe disease or those with extra-GI complications. It is worth noting that viral gastroenteritis often presents with mainly UGI symptoms like N&V more so than diarrhoea.
A 76 year old woman admitted with a chest infection develops non-bloody diarrhoea on the ward. She was on cefuroxime and erythromycin for her chest. She appears unwell and there is a fever. CRP is elevated.
What is the diagnosis? A. Clostridium difficile B. Amoebic dysentery C. Crohn's disease D. Ulcerative colitis E. Malabsorption F. Thyrotoxicosis G. Cancer of the colon H. Cancer of the rectum I. Bacterial gastroenteritis J. Diverticular disease K. Drug induced L. Irritable bowel syndrome
A. Clostridium difficile
This is infection with clostridium difficile with the major risk factor here of antibiotic exposure due to the recent chest infection. The most common ones implicated are ampicillin, second and third generation cephalosporins, clindamycin and fluoroquinolones, especially if used in the preceding 3 months (though most manifestations occur on days 4 through to 9 of antibiotic therapy). Diarrhoea may range from a few loose stools to severe diarrhoea, though absence could be related to toxic megacolon to paralytic ileus. Abdominal pain is also common as is fever. C. difficile produces 2 exotoxins which are responsible for its pathogenicity. These are called toxin A and toxin B (A is thought to be more important than B) which lead to an inflammatory response in the large bowel, increased vascular permeability and the formation of pseudomembranes. Colonic pseudomembranes look like raised yellow and white plaques against an inflamed mucosa and are composed of neutrophils, fibrin, mucin and cellular debris. The diagnostic standard is with cytotoxic tissue culture assay. Treatment involves discontinuing the implicated antibiotic and beginning oral metronidazole or vancomycin. 5-20% will have a recurrence on discontinuing treatment and will need a second course.
A 30 year old female presents with a 3 month history of bloody diarrhoea and vague lower abdominal cramps. She gave up smoking a few months ago. The doctor feels that this could have contributed to her condition.
What is the diagnosis? A. Clostridium difficile B. Amoebic dysentery C. Crohn's disease D. Ulcerative colitis E. Malabsorption F. Thyrotoxicosis G. Cancer of the colon H. Cancer of the rectum I. Bacterial gastroenteritis J. Diverticular disease K. Drug induced L. Irritable bowel syndrome
D. Ulcerative colitis
While this could be Crohn’s disease, bloody diarrhoea is more commonly a presentation of UC than Crohn’s. UC is characterised by diffuse mucosal inflammation running a relapsing and remitting course. Bloody diarrhoea is commonly experienced by patients who may also complain of other symptoms such as (lower) abdominal pain, faecal urgency and the host of extra-intestinal manifestations associated with UC. These include erythema nodosum, pyoderma gangrenosum, sacroiliitis, ankylosing spondylitis, PSC, aphthous ulcers, episcleritis, peripheral arthropathy and anterior uveitis. Another clue in this question which makes you pick UC instead of Crohn’s is the fact the patient has given up smoking. While I remain convinced this link as a risk factor is a weak one, you should try to think like an EMQ when answering EMQs (generally the information is there for a reason). There is a weak risk of UC development in non-smokers and those who were a former smoker (though it is an established link). This is based on a review paper published by some German medics in an exciting journal named ‘Inflammatory Bowel Diseases’. Should be you interested you can check it out: Inflammatory Bowel Diseases. 10(6):848-859, November 2004 (just read the abstract if you want)
Diagnosis of UC requires endoscopy with biopsy and a negative stool culture to rule out infectious gastroenteritis. Flare ups are usually linked to pathogens so a stool culture will always be needed in these cases. Toxic megacolon is a complication which is associated with a risk of perforation. UC is also linked with bowel adenocarinoma and PSC. Treatment involves mesalazine (5-ASA) used to induce and maintain remission.
An 18 year old girl has felt unwell with myalgia and general malaise for a week develops sharp chest pains which are worse when she lies flat. The pain is constant and unrelated to exertion. There have also been fevers.
What is the diagnosis? A. Atrial septal defect B. Dilated cardiomyopathy C. Infective endocarditits D. Mitral regurgitation E. Mitral stenosis F. Pulmonary fibrosis G. Pericarditis H. Conduction system disease I. Pericardial effusion J. Aortic valve disease K. Tuberculosis L. Hypertensive cardiomyopathy
G. Pericarditis
This patient has presented with pericarditis – most likely viral following a viral infection (as suggested by the prodrome and fever). Symptoms include a sharp and severe chest pain retrosternally which is worse on inspiration and when supine, relieved by sitting forwards. The classical finding on examination is a friction rub which is said to sound like ‘walking on snow’ – a monophasic, biphasic or triphasic friction rib is pathognomic with close to 100% specificity. There may be diffuse ST elevations on ECG, an effusion on echocardiography and blood results suggesting inflammation. Complications include tamponade and constrictive pericarditis. Prior viral infection is a risk factor with the most common pericardial infection being viral. Bacterial purulent pericarditis also occurs. The inflammation is due either to direct viral attack or immune mediated damage. Other risk factors include male gender, post-MI (both ‘early’ and Dressler’s), post-pericardiotomy syndrome, neoplasm from local tumour invasion, uraemia and autoimmune conditions such as RA and SLE.
During the month following his acute MI, a 56 year old man has become progressively more breathless. O/E he has a loud pan-systolic murmur
What is the diagnosis? A. Atrial septal defect B. Dilated cardiomyopathy C. Infective endocarditits D. Mitral regurgitation E. Mitral stenosis F. Pulmonary fibrosis G. Pericarditis H. Conduction system disease I. Pericardial effusion J. Aortic valve disease K. Tuberculosis L. Hypertensive cardiomyopathy
D. MR can occur as a complication of MI which may cause structural damage to the mitral valve apparatus. MR is loudest at the apex and radiates to the axilla and tends to be around grade 4. It is associated with a systolic thrill at the apex. TTE is the investigation of choice for diagnosis. Chronic MR is associated with a laterally displaced apex beat with LV dilatation. This case of acute MR in the setting of an acute MI is very serious can lead to high LA pressure and pulmonary oedema secondary to reduced LA compliance. Occasionally no murmur is heard. Note that while a VSD also gives a pansystolic murmur, which is generally easily heard, and is loudest at the left parasternal region, with no axillary radiation.
A 24 year old Asian male chef is referred by his GP after a 2 month history of cough, fever, night sweats and weight loss. The GP has prescribed anti-biotics with no improvement. He is admitted with SOB and haemoptysis. His CXR shows a normal heart size.
What is the diagnosis? A. Atrial septal defect B. Dilated cardiomyopathy C. Infective endocarditits D. Mitral regurgitation E. Mitral stenosis F. Pulmonary fibrosis G. Pericarditis H. Conduction system disease I. Pericardial effusion J. Aortic valve disease K. Tuberculosis L. Hypertensive cardiomyopathy
K. Tuberculosis
It is important to have a high level of suspicion when evaluating patients with risk factors who present with suggestive symptoms. Night sweats, fever, weight loss, malaise, cough, haemoptysis and erythema nodosum are all suggestive. In the first half of the 20th century, tuberculosis accounted for over 90% of cases of erythema nodosum. Other key risk factors for pulmonary TB include exposure to infection and returning from or being born in a high-risk region such as Asia, Africa and Latin America (highly possible in this case). If TB is suspected, the patient should be placed in isolation and a CXR obtained with 3 sputum samples cultured for AFB being the gold standard of diagnosis. Culture takes several weeks so sputum smears will be done before culture results are known. Interferon-gamma release assays (IGRAs) are now used by some hospitals to rapidly determine a patient’s TB status. All patients who have TB should be tested for HIV within 2 months of diagnosis. Specific anti-TB medication is required, not standard antibiotics for community-acquired pneumonia.
The CXR in pulmonary TB is almost always abnormal in patients who are not immunocompromised. Patients with, for instance, advanced HIV, may have a normal CXR. Primary disease common presents as middle and lower zone infiltrates and ipsilateral adenopathy, atelectasis from airway compression and pleural effusion can be seen. Post-primary classically involves apical changes, spreading to other lobes/segments as the disease progresses. The CXR may be normal in normal individuals but it is rare and it is likely only part of this patient’s CXR is reported here so as not to completely give the game away in this EMQ. Or whoever was interpreted it should not have been allowed to pass finals, which is also possible.
A 42 year old alcoholic is admitted with SOB. He has no murmurs but the apex is laterally displaced and there are crackles at the lung bases with raised JVP. There is also hepatomegaly, clubbing and multiple spider naevi.
What is the diagnosis? A. Atrial septal defect B. Dilated cardiomyopathy C. Infective endocarditits D. Mitral regurgitation E. Mitral stenosis F. Pulmonary fibrosis G. Pericarditis H. Conduction system disease I. Pericardial effusion J. Aortic valve disease K. Tuberculosis L. Hypertensive cardiomyopathy
B. Dilated cardiomyopathy
It is worth noting that ventricular hypertrophy due to hypertension causes concentric hypertrophy i.e. the wall of the ventricle gets thicker inwards. Hence the apex beat is not displaced unlike in DCM. DCM is characterised by LV dilation and systolic dysfunction without significant coronary artery disease or abnormal loading conditions. RV dilation is often also present. 25-35% are familial (there may be FH of sudden death). Causes are extensive and include post-myocarditis, alcohol, chemotherapy agents, haemochromatosis, AI conditions and acromegaly. This case is alcohol related DCM with a history of alcohol excess, signs of chronic liver disease on examination and signs of systolic dusfunction on examination (crackles at lung bases, JVP distension and there may also be peripheral oedema). ECG may show non-specific ST-T changes, CXR can show an enlarged cardiac shadow and echo also give consistent results (wall thickness, LV dilation). LFTs, serum albumin and clotting profile may all be abnormal here too, and GGT would especially be expected to be elevated due to alcohol abuse.
A 55 year old man with known carcinoma of the lungs, develops SOB over a few days. He has a large cardiac silhouette on his CXR but no pulmonary oedema.
What is the diagnosis? A. Atrial septal defect B. Dilated cardiomyopathy C. Infective endocarditits D. Mitral regurgitation E. Mitral stenosis F. Pulmonary fibrosis G. Pericarditis H. Conduction system disease I. Pericardial effusion J. Aortic valve disease K. Tuberculosis L. Hypertensive cardiomyopathy
I. Pericardial effusion
This is a malignant effusion (one of the most likely to lead to tamponade) caused by lung cancer. Other prevalent malignant causes include breats cancer, lymphomas and leukaemias. This may also be the first sign of metastatic disease. The history of lung cancer here should make you suspicious. Other causes of a pericardial effusion include hypothyroidism (high protein content and accumulate very slowly due to capillary leak), cardiac causes such as CHF and dissection of the proximal aorta, trauma, radiation-related, uraemia, immune-mediated such as SLE, Dressler’s, amyloidosis and Wegener’s, infectious or idiopathic (which is generally assumed to be viral). Symptoms may coexist with those of pericarditis sometimes. ECG and CXR are indicated here. Most patients also get an echocardiogram whic is the preferred test to establish the diagnosis. On ECG there may be diffuse ST elevation and PR depression with epicardial inflammation. If the effusion is large enough there may be electrical alternans, which is beat-to-beat variation of the ventricular axis (find an image of this to cement it in your memory). The cardiac shadow on CXR is said to be ‘water-bottle shaped’. Pericardiocentesis may be necessary depending on the clinical case.
A 40 year old female who had been taking ibuprofen for pain relief when she gets headaches, presents to A&E with a history of weight loss and melaena with pain in her epigastric region. The pain gets worse with eating.
What is the diagnosis? A. Meckel's diverticulum B. Duodenal ulcer C. Ulcerative colitis D. Oesophageal varices E. Oesophageal malignancy F. Mallory-Weiss tear G. Gastric ulcer H. Crohn's disease I. Oesophagitis
G. Gastric ulcer
The patient has a bleeding peptic ulcer (the black tarry stools from the UGI bleed). Epigastric pain and tenderness related to eating a meal is typical of a peptic ulcer. 80% are duodenal and 20% are gastric. Ulcers may cause iron deficiency anaemia and associated symptoms may feature. Key risk factors are NSAID use, like in this patient, H. pylori infection, smoking and a family history of PUD. Zollinger-Ellison syndrome should be considered if there are multiple ulcers or ulcers refractory to treatment.
Gastric ulcers classically cause pain which is exacerbated by eating and immediately relieved on vomiting. There is usually also weight loss due to a fear of food and its association with pain. Duodenal ulcers are classically made worse by hunger and are relieved by eating and the patient may wake at night with the pain. As a result, weight gain is typically a feature. In reality, it is difficult to differentiate the site of the ulcer based on these features.
The most specific and sensitive test is an upper GI endoscopy which is initially ordered if the patient has ‘red flag’ symptoms, is >55 years of age or fails to respond to treatment. Duodenal ulcers rarely undergo malignant transformation so do not require a compulsory biopsy but gastric ulcers require biopsies to rule this out. In patients who are 55 or younger without ‘red flags’, testing for Helicobacter pylori (breath testing with radiolabelled urea or stool antigen testing) is necessary. Management is aimed at correcting the underlying cause such as discontinuing NSAIDs. H. pylori eradication should be started if the organism is present with triple therapy. Otherwise, a PPI is indicated.
A 25 year old Jewish man presents to A&E with some abdominal discomfort, weight loss with associated loss of appetite. His history revealed loose and bloody stools. Examination reveals tenderness in the RLQ. He is booked in for endoscopy.
What is the diagnosis? A. Meckel's diverticulum B. Duodenal ulcer C. Ulcerative colitis D. Oesophageal varices E. Oesophageal malignancy F. Mallory-Weiss tear G. Gastric ulcer H. Crohn's disease I. Oesophagitis
H. Crohn’s disease
This patient gives a history of IBD. This could well be UC where the mainstay of treatment is with 5-ASA. A colonoscopy is required to assess the extent of disease and for a definitive diagnosis. Biopsy in CD will show transmural granulomatous inflammation. CD can affect the whole GIT but favours the TI (RLQ pain) and proximal colon and is macroscopically characterised by skip lesions. UC on the other hand is characterised by the presence of crypt abscesses, which is pathognomic. CD risk is increased 3-4 fold by smoking whereas smoking seems protective in UC. The mainstay of treatment in CD is with steroids and azathioprine to revent relapses and for those suffering side effects of steroid treatment. TNF-alpha inhibitors also have a role. Surgery in CD is only indicated in a small number of patients who bleed, for bowel perforation and cases of complete obstruction. The aim is to rest distal disease by temporarily diverting faecal flow.
A 36 year old gentleman presents with a 36 hour history of diarrhoea and vomiting following a takeaway meal the night before. In the last few hours he has increasing amounts of bright red blood in his vomit.
What is the diagnosis? A. Meckel's diverticulum B. Duodenal ulcer C. Ulcerative colitis D. Oesophageal varices E. Oesophageal malignancy F. Mallory-Weiss tear G. Gastric ulcer H. Crohn's disease I. Oesophagitis
F. Mallory-Weiss tear
This occurs after a rise in abdominal pressure which induces a tear in the oesophageal mucosa, causing subsequent GI bleeding. It commonly presents with haematemesis after an episode of retching/vomiting/coughing/straining. Hence, risk factors include anything which can cause vomiting like heavy alcohol use, which is commonly the case in EMQs. Also, other conditions would include food poisoning like in this case, bowel obstruction, hyperemesis gravidarum, bulimia, the chronic cough of COPD, meningitis etc… you name it really. Classically, MWT presents with a small self limiting episode of haematemesis. Definitive diagnosis is made by OGD. Treatment is supportive because most cases are self limiting and emergency treatment is not offered unless the patient is showing signs of clinical instability. If the patient is actively bleeding, treatment will be with therapeutic endoscopy in most cases, and very very few cases will require more intervention such as angiography with embolisation.
An 80 year old man presents with a 6 month history of increasing weakness and 8kg weight loss. He also has some vague abdominal pain and a few episodes of black stools. He is a long term smoker.
What is the diagnosis? A. Meckel's diverticulum B. Duodenal ulcer C. Ulcerative colitis D. Oesophageal varices E. Oesophageal malignancy F. Mallory-Weiss tear G. Gastric ulcer H. Crohn's disease I. Oesophagitis
E. Oesophageal malignancy
Such levels of extreme weight loss over a short period of time with GI symptoms here points to GI malignancy which is bleeding. The only option on the list is oesophageal. EMQs normally mention dysphagia, which occurs when there is obstruction of more than 2/3 of the lumen and presence indicates locally advanced disease however this is absent here. There may additionally be odynophagia. Men are twice as likely to develop oesophageal cancer. GORD, Barrett’s oesophagus, FH, tobacco and alcohol are all risk factors. The two main types are squamous cell carcinoma and adenocarcinoma. Tumours in the upper 2/3 of the oesophagus are SCC whereas those that lie in the lower 1/3 are adenocarcinomas. The main test to order is an OGD with biopsy. Treatment is either surgical resection or with chemo or radiotherapy alongside endoscopic ablation with or without stenting and brachytherapy.
A 38 year old man presents with a 2 month history of intermitted pain in the upper abdomen which he describes as dull in nature. It sometimes wakes him up at night and is relieved by food and particularly when he has a glass of milk. He has had a similar episode before where he remembers the doctor prescribed him some pills, which helped. Examination reveals mild epigastric tenderness.
What is the diagnosis? A. Meckel's diverticulum B. Duodenal ulcer C. Ulcerative colitis D. Oesophageal varices E. Oesophageal malignancy F. Mallory-Weiss tear G. Gastric ulcer H. Crohn's disease I. Oesophagitis
B. Duodenal ulcer
The patient has a duodenal ulcer. Epigastric pain and tenderness related to eating a meal is typical of a peptic ulcer. 80% are duodenal and 20% are gastric. Ulcers may cause iron deficiency anaemia and associated symptoms may feature. Key risk factors are NSAID use, like in this patient, H. pylori infection, smoking and a family history of PUD. Zollinger-Ellison syndrome should be considered if there are multiple ulcers or ulcers refractory to treatment.
Gastric ulcers classically cause pain which is exacerbated by eating and immediately relieved on vomiting. There is usually also weight loss due to a fear of food and its association with pain. Duodenal ulcers are classically made worse by hunger and are relieved by eating and the patient may wake at night with the pain. As a result, weight gain is typically a feature. In reality, it is difficult to differentiate the site of the ulcer based on these features.
The most specific and sensitive test is an upper GI endoscopy which is initially ordered if the patient has ‘red flag’ symptoms, is >55 years of age or fails to respond to treatment. Duodenal ulcers rarely undergo malignant transformation so do not require a compulsory biopsy but gastric ulcers require biopsies to rule this out. In patients who are 55 or younger without ‘red flags’, testing for Helicobacter pylori (breath testing with radiolabelled urea or stool antigen testing) is necessary. Management is aimed at correcting the underlying cause such as discontinuing NSAIDs. H. pylori eradication should be started if the organism is present with triple therapy. Otherwise, a PPI is indicated.
A 30 year old Afro-Caribbean patient comes to A&E complaining of coughing up blood and a rash on his cheeks, nose and shins. The CXR shows hilar lymphadenopathy bilaterally.
What is the diagnosis? A. Tuberculosis B. Bronchiectasis C. Bronchial carcinoma D. Primary pulmonary hypertension E. Pulmonary embolus F. Streptococcus pneumoniae G. Trauma H. Left ventricular failure I. Mycoplasma pneumoniae J. Idiopathic pulmonary fibrosis K. Sarcoidosis L. COPD
K. Sarcoidosis
Sarcoidosis is a chronic multisystem disease with an unknown aetiology but pulmonary involvement usually dominates. Hypercalcaemia occurs in these granulomatous conditions (also including TB and leprosy) as a result of tissue being able to 1-alpha-hydroxylate 25(OH) D leading to vitamin D (the 1,25-dihydroxyvitamin D3) excess. Erythema nodosum, tender erythematous nodules and lupus pernio, indurated plaques with discoloration on the face, are typical skin manifestations of sarcoidosis which this patient has. CXR will typically show bilateral hilar lymphadenopathy and CXR findings are used in the staging of disease. Additionally, serum calcium and ACE levels may be raised. A transbronchial biopsy is essential for diagnosis in most cases and shows the presence of non-caseating granulomas. Black people have a higher lifetime risk of sarcoidosis, as do those of Scandinavian origin. The mainstay of treatment for severe disease involves systemic corticosteroids.
A 49 year old lady presents to A&E with severe haemoptysis. She has a history of continuous production of foul-smelling khaki-coloured sputum. She had whooping cough as a child.
What is the diagnosis? A. Tuberculosis B. Bronchiectasis C. Bronchial carcinoma D. Primary pulmonary hypertension E. Pulmonary embolus F. Streptococcus pneumoniae G. Trauma H. Left ventricular failure I. Mycoplasma pneumoniae J. Idiopathic pulmonary fibrosis K. Sarcoidosis L. COPD
B. Bronchiecstasis
Bronchiectasis is permanent bronchi dilatation due to bronchial wall damage and loss of elasticity. It is often as a consequence of recurrent/severe infections (whooping cough in this case caused by Bordetella pertussis) and most present with chronic productive mucopurulent cough. The most common identifiable cause is CF. Many patients will have crackles on auscultation of the lungs and high-pitched inspiratory squeaks and pops are also commonly heard. SOB is present in the majority of patients, especially with exertion (and is a good correlate of the severity on CT) and more than half will have recurrent episodes of fever, which is also a sign of an acute exacerbation. Daily sputum production is present in two thirds of patients and bloody sputum in half. The most common identifiable cause is CF and clubbing is a sign of bronchiectasis. Chest CT is the diagnostic test. Diagnosis is aided by sputum analysis.
A 45 year old male from India, presents with a 3 week history of tiredness, loss of weight and haemoptysis. His left lung base is stony-dull to percussion.
What is the diagnosis? A. Tuberculosis B. Bronchiectasis C. Bronchial carcinoma D. Primary pulmonary hypertension E. Pulmonary embolus F. Streptococcus pneumoniae G. Trauma H. Left ventricular failure I. Mycoplasma pneumoniae J. Idiopathic pulmonary fibrosis K. Sarcoidosis L. COPD
A. Tuberculosis
It is important to have a high level of suspicion when evaluating patients with risk factors who present with suggestive symptoms. Night sweats, fever, weight loss, malaise, cough, haemoptysis and erythema nodosum are all suggestive. In the first half of the 20th century, tuberculosis accounted for over 90% of cases of erythema nodosum. Other key risk factors for pulmonary TB include exposure to infection and returning from or being born in a high-risk region such as Asia, Africa and Latin America (India in this case). The examination findings here are consistent with a parapneumonic effusion. If TB is suspected, the patient should be placed in isolation and a CXR obtained with 3 sputum samples cultured for AFB being the gold standard of diagnosis. Culture takes several weeks so sputum smears will be done before culture results are known. Interferon-gamma release assays (IGRAs) are now used by some hospitals to rapidly determine a patient’s TB status. All patients who have TB should be tested for HIV within 2 months of diagnosis.
A 60 year old patient presents with SOB and haemoptysis. O/E the patient is tachycardic, tachypnoeic with swollen ankles and bilateral basal crepitations
What is the diagnosis? A. Tuberculosis B. Bronchiectasis C. Bronchial carcinoma D. Primary pulmonary hypertension E. Pulmonary embolus F. Streptococcus pneumoniae G. Trauma H. Left ventricular failure I. Mycoplasma pneumoniae J. Idiopathic pulmonary fibrosis K. Sarcoidosis L. COPD
H. Left ventricular failure
LVF causes congestion in the pulmonary circulation so the symptoms are respiratory with evidence here of pulmonary oedema. As seen in this patient, there is SOB and there may also be orthopnoea. This is why you can ask patients in a cardiac history how many pillows they sleep with. PND can also occur as well as ‘cardiac asthma’. RVF leads to a backlog of blood and congestion of the systemic capillaries. This causes peripheral oedema and ascites and hepatomegaly may develop. Nocturia may be a symptom as fluid returns from the legs when the patient lies down flat. This patient does have peripheral oedema too so technically has CCF (congestive cardiac failure), but the best option on the list is LVF.
A 69 year old lady presents with a sudden onset of fever and coughing up a purulent, rusty coloured sputum. Examination of her chest showed signs of consolidation.
What is the diagnosis? A. Tuberculosis B. Bronchiectasis C. Bronchial carcinoma D. Primary pulmonary hypertension E. Pulmonary embolus F. Streptococcus pneumoniae G. Trauma H. Left ventricular failure I. Mycoplasma pneumoniae J. Idiopathic pulmonary fibrosis K. Sarcoidosis L. COPD
F. Streptococcus pneumoniae
The rusty coloured sputum is hinting at a pneumococcal pneumonia.The patient has presented with common symptoms of fever and a productive cough. Examination findings are also consistent – have a think about what would actually be found while performing a respiratory examination on this patient. There may also be SOB, chills, rigors and pleuritic chest pain. The most specific and sensitive test is a CXR (PA and lateral) and initial treatment of a CAP is empirical with antibiotics. Often diagnosis is made solely on history and examination findings. Management is guided by the patient’s CURB-65 score.
A 21 year old male has a 3 day history of hoarseness. He has pain in his throat which is worse on talking and eating. O/E his throat appears normal.
What is the diagnosis? A. Laryngitis B. Acromegaly C. Vocal cord nodules D. Sjogren's syndrome E. Hypothyroidism F. Wegener's syndrome G. Carcinoma of the larynx H. Angioedema I. Laryngeal nerve palsy J. Foreign body
A. Laryngitis
Laryngitis, as the name would suggest, is inflammation of the larynx, which can lead to oedema of the true vocal folds. It has both infectious and noninfectious causes such as vocal strain. Symptoms of acute disease are most commonly hoarseness, generally over a period of less than a week, usually preceded by viral URTI and usually self limiting. The pain on swallowing and sore throat is common of URTIs. An exudate or cervical lymphadenitis would suggest bacterial infection instead. Treatment begins, as always, with ABC and airway assessment. Chronic laryngitis presents with hoarseness lasting more than 3 weeks and this needs investigating due to the fact that symptoms may be similar to cancer of larynx. Antibiotics are given in bacterial cases or otherwise voice rest and hydration is sufficient.
A 25 year old man suddenly developed hoarseness, wheeze and stridor whilst eating peanuts in a bar. Looking in his mouth you notice a swollen tongue.
What is the diagnosis? A. Laryngitis B. Acromegaly C. Vocal cord nodules D. Sjogren's syndrome E. Hypothyroidism F. Wegener's syndrome G. Carcinoma of the larynx H. Angioedema I. Laryngeal nerve palsy J. Foreign body
H. Angioedema
Angio-oedema is swelling involving the deeper layers of the subdermis (occuring in association with urticaria in around 40% of cases). In this case it involves the face/neck and is dangerous – the risk being airway compromise and this requires rapid treatment with adrenaline. The food trigger here is obvious – this person has just consumed peanuts and this is allergic in nature, causing an IgE mediated reaction. Common triggers aside from nuts include eggs and shellfish although any food can be implicated. As mentioned, airway management and adrenaline is crucial here and you would also give antihistamines, IV corticosteroids and tell the patient to avoid the trigger.
A 55 year old woman develops hoarseness 2 days after a partial thyroidectomy for thyrotoxicosis.
What is the diagnosis? A. Laryngitis B. Acromegaly C. Vocal cord nodules D. Sjogren's syndrome E. Hypothyroidism F. Wegener's syndrome G. Carcinoma of the larynx H. Angioedema I. Laryngeal nerve palsy J. Foreign body
I. Laryngeal nerve palsy
This patient has just had neck surgery and the hoarseness here results from damage to the recurrent laryngeal nerve, which is a branch of the vagus nerve which supplies motor function and sensation to the larynx. This nerve runs posterior to the thyroid and results in hoarseness when damaged. Bilateral damage is even worse and the patient could have difficulty breathing and the complete inability to speak. The right recurrent laryngeal is more prone to damage as it is located relatively more medial than the left.
A 58 year old male smoker has a 2 month history of progressive persistent hoarseness and pain in his left ear on swallowing. He has enlarged left cervical lymph nodes.
What is the diagnosis? A. Laryngitis B. Acromegaly C. Vocal cord nodules D. Sjogren's syndrome E. Hypothyroidism F. Wegener's syndrome G. Carcinoma of the larynx H. Angioedema I. Laryngeal nerve palsy J. Foreign body
G. Carcinoma of the larynx
Laryngeal cancer is frequently associated with two big risk factors: smoking and alcohol use. Major signs are persistent (>3 weeks) of hoarseness, dysphonia, sore throat, dysphagia, referred otalgia (seen here) and neck masses/adenopathy. These patients need to be evaluated by a specialist and as mentioned this can resemble chronic laryngitis in presentation. An MDT approach is taken to try and preserve the organ as much as possible, with salvage surgical resection offered in advanced disease.
A 40 year old woman develops a progressively hoarse voice over 6 months. She has also gained 8kg in weight and complains of constipation.
What is the diagnosis? A. Laryngitis B. Acromegaly C. Vocal cord nodules D. Sjogren's syndrome E. Hypothyroidism F. Wegener's syndrome G. Carcinoma of the larynx H. Angioedema I. Laryngeal nerve palsy J. Foreign body
E. Hypothyroidism
This woman is in a hypothyroid state. The hoarseness may be a symptom of a goitre (enlarged thyroid). Worldwide, the most common cause is iodine deficiency. Other causes include Hashimoto’s or secondary and tertiary hypothyroidism. It can also result from viral de Quervain’s thyroiditis or postpartum thyroiditis. Symptoms include those mentioned as well as depression, bradycardia, sluggish reflexes, cold intolerance and muscle cramps. Diagnosis is based on measurement of TSH and thyroid hormones. Treatment is by replacement of T4 with or without T3 in combination. If the patient has normal T3 and T4 but mildly elevated TSH, this is described as subclinical hypothyroidism.
A 43 year old man with a long history of excess alcohol consumption presents with haematemesis. O/E his is clubbed and has spider naevi.
What is the most suitable investigation? A. Serum sodium B. U&E C. Bronchoscopy D. Echocardiogram E. TFT F. Lung(pulmonary) function tests G. Abdominal ultra sound scan (USS) H. Colonoscopy I. FBC J. Liver function tests K. Stool culture L. Sputum culture M. CXR
G. Abdominal ultra sound scan (USS)
This is hepatic cirrhosis leading to clubbing. The haematemesis is secondary to oesophageal varices and he has signs of chronic liver disease. LFTs are non-specific however ultrasound can show signs of advanced cirrhosis. There may be liver surface nodularity (remember cirrhosis entails nodular regeneration), small liver and possible left/caudate lobe hypertrophy. Signs of portal hypertension may also be picked up such as ascites, splenomegaly and increased diameter of the hepatic portal vein. The most specific and sensitive test is a liver biopsy, which is not given as an option here. Additionally abdominal CT or MRI can also be done similar to USS, with similar findings.
A 47 year old demolition expert presents with SOB. O/E he has some clubbing and signs of pleural effusion.
What is the most suitable investigation? A. Serum sodium B. U&E C. Bronchoscopy D. Echocardiogram E. TFT F. Lung(pulmonary) function tests G. Abdominal ultra sound scan (USS) H. Colonoscopy I. FBC J. Liver function tests K. Stool culture L. Sputum culture M. CXR
M. CXR
Possible mesothelioma. Possible pulmonary fibrosis. Either way, CXR is the way to go.
A 19 year old woman who had cardiac surgery as a child, presents with decreasing exercise tolerance. O/E she is cyanosed and has clubbed nails.
What is the most suitable investigation? A. Serum sodium B. U&E C. Bronchoscopy D. Echocardiogram E. TFT F. Lung(pulmonary) function tests G. Abdominal ultra sound scan (USS) H. Colonoscopy I. FBC J. Liver function tests K. Stool culture L. Sputum culture M. CXR
D. Echocardiogram
The cause here is cardiac and likely Eisenmenger’s syndrome. This is clubbing due to congenital cyanotic heart disease and you would want to perform an echocardiogram here to look for structural heart defects.
A 35 year old woman with a history of recurrent lower abdominal pain, bloody diarrhoea and passing mucus PR. O/E she has lower abdominal tenderness and clubbing.
What is the most suitable investigation? A. Serum sodium B. U&E C. Bronchoscopy D. Echocardiogram E. TFT F. Lung(pulmonary) function tests G. Abdominal ultra sound scan (USS) H. Colonoscopy I. FBC J. Liver function tests K. Stool culture L. Sputum culture M. CXR
H. Colonoscopy
This is clubbing due to inflammatory bowel disease (Crohn’s or UC) and diagnosis of this would be made on colonoscopy. Biopsy in CD will show transmural granulomatous inflammation. CD can affect the whole GIT but favours the TI (RLQ pain) and proximal colon and is macroscopically characterised by skip lesions. UC on the other hand is characterised by the presence of crypt abscesses, which is pathognomic.
A 49 year old heavy smoker presents with SOB and weight loss. O/E she is clubbed and her CXR shows a perihilar shadow.
What is the most suitable investigation? A. Serum sodium B. U&E C. Bronchoscopy D. Echocardiogram E. TFT F. Lung(pulmonary) function tests G. Abdominal ultra sound scan (USS) H. Colonoscopy I. FBC J. Liver function tests K. Stool culture L. Sputum culture M. CXR
C. Bronchoscopy
This is likely lung cancer and diagnosis relies on pathological confirmation from a tissue sample, often obtained from bronchoscopy. A CXR will of course be done in the first instance as the initial investigation but the best test on the list for diagnosis is a bronchoscopy.
A 50 year old woman has developed weight loss and passes loose pale stools. She has mouth ulcers and is anaemic. She is taking thyroxine for myxoedema.
What is the most suitable investigation? A. ERCP B. Faecal elastase-1 C. Abdominal ultrasound D. Liver function tests E. HIV test F. Skin biopsy G. Immunoglobulin H. Endomysial antibodies I. Sweat test J. Hydrogen breath test K. Abdominal X-ray L. Thyroid function M. Colonoscopy
H. Endomysial antibodies
This is a common condition in the US and Europe. Coeliac disease most commonly presents with IDA, although it can also lead to a macrocytic anaemia with mainly folate deficiency (though B12 is also affected but hepatic stores last several years). The mouth ulcers are a sign of this. There are also GI symptoms resulting from malabsorption. It is an autoimmune condition (the presence of another autoimmune condition here is a risk factor) triggered by gluten peptides found in wheat, rye and barley. The ultimate best test is duodenal biopsy and histology to show intra-epithelial lymphocytes, villous atrophy and crypt hyperplasia. Macroscopic changes may be present but endoscopy is generally unhelpful. The test of choice before performing such an invasive confirmatory test is to look for elevated anti-gliadin antibodies. Anti-tissue transglutaminase is less accurate and endomysial antibody is more expensive and has lower sensitivity, though is the only option on this list specific for coeliac.
It is worth knowing about the Schilling test as it is frequently examined. However, it is no longer routinely done in clinical practice. In this test, IM vitamin B12 is given to saturate stores. Then oral radiolabelled B12 is given and urine is collected over 24 hours. The amount excreted is lower in B12 malabsorption. If this is not corrected by IF the problem is with the ileum and not inadequate IF.
A 35 year old man presents with weight loss, diarrhoea and pain on swallowing. O/E he has oral candidiasis & molluscum contagiosum.
What is the most suitable investigation? A. ERCP B. Faecal elastase-1 C. Abdominal ultrasound D. Liver function tests E. HIV test F. Skin biopsy G. Immunoglobulin H. Endomysial antibodies I. Sweat test J. Hydrogen breath test K. Abdominal X-ray L. Thyroid function M. Colonoscopy
E. HIV test
Molluscum contagiosum is an umbilicated, pearl like, smooth papules and at least a third of patients will also develop symptoms of local erythema, swelling or pruritis. HIV is a strong risk factor for MC. It is transmitted skin-to-skin or fomite in children and sexually transmitted in adulthood. Oral candidiasis is also an opportunistic infection associated with the immunocompromised state of HIV. Weight loss is also seen in HIV and may result from malnutrition, TB or HIV wasting syndrome. Diarrhoea is also common. An HIV test is needed in this patient and contact tracing will be necessary.
A 10 year old girl with a history of recurrent chest infections has developed pale floating stools and weight loss.
What is the most suitable investigation? A. ERCP B. Faecal elastase-1 C. Abdominal ultrasound D. Liver function tests E. HIV test F. Skin biopsy G. Immunoglobulin H. Endomysial antibodies I. Sweat test J. Hydrogen breath test K. Abdominal X-ray L. Thyroid function M. Colonoscopy
I. Sweat test
CF is autosomal recessive and the mean age of death is around 40. There is currently no cure for this condition. The reccurent chest infections and greasy stools (fat malabsorption due to pancreatic insufficiency) should make you think of CF. A persistent cough which is productive would also raise suspicions. Additionally, you may find nasal polyps and hepatomegaly and/or splenomegaly and a congenital absence of the vas deferens in males. There may also be failure to thrive in infants. The most conclusive diagnostic test is the sweat test which is positive if sweat chloride is >60mmol/L. Serum IRT from a heel prick blood spot allows screening of newborns. CF is a genetic condition with abnormal salt and water transport due to mutations in the CFTR (an apical anion channel). Heterozygotes generally do not demonstrate disease.
A 45 year old man has recurrent epigastric pain, weight loss and steatorrhoea. He has a previous history of alcoholism.
What is the most suitable investigation? A. ERCP B. Faecal elastase-1 C. Abdominal ultrasound D. Liver function tests E. HIV test F. Skin biopsy G. Immunoglobulin H. Endomysial antibodies I. Sweat test J. Hydrogen breath test K. Abdominal X-ray L. Thyroid function M. Colonoscopy
A. ERCP
This is chronic pancreatitis which is most commonly associated with chronic alcohol abuse. Features include the epigastric pain here, which classically radiates to the back, and steatorrhoea from malabsorption (pale, foul-smelling and difficult to flush stools). There may additionally be DM due to pancreatic failure and the patient may be malnourished. The diagnosis is based on findings and imaging – your options are USS which is less sensitive, or CT, which is more sensitive but involves radiation exposure. AXR is not a sensitive enough test. However, this question is looking for the best test which is ERCP, commonly considered the most accurate test with high sensitivity and specificity. It is limited in use though due to cost and the risk to the patient. Characteristically ERCP would show beading of the main pancreatic duct as well as irregularities in the side branches. Faecal elastase-1 is inaccurate for diagnosing mild to moderate pancreatic insufficiency, and anyway has unacceptably low sensitivity.
There is no real definitive treatment, which is mainly symptomatic and the underlying and precipitating factors are treated – in this case, this man’s alcohol excess. Complications of chronic pancreatic imflammation include the development of pseudocysts, calficiation, DM and malabsorption.
A 20 year old man has a 4 month history of diarrhoea & weight loss. He is pale, has mouth ulcers and clubbing.
What is the most suitable investigation? A. ERCP B. Faecal elastase-1 C. Abdominal ultrasound D. Liver function tests E. HIV test F. Skin biopsy G. Immunoglobulin H. Endomysial antibodies I. Sweat test J. Hydrogen breath test K. Abdominal X-ray L. Thyroid function M. Colonoscopy
M. Colonoscopy
This is a history of inflammatory bowel disease. A colonoscopy is required to assess the extent of disease and for a definitive diagnosis. Biopsy in CD will show transmural granulomatous inflammation. CD can affect the whole GIT but favours the TI (RLQ pain) and proximal colon and is macroscopically characterised by skip lesions. UC on the other hand is characterised by the presence of crypt abscesses, which is pathognomic.
A 50 year old housewife presents with pruritis and jaundice with pale stools, dark urine and steatorrhea, pigmentation and xanthelasma. Examination reveals splenomegaly. Anti-mitochondrial antibodies are present.
What is the diagnosis? A. Hepatitis B. Gall stones C. Gilbert's syndrome D. Primary sclerosing cholangitis E. Haemolytic anaemia F. Dubin-Johnson syndrome G. Carcinoma of the pancreas H. Primary biliary cirrhosis
H. Primary biliary cirrhosis
Primary biliary cirrhosis (PBC) is a chronic condition where the intrahepatic small bile ducts are progressively damaged (and eventually lost) occuring on a background of portal tract inflammation. Fibrosis develops, ultimately leading to cirrhosis (which is defined as fibrosis with nodular regeneration). It is widely believed to be autoimmune in aetiology as almost all patients have AMA (present here). The pointers in this question which would raise your suspicion, is xanthelasma around the eyes, pruritis in the absence of an obvious dermatological cause, fatigue and the features of liver disease typical of cirrhosis (obstructive jaundice) and splenomegaly as a feature of portal hypertension.
A 25 year old man presents to you with an incidental finding of a raised bilirubin (31 umol). No other signs of liver disease are present. Further investigations show a raised unconjugated bilirubin. When asked he tells you that other family members have suffered from jaundice.
What is the diagnosis? A. Hepatitis B. Gall stones C. Gilbert's syndrome D. Primary sclerosing cholangitis E. Haemolytic anaemia F. Dubin-Johnson syndrome G. Carcinoma of the pancreas H. Primary biliary cirrhosis
C. Gilbert’s syndrome
Gilbert’s occurs in an asymptomatic patient, often as an incidental finding or mild jaundice occuring in adolescence/young adult age. There is elevated unconjugated BR with other liver tests being normal. The blood smear is also normal with normal reticulocyte count, and normal Hb indicating that this is not due to haemolysis. It is a common syndrome and is not really a disease, more a physiological variant. No treatment is needed and this condition is due to decreased UDPGT activity leading to decreased conjugation of unconjugated bilirubin, leading to elevated levels. Positive FH is common as this condition is most likely transmitted in an autosomal recessive pattern.
A 65 year old ex-smoker is deeply jaundiced. He has epigastric pain radiating to his back. A dilated gall bladder is palpable and there is hepatomegaly. He has lost about 5kg in weight.
What is the diagnosis? A. Hepatitis B. Gall stones C. Gilbert's syndrome D. Primary sclerosing cholangitis E. Haemolytic anaemia F. Dubin-Johnson syndrome G. Carcinoma of the pancreas H. Primary biliary cirrhosis
G. Carcinoma of the pancreas
Pancreatic cancer (of the head) typically presents with painless obstructive jaundice and weight loss and generally presents late. There is however epigastric pain in this case, which is a possible presentation. Whipple’s procedure or Traverso-Longmire procedure (pancreaticoduodenectomy) offers the only hope of a cure but only a small minority are elegible for these procedures. The first tests to order are an abdominal USS and LFTs. Note Courvoisier’s law: Jaundice and a palpable painless gallbladder is unlikely to be caused by gallstones. The tumour marker for pancreatic cancer is CA19-9 which is useful in preoperative staging.
A 22 year old man comes to see you on his return from a holiday in Spain. He has a 3-4 day history of fever, malaise, nausea, vomiting and abdominal discomfort. He is noticeably jaundiced with dark urine and pale stools. There is also tender hepatomegaly on examination. He wonders if this is related to his meal of shellfish from a street vendor.
What is the diagnosis? A. Hepatitis B. Gall stones C. Gilbert's syndrome D. Primary sclerosing cholangitis E. Haemolytic anaemia F. Dubin-Johnson syndrome G. Carcinoma of the pancreas H. Primary biliary cirrhosis
A. Hepatitis A
This is likely hepatitis A which is primarily transmitted via the faecal-oral route. After the virus is consumed and absorbed, it replicates in the liver and is excreted in the bile (to be re-transmitted). Transmission usually precedes symptoms by about 2 weeks and patients are non-infectious 1 week after onset of jaundice. The history can reveal risk factors such as living in an endemic area, contact with an infected person, homosexual sex or a known food-borne outbreak. This is classically, in EMQs, associated with shellfish which is harvested from sewage contaminated water. If the patient has other liver diseases such as HBV or HCV or cirrhosis then there is a higher risk of fulminant HAV infection. The clinical course of HAV consists of a pre-icteric phase, lasting 5-7 days, consisting characteristically of N&V, abdominal pain, fever, malaise and headache. Rarer symptoms may be present such as arthralgias and even severe thrombocytopenia and signs that may be found include splenomegaly, RUQ tenderness and tender hepatomegaly as well as bradycardia. The icteric phase is characterised by dark urine, pale stools, jaundice and pruritis. When jaundice comes on, the pre-icteric phase symptoms usually diminish, and jaundice typically peaks at 2 weeks. However, a fulminant course runs in <1% of patients with worsenining jaundice and encephalopathy. Serum transaminases may reach in excess of 10,000 units, although there is little correlation between the level and disease severity. ALT is typically higher than AST.
A 6 year old presents with mild jaundice and some pain and swelling of his fingers. O/E you note splenomegaly.
What is the diagnosis? A. Hepatitis B. Gall stones C. Gilbert's syndrome D. Primary sclerosing cholangitis E. Haemolytic anaemia F. Dubin-Johnson syndrome G. Carcinoma of the pancreas H. Primary biliary cirrhosis
E. Haemolytic anaemia
Africans have higher incidence of sickle cell anaemia. This is a presentation of bone pain here with dactylitis, consistent with hand-foot syndrome which can be what young infants and children present with (it is often a child’s first presentation of disease). The jaundice here is due to haemolysis and so while this is sickle cell anaemia, the options are trying to get you to think a bit about the best fit here which would be haemolytic anaemia. About 8% of black people carry the gene and the prevalence is high in sub-Saharan Africa. The condition is autosomal recessive and therefore occurs in 1 in 4 pregnancies where both parents carry the sickle gene. Sickling occurs when RBCs containing HbS become distorted into a crescent shape. Patients with sickle cell anaemia have no HbA at all. If both parents carry the sickle cell gene, there is a 1 in 4 chance of giving birth to a child with sickle cell anaemia. Sickle cell disease also includes other conditions such as HbS from one parent with another abnormal Hb or beta thalassaemia from the other parent such as HbS-Beta thal and HbSC. Treatment goals here include fluid replacement therapy, pain management and symptomatic control.
A 25 year old female with recent onset of depression takes 50 paracetamol capsules, each containing 500mg of active drug. In several days her liver is most likely to show what?
A. Extensive cirrhosis B. Enlarged right lobe C. Pancreatic carcinoma D. Hypervascularity E. Hepatitis B F. Cholecystitis G. Arterio-venous malformations H. Hepatocellular carcinoma I. Extensive necrosis J. Hepatitis C K. Pancreatic pseudocyst L. Portal chronic inflammation
I. Extensive necrosis
Paracetamol OD can occur after a single large OD or repeated ODs. Often, the patient is asymptomatic at initial presentation but if untreated may cause liver injury over the 2-4 days after ingestion, including fulminant liver failure. Massive hepatic necrosis will occur and will be the cause of fulminant liver failure. Paracetamol is the most frequent intentional OD drug in this country. The risk of liver damage is increased after taking drugs which induce CYP 450. Inducers include St John’s wort, barbiturates, phenytoin, tetracycline, chronic alcohol use and carbamazepine. A serum paracetamol level is important to order as early as possible, but at the earliest 4 hours post-ingestion.Treatment if indicated is with N-acetylcysteine with the level based on a paracetamol treatment graph.
A 40 year old male has a long history of alcoholism. His liver is firm on palpation. You finally convince him to stop drinking and join Alcoholics Anonymous. Despite abstinence he remains at risk for developing which disease?
A. Extensive cirrhosis B. Enlarged right lobe C. Pancreatic carcinoma D. Hypervascularity E. Hepatitis B F. Cholecystitis G. Arterio-venous malformations H. Hepatocellular carcinoma I. Extensive necrosis J. Hepatitis C K. Pancreatic pseudocyst L. Portal chronic inflammation
H. Hepatocellular carcinoma
Patients with cirrhosis, especially those with alcoholic liver disease, are at a high risk of developing HCC. Cirrhosis is irreversible so despite stopping drinking, he is still at risk of HCC (hepatoma). Patients with cirrhosis should be screened for HCC with serum AFP and USS at 6 month intervals.
A 40-year-old female, rather overweight, has episodes of right upper quadrant pain and fever.
What is the diagnosis? A. Extensive cirrhosis B. Enlarged right lobe C. Pancreatic carcinoma D. Hypervascularity E. Hepatitis B F. Cholecystitis G. Arterio-venous malformations H. Hepatocellular carcinoma I. Extensive necrosis J. Hepatitis C K. Pancreatic pseudocyst L. Portal chronic inflammation
F. Cholecystitis
Cholecystitis is acute GB inflammation caused by an obstruction at the cystic duct. It occurs as a major complication of gallstones and classically presents with RUQ pain and fever. Gallstones in EMQs classically involves the Fs (Fat, Forty, Female, Fertile, Fair). USS is the definitive initial investigation. HIDA scanning and MRI may help if the diagnosis remains unclear. Treatment is with cholecystectomy.
A 60 year old alcoholic is hospitalised after an episode of haematemesis. He is about to undergo endoscopy. What would his liver biopsy likely low evidence of?
A. Extensive cirrhosis B. Enlarged right lobe C. Pancreatic carcinoma D. Hypervascularity E. Hepatitis B F. Cholecystitis G. Arterio-venous malformations H. Hepatocellular carcinoma I. Extensive necrosis J. Hepatitis C K. Pancreatic pseudocyst L. Portal chronic inflammation
A. Extensive cirrhosis
This is a case of haematemesis secondary to oesophageal varices. Oesophageal varices are a direct result of portal hypertension, which occurs as a progressive complication of cirrhosis, which is what liver biopsy will show. Diagnosis and surveillance by endoscopy is an important part of management of this condition and in terms of prophylaxis against variceal bleeding before it has occured, non-selective beta blockers and/or endoscopic ligation can be used.
On liver biopsy a moderate chronic inflammation is observed. Special stains identify antigens from a double stranded DNA virus within the cytoplasm of hepatocytes.
What is the diagnosis? A. Extensive cirrhosis B. Enlarged right lobe C. Pancreatic carcinoma D. Hypervascularity E. Hepatitis B F. Cholecystitis G. Arterio-venous malformations H. Hepatocellular carcinoma I. Extensive necrosis J. Hepatitis C K. Pancreatic pseudocyst L. Portal chronic inflammation
E. Hepatitis B
Hepatitis B is a DNA virus which is transmitted percutaneously and permucosally. It is also a STI. HCV is an RNA virus and RNA-PCR will be positive. A brief bit about hepatitis B markers: HBsAb appears several weeks after HBsAg disappears and in most patients suggests a resolved infection and life-long immunity (it is also detectable and titres are measured in those immunised with the HBV vaccine). HBsAg on the other hand appears 2-10 weeks after exposure to HBV and usually, in self-limiting acute cases, becomes undetectable after 4-6 months of infection. Persistence for >6 months implies chronic infection. Core antibody (IgM) appears within weeks of acute infection and remains detectable for 4-8 months and can be the only way to diagnose acute infection during the period when surface antigen disappears but before surface antibody has appeared. Chronic infection is indicated by IgG core antibody. The best single test to screen household contacts of infected individuals to determine the need to vaccinate is still HBcAb. E antigen is a soluble viral protein in serum which is part of the early acute infection and disappears soon after peak ALT levels. Presence >3 months indicates chronic infection is likely. E antigen being present in those with surface antigen indicates greater infectivity and a high level of viral activity and replication.
A 50 year old man took an overdose of his antidepressants one hour ago. He has a dry mouth and dilated pupils but is not drowsy.
What is the best treatment? A. N-acetlycysteine B. IV-ethanol C. Gastric lavage D. IV-glucagon E. Activated charcoal F. Forced emesis G. Haemodialysis H. IV-naloxone I. Forced alkaline diuresis J. Oral methionine K. Hyperbaric oxygen
E. Activated charcoal
This is an overdose of tricyclic antidepressants which are a class of drugs with a narrow therapeutic index and therefore become potent toxins in moderate doses to both the CNS and cardiovascular system. The main aim in treatment is to provide respiratory and cardiovascular support until the medicine has been fully metabolised and eliminated. GI decontamination should be considered in those presenting with early overdose (under 2 hours after ingestion) provided that the airway can be protected. There is no shown clear benefit to repeated doses of activated charcoal. The warm, dry skin is part of the anticholinergic effects (physostigmine should NOT be used to reverse this as it has been in rare cases been associated with asystole – would you rather have a patient who is flushed or flatlined?). Other anticholinergic effects include dilated pupils, urinary retention, decreased or absent bowel sounds and changes in mental status. Hypotension is common and is due to alpha 1 antagonism. Classic ECG changes are of sinus tachycardia progressing to wide complex tachycardia and ventricular arrhythmias (with increasing severity and intoxication). Condution problems and hypotension is improved with hypertonic sodium bicarbonate and if arrhythmias are present, treatment of these involves correcting the acidosis, hypoxia and electrolyte abnormalities. Anti-arrhythmics are generally avoided. If hypotension is refractory then a vasopressor can be used. BZDs can be used for any seizures.
A 30 year old woman with toothache has taken 50 paracetamol 500mg tablets in the last 24 hours. She feels nauseated and still has toothache but is otherwise well.
What is the best treatment? A. N-acetlycysteine B. IV-ethanol C. Gastric lavage D. IV-glucagon E. Activated charcoal F. Forced emesis G. Haemodialysis H. IV-naloxone I. Forced alkaline diuresis J. Oral methionine K. Hyperbaric oxygen
A. N-acetylcysteine
Paracetamol OD can occur after a single large OD or repeated ODs. Often, the patient is asymptomatic at initial presentation but if untreated may cause liver injury over the 2-4 days after ingestion, including fulminant liver failure. Paracetamol is the most frequent intentional OD drug in this country. The risk of liver damage is increased after taking drugs which induce CYP 450. Inducers include St John’s wort, barbiturates, phenytoin, tetracycline, chronic alcohol use and carbamazepine. A serum paracetamol level is important to order as early as possible, but at the earliest 4 hours post-ingestion.Treatment if indicated is with N-acetylcysteine with the level based on a paracetamol treatment graph.
A 20 year old heroin addict arrives in casualty, unconscious and cyanosed. His resp rate is 6/min and he has pin-point pupils.
What is the best treatment? A. N-acetlycysteine B. IV-ethanol C. Gastric lavage D. IV-glucagon E. Activated charcoal F. Forced emesis G. Haemodialysis H. IV-naloxone I. Forced alkaline diuresis J. Oral methionine K. Hyperbaric oxygen
H. IV-naloxone
Signs of opiate OD include CNS depression, miosis (pinpoint pupils) and apnoea. Naloxone is indicated both therapeutically and diagnostically. If there is a response, then it is diagnostic. Another diagnosis should be sought if the patient is unresponsive. IV is the preferred route of administration although naloxone can be given IM or SC if IV access cannot be established. Ventilatory support is key with 100% oxygen.
A 40 year old woman with a history of hypertension was brought in to casualty two hours ago having taken a whole bottle of her medication in an attempt to commit suicide. She suddenly collapses with a pulse of 30bpm and a BP of 70/30.
What is the best treatment? A. N-acetlycysteine B. IV-ethanol C. Gastric lavage D. IV-glucagon E. Activated charcoal F. Forced emesis G. Haemodialysis H. IV-naloxone I. Forced alkaline diuresis J. Oral methionine K. Hyperbaric oxygen
D. IV-glucagon
Glucagon stimulates adenyl cyclase which acts to increase intracellular cAMP and to therefore increase cytosolic calcium and cardiac contractility. Hypotension and bradyarrhythmias are the most common initial findings of beta blocker toxicity. If IV glucogon is not available then high-dose insulin can be used instead with co-administration of dextrose to maintain blood glucose levels.
A 45 year old homeless man complains of headache, abdominal pain, nausea and dizziness. He admits to having drunk anti-freeze on the previous night. He is hyperventilating and slightly drowsy.
What is the best treatment? A. N-acetlycysteine B. IV-ethanol C. Gastric lavage D. IV-glucagon E. Activated charcoal F. Forced emesis G. Haemodialysis H. IV-naloxone I. Forced alkaline diuresis J. Oral methionine K. Hyperbaric oxygen
B. IV-ethanol
Antifreeze is ethylene glycol. It is a sweet-tasting, odourless and colourless liquid and the substance itself is non-toxic and initially causes inebriation. Toxicity appears within 12-24 hours and is due to metabolic acidosis and the formation of calcium oxalate from one of the metabolites. Oxalate deposits in the lungs, myocardium and kidneys leading to organ damage and renal failure, and hypocalcaemia may also occur due to the consumption of circulating calcium. Ethylene glycol is not absorbed by activated charcoal and gastric decontamination is pointless regardless of time since consumption. The first line treatment is fomepizole (4-methylpyrazole) which is a competitive inhibitor of alcohol dehydrogenase, an enzyme involved in catalysing the initial steps in metabolism of ethylene glycol and methanol into toxic metabolites. However, this is not on the list, and oral ethanol (loading dose or infusion) can be used in this case (have a think about why ethanol would work as an antidote, if you think back to how ethanol is metabolised). Dialysis may well be required.
A 23 year old woman presents with a 24 hour history of right iliac fossa pain. There is tenderness & guarding in the right iliac fossa. There are no menstrual symptoms. Abdominal & pelvic ultrasound is normal.
What is the most suitable investigation? A. ECG B. PR exam C. Diagnostic laparotomy D. CT scan E. AXR F. Endoscopy G. CXR H. Laxatives I. Oral antibiotics J. Ultrasound scan K. Palliative care L. Acute pancreatitis
C. Diagnostic laparotomy
An abdominal and pelvic CT scan would normally be ordered in situations like this, with possible appendicitis, but it is assumed here that the doctors were thinking of pregnancy as a possibility so a sonogram was done instead, which turns out to be inconclusive. Now, in this situation, you could do an abdominal MRI (especially in early pregnancy) or go ahead with a CT scan anyway, but a diagnostic laparotomy is the best option here to diagnose and treat at the same time. The main differential here is either obstetric, such as a ruptured ectopic pregnancy, or acute appendicitis. You would have imagined they would have done the usual important tests like FBC and a urinary pregnancy test… but these results are not available, nor are they an option, but a prudent doctor would have ordered them in the diagnostic work up. However, given USS does not show a mass in the fallopian tubes, this may push you away from an ectopic pregnancy… however, USS is operator dependent, this is a female of childbearing age (this age is getting lower and lower in the UK) and the doctor has failed to obtain either serum or urine HCG levels or asked about any missed menstrual periods.
This patient, should be made NBM with maintenance IV fluids like lactated Ringer’s, and have a laparotomy which can be both diagnostic and therapeutic. You can take the appendix out if this is the problem or deal with the ectopic, if that is the problem, or deal with whatever it could be.. say for instance, a rare Meckel’s diverticulitis.
A 30 year old man presents with severe left loin pain, colicky in nature. It radiates towards the left groin.
What is the most suitable investigation? A. ECG B. PR exam C. Diagnostic laparotomy D. CT scan E. AXR F. Endoscopy G. CXR H. Laxatives I. Oral antibiotics J. Ultrasound scan K. Palliative care L. Acute pancreatitis
D. CT scan
This patient has renal colic which classically presents with severe flank pain radiating to the groin. Infection may complicate renal calculi. Microscopic haematuria is present in up to 90% of cases. Up to 85% of stones are visible on a plain KUB although urate stones are radiolucent. If the stone is radio-opaque, calcification will be seen within the urinary tract. In pregnancy though, a renal USS is first line. The IVP has now been replaced by the CT scan which is the new diagnostic standard. A non-contrast helical (or spiral) CT is preferred due to high sensitivity and specificity and acurately determines presence, site and size of stones. Stones are analysed after they are extracted or when they are expelled to check their composition.
In reality the first test to order is urinalysis – it is quick and simple. You’d also always exclude ectopic pregnancy with a urine pregnancy test if this were a female of childbearing age, look for hypercalcaemia and hyperuricaemia and perform a FBC to look for infection.
A 45 year old man presents with sudden onset epigastric pain, constant in nature. He has had several previous episodes. He drinks half a bottle of whisky per day.
What is the most suitable investigation? A. ECG B. PR exam C. Diagnostic laparotomy D. CT scan E. AXR F. Endoscopy G. CXR H. Laxatives I. Oral antibiotics J. Ultrasound scan K. Palliative care L. Acute pancreatitis
L. Acute pancreatitis
This patient has acute pancreatitis – the cause here being alcohol. He is describing mid-epigastric pain. This pain classically radiates around to the back, which in itself is almost diagnostic. Complicated haemorrhagic pancreatitis may exhibit Cullen’s sign, Grey-Turner’s sign and Fox’s sign. Make sure you know what these are and you are familiar with the causes of acute pancreatitis (GET SMASHED). Those caused by hypocalcaemia may also display Chvostek’s sign and Trousseau’s sign.
Key to diagnosis is serum amylase or lipase levels which are massively elevated. Prognostic criteria are outlined in Ranson’s criteria applied on admission and after 48 hours, or the modified Glasgow score which you can find in your Oxford Handbook. An abdominal CT is however the most sensitive and specific study and findings may include enlargement of the pancreas with irregular contours, necrosis, pseudocysts and peripancreatic fat obliteration.
A 77 year old woman presents with a 3 day history of constant left iliac fossa pain. She has a temp of 38oC and O/E is tender with guarding in the left iliac fossa. CT scan demonstrates an inflamed sigmoid colon with numerous diverticulae.
What is the most suitable investigation? A. ECG B. PR exam C. Diagnostic laparotomy D. CT scan E. AXR F. Endoscopy G. CXR H. Laxatives I. Oral antibiotics J. Ultrasound scan K. Palliative care L. Acute pancreatitis
I. Oral antibiotics
This patient obviously has diverticulitis and does not need further investigation. Symptomatic diverticulitis presents with fever, high WCC and LLQ pain. Risk factors for diverticular disease include low dietary fibre and advanced age. Oral antibiotic therapy and analgesia is indicated. If there is no improvement in 72 hours after oral antibiotics then IV antibiotics are indicated. Make sure you understand the differences in the terms: diverticulosis, diverticulitis and diverticular disease.
A 48 year old woman presents with a 1 day history of constant right upper quadrant pain radiating round the right side of her chest. She says her urine may be darker than usual. Her GP started her on oral antibiotics. Amylase has already been ordered.
What is the most suitable investigation? A. ECG B. PR exam C. Diagnostic laparotomy D. CT scan E. AXR F. Endoscopy G. CXR H. Laxatives I. Oral antibiotics J. Ultrasound scan K. Palliative care L. Acute pancreatitis
I. Ultrasound scan
Abdominal ultrasound is ordered when a patient presents with biliary pain and is the single best test for cholelithiasis (though has a low sensitivity for choledocholithiasis). Note that cholelithiasis refers to stones in the gallbladder and choledocholithiasis refers to stones in the bile duct. If stones are found then this would give weight to a diagnosis of acute cholecystitis. There are symptoms here of obstructive jaundice due to gallstone obstruction of bile outflow. Serum amylase would also be ordered in any patient presenting with pain located in the epigastric region, to rule out acute pancreatitis. This has been done here. In this patient you would also order LFTs, FBC looking for evidence of inflammation. MRCP, ERCP and EUS can be considered if necessary.
A 30 year old male is brought into A&E having been found unrousable by his partner on the floor. He is breathing very occasionally and has small pupils. He has track marks in his antecubital fossa.
What is the best treatment? A. IV adrenaline B. IV dextrose C. Urgent CT scan D. IV carbamazepine E. Phenytoin infusion F. IM benzylpenicillin G. Elevate legs H. IM adrenaline I. IV lorazepam J. IV diazepam K. IV naloxone L. IV propofol M. IV midazolam N. CPR
K. IV naloxone
Signs of opiate OD include CNS depression, miosis (pinpoint pupils) and apnoea. Naloxone is indicated both therapeutically and diagnostically. If there is a response, then it is diagnostic. Another diagnosis should be sought if the patient is unresponsive. IV is the preferred route of administration although naloxone can be given IM or SC if IV access cannot be established. Ventilatory support is key with 100% oxygen.
A 50 year old male collapses in hospital while you are taking a history from the patient next to him. After 10 seconds, he is rapidly jerking his head with tonic stiffening arms quickly followed by clonic jerking. He becomes incontinent of urine and unresponsive.
What is the best treatment? A. IV adrenaline B. IV dextrose C. Urgent CT scan D. IV carbamazepine E. Phenytoin infusion F. IM benzylpenicillin G. Elevate legs H. IM adrenaline I. IV lorazepam J. IV diazepam K. IV naloxone L. IV propofol M. IV midazolam N. CPR
I. IV lorazepam
This is a tonic-clonic, generalised seizure. It is characterised by LOC and widespread motor tonic contractions followed by clonic jerking movements. There will characteristically be a suppressed level of arousal following the event. This may either reflect a primary generalised episode or a focal seizure with secondary generalisation. The main aim of acute treatment is to terminate the seizure and to protect the airway. Management always starts with basic life-support (like every acute emergency) and your ABCs. IV access needs to be established (bloods sent to the lab too and serum glucose measured to test for reversable causes of seizure activity – thiamine should also be given to the patient if there is any concern about deficiency and hypoglycaemia, for instance in alcohol abuse). The following are needed: ECG, pulse oximetry, ABG. IV lorazepam is the preferred initial therapy, though rectal diazepam can be used if there is no IV access. If BZDs fail to stop the seizure then phenytoin or fosphenytoin can be tried.
After the episode, MRI and EEG are essential in diagnosing an epilepsy syndrome. During the episode of generalised tonic-clonic activity, the EEG will show bilateral synchrony in the epileptiform activity. If this is a one-off seizure in which a provoking factor, such as electrolyte disturbance or hypoglycaemia, has been identified then there is no need for therapy for epilepsy. In unprovoked cases, this depends on history, examination, EEG and MRI. Treatment may not be needed the first time but after a second unprovoked instance, therapy is generally recommended.
An 18 year old man attends his GP to have a routine blood test. He has no significant past medical history. While having the blood test he becomes pale, clammy and says he feels sick. He subsequently becomes unresponsive.
What is the best treatment? A. IV adrenaline B. IV dextrose C. Urgent CT scan D. IV carbamazepine E. Phenytoin infusion F. IM benzylpenicillin G. Elevate legs H. IM adrenaline I. IV lorazepam J. IV diazepam K. IV naloxone L. IV propofol M. IV midazolam N. CPR
G. Elevate legs
This is a case of vasovagal syncope. Elevation of the legs will help move blood towards the head. The other options on the list are not necessary.
A 13-year-old boy collapses at the playground. He has recurrent seizures for over 30 minutes. It seems he has not regained consciousness in between the seizures.
What is the best treatment? A. IV adrenaline B. IV dextrose C. Urgent CT scan D. IV carbamazepine E. Phenytoin infusion F. IM benzylpenicillin G. Elevate legs H. IM adrenaline I. IV lorazepam J. IV diazepam K. IV naloxone L. IV propofol M. IV midazolam N. CPR
I. IV lorazepam
This patient is in status epilepticus defined by 30 minutes or more of continuous seizure activity, or repetitive seizures with no intervening recovery of consciousness. SE can be either generalised convulsive or non-convulsive (simple or complex partial). In children, seizures of a shorter duration may also be considered to be status epilepticus. The initial treatment is as 2) and should start with BLS measures, continuous monitoring and benzodiazepines as first line therapy – with IV lorazepam. Securing the patient’s airwar may prove difficult due to the convulsions and neuromuscular blockade with a short-acting drug such as vecuronium may be necessary.
Unresponsive cases can get anticonvulsants or phenobarbitone. It is worth noting that phenytoin infusions may lead to venous irritation and tissue damage if the undiluted drug is given through a small bore cannula. If SE persists, the next step to take is to intubate and start general anaesthesia. The best initial agents to use are midazolam and propofol though other options include pentobarbital and thiopental, the former being an active metabolite of the latter. GA should be tapered off after a minimum of 12 hours, and if the seziure recurs then the infusion should be restarted for another 12-24 hours.
A 22-year-old student collapses in her room. She is febrile and you notice a rash over her body.
What is the best treatment? A. IV adrenaline B. IV dextrose C. Urgent CT scan D. IV carbamazepine E. Phenytoin infusion F. IM benzylpenicillin G. Elevate legs H. IM adrenaline I. IV lorazepam J. IV diazepam K. IV naloxone L. IV propofol M. IV midazolam N. CPR
F. IM benzylpenicillin
This is suspected bacterial meningitis and in the community setting the patient should receive immediate IM benzylpenicillin before being transferred to hospital as an emergency case.
For each disease/syndrome, choose the most likely mode of inheritance.
Duchenne muscular dystrophy
A. Autosomal recessive B. None/unknown C. X-linked recessive D. X-linked dominant E. Mitochondrial inheritance F. Chromosomal abnormality G. Autosomal dominant
C. X-linked recessive
Here is a list of the important conditions you should be aware of:
Autosomal dominant: Achrondroplasia, APKD, dystrophia myotonica, familial hypercholesterolaemia, Huntington’s, Marfan’s, NF, tuberous sclerosis, osteogenesis imperfecta
Autosomal recessive: CF, hereditary haemochromatosis, sickle cell disease, Wilson’s, Friedreich’s ataxia, CAH
X-linked recessive: DMD, Fragile X syndrome, Haemophilia A and B, G6PDH deficiency, Alport’s
You should be aware that Down’s is trisomy 21, Edwards’ is trisomy 18 and Patau’s is trisomy 13.
For each disease/syndrome, choose the most likely mode of inheritance.
Cystic fibrosis
A. Autosomal recessive B. None/unknown C. X-linked recessive D. X-linked dominant E. Mitochondrial inheritance F. Chromosomal abnormality G. Autosomal dominant
A. Autosomal recessive
Here is a list of the important conditions you should be aware of:
Autosomal dominant: Achrondroplasia, APKD, dystrophia myotonica, familial hypercholesterolaemia, Huntington’s, Marfan’s, NF, tuberous sclerosis, osteogenesis imperfecta
Autosomal recessive: CF, hereditary haemochromatosis, sickle cell disease, Wilson’s, Friedreich’s ataxia, CAH
X-linked recessive: DMD, Fragile X syndrome, Haemophilia A and B, G6PDH deficiency, Alport’s
You should be aware that Down’s is trisomy 21, Edwards’ is trisomy 18 and Patau’s is trisomy 13.
For each disease/syndrome, choose the most likely mode of inheritance.
Achondroplasia
A. Autosomal recessive B. None/unknown C. X-linked recessive D. X-linked dominant E. Mitochondrial inheritance F. Chromosomal abnormality G. Autosomal dominant
G. Autosomal dominant
Here is a list of the important conditions you should be aware of:
Autosomal dominant: Achrondroplasia, APKD, dystrophia myotonica, familial hypercholesterolaemia, Huntington’s, Marfan’s, NF, tuberous sclerosis, osteogenesis imperfecta
Autosomal recessive: CF, hereditary haemochromatosis, sickle cell disease, Wilson’s, Friedreich’s ataxia, CAH
X-linked recessive: DMD, Fragile X syndrome, Haemophilia A and B, G6PDH deficiency, Alport’s
You should be aware that Down’s is trisomy 21, Edwards’ is trisomy 18 and Patau’s is trisomy 13.
For each disease/syndrome, choose the most likely mode of inheritance.
Down’s syndrome
A. Autosomal recessive B. None/unknown C. X-linked recessive D. X-linked dominant E. Mitochondrial inheritance F. Chromosomal abnormality G. Autosomal dominant
F. Chromosomal abnormality
Here is a list of the important conditions you should be aware of:
Autosomal dominant: Achrondroplasia, APKD, dystrophia myotonica, familial hypercholesterolaemia, Huntington’s, Marfan’s, NF, tuberous sclerosis, osteogenesis imperfecta
Autosomal recessive: CF, hereditary haemochromatosis, sickle cell disease, Wilson’s, Friedreich’s ataxia, CAH
X-linked recessive: DMD, Fragile X syndrome, Haemophilia A and B, G6PDH deficiency, Alport’s
You should be aware that Down’s is trisomy 21, Edwards’ is trisomy 18 and Patau’s is trisomy 13.
For each disease/syndrome, choose the most likely mode of inheritance.
Multiple sclerosis
A. Autosomal recessive B. None/unknown C. X-linked recessive D. X-linked dominant E. Mitochondrial inheritance F. Chromosomal abnormality G. Autosomal dominant
B. None/ unknown
Here is a list of the important conditions you should be aware of:
Autosomal dominant: Achrondroplasia, APKD, dystrophia myotonica, familial hypercholesterolaemia, Huntington’s, Marfan’s, NF, tuberous sclerosis, osteogenesis imperfecta
Autosomal recessive: CF, hereditary haemochromatosis, sickle cell disease, Wilson’s, Friedreich’s ataxia, CAH
X-linked recessive: DMD, Fragile X syndrome, Haemophilia A and B, G6PDH deficiency, Alport’s
You should be aware that Down’s is trisomy 21, Edwards’ is trisomy 18 and Patau’s is trisomy 13.
