Mock Exam 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 most likely diagnosis?
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 most likely diagnosis?
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 most likely diagnosis?
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 most likely diagnosis?
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 most likely diagnosis?
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 most likely chromosomal 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 most likely chromosomal 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 most likely chromosomal 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 most likely chromosomal 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 most likely chromosomal 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.
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 most like causative poison or group of poisons?
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 most like causative poison or group of poisons?
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 most like causative poison or group of poisons?
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 most like causative poison or group of poisons?
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 most like causative poison or group of poisons?
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 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 most likely diagnosis?
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).
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.
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 most likely diagnosis?
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 most likely diagnosis?
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 breast 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.
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 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.
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 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 single most useful investigation?
Endomysial antibodies (or anti-gliadin antibodies, or Anti-tissue transglutaminase) 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 45 year old man has recurrent epigastric pain, weight loss and steatorrhoea. He has a previous history of alcoholism. What is the single most useful investigation?
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 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 most likely diagnosis?
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.
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?
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 most beneficial treatment?
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 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 most beneficial treatment?
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 most beneficial treatment?
First line treatment is fomepizole (4-methylpyrazole), second line = 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.
Calcium channel blocker OD can be treated with…
Calcium chloride. Glucagon can be tried if calcium replacement alone is insufficient.
Sodium channel blocker toxicity can be treated with…
Sodium bicarbonate depending on the QRS length.
Salicylate or phenobarbital OD can be treated with…
Urine alkalinisation with IV sodium bicarbonate. Phenobarbital responds well to multidose charcoal.
Cholinesterase toxicity can be treated with…
IV atropine if there is symptomatic bradycardia. Severe cases can benefit also from IV pralidoxime.
