Mock exam errors Flashcards

1
Q

Diagnosis:
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.

A

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.

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2
Q

Diagnosis:
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.

A

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.

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3
Q

Diagnosis:
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).

A

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.

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4
Q

Causative agent:
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.

A

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.

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5
Q

Causative agent:
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.

A

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.

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6
Q

Diagnosis:
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.

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.

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7
Q

Diagnosis:
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.

A

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.

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8
Q

Diagnosis:
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.

A

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.

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9
Q

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

A

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.

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10
Q

Diagnosis:
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.

A

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.

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11
Q

Diagnosis:
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.

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.

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12
Q

Ix:
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.

A

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.

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13
Q

Ix:
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.

A

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.

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14
Q

Ix:

A 10 year old girl with a history of recurrent chest infections has developed pale floating stools and weight loss.

A

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 prict 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.

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15
Q

Ix:

A 45 year old man has recurrent epigastric pain, weight loss and steatorrhoea. He has a previous history of alcoholism.

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.

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16
Q

Diagnosis:

A 6 year old presents with mild jaundice and some pain and swelling of his fingers. O/E you note splenomegaly.

A

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.

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17
Q

Diagnosis:
On liver biopsy a moderate chronic inflammation is observed. Special stains identify antigens from a double stranded DNA virus within the cytoplasm of hepatocytes.

A

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.

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18
Q

Mgx:
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.

A

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.

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19
Q

Mgx:
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.

A

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.

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20
Q

Ix:
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.

A

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.

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21
Q

Mgx:
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.

A

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.

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22
Q

Mode of inheritance:

Duchenne muscular dystrophy

A

X-linked recessive

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23
Q

Mode of inheritance:

Achondroplasia

A

Autosomal dominant

24
Q

Diagnosis:
An overweight 30 year old lady presents to A&E with an intense, colicky abdominal pain and vomiting which started last night. She says she has noticed weight gain and pelvic pain for a few months. She has also had vaginal discharge. On examination there is gross swelling of the abdomen.

A

Labour

Abdominal pain throughout pregnancy is common although reproductive organs share the name visceral innvervations as the lower ileum, sigmoid colon and rectum so it may be difficult to differentiate GI pain from gynaecological pain. This acute abdomen would require some consideration as the clinical picture may be distorted by the fact that pregnancy stretches the anterior abdominal wall so peritoneal signs are often different due to a lack of contact with the underlying inflammation, if an inflammatory process were to be present. The case described here could well be labour and the already overweight woman has simply been unaware of the fact she is pregnant (which although uncommon, can occur). The gross abdominal distension (which she may not attribute to anything abnormal if she is already fat) and symptoms are pointing to labour and there may also be uterine contractions. Blood or mucus on vaginal examination may be seen and you would expect the cervix to be soft, effaced and possibly dilated. However, this could be another complication of pregnancy or even a non-gynaecological condition and these need to also be considered during the diagnostic work-up. An ultrasound scan, which is safe to use in pregnancy, should be done here.

25
Q

Diagnosis:
A 33 year old lady with no children has been suffering worsening pelvic pain particularly prior to menstruation and is now complaining of deep dysareunia.

A

Endometriosis

Endometriosis is a chronic inflammatory condition defined by endometrial stroma and glands located outside of the uterine cavity – the most common sites being the pelvic peritoneum and ovaries. It may present as an incidental finding in asymptomatic patients but more commonly it presents in women of reproductive age with chronic pelvic pain and/or subfertility. This woman has symptoms which make this diagnosis likely. There is dyspareunia which is pain during sexual intercourse, particularly on deep penetration, and may be caused by a distortion in the pelvic anatomy and rectovaginal involvement. There is also well documented genetic predisposition so a positive FH may be found. Additionally, nulliparous women are more likely to be diagnosed with endometriosis than parous women. The diagnosis can be confirmed on visualising the ectopic tissue directly and focused biopsies during laparoscopy but this is not generally necessary as clinical suspicion is enough to start treatment. Options for treatment include NSAIDs, COCPs, GnRH agonists, danazol or related androgens and surgical destruction of lesions. Those who present with subfertility may be considered for ovarian hyperstimulation and IVF.

26
Q

Diagnosis:
A 55 year old lady on HRT, complains of non-specific pelvic pain and occasional spotting of blood prioir to her withdrawal bleed on HRT.

A

Endometrial cancer

This is a common malignancy and is usually an adenocarcinoma. Obesity is associated with an increased incidence of endometrial cancer and also poorer outcome. Risk factors to consider aside from obesity include HRT, tamoxifen use, age over 50, unopposed oestrogen and radiotherapy. FH and a history of other cancers are also risks. A good history is important to establish that PV bleeding does not have another obvious cause such as intercourse or that associated with HRT, and that is is unlikely to be related to another malignancy like cervical cancer. Examination tends to be challenging due to the prevalence of obesity in those with endometrial cancer. The presentation is typically with post-menopausal bleeding PV and often the disease is surgically curable. Diagnosis will need to be confirmed by biopsy and histology with histopathology showing adenocarcinoma.

27
Q

Diagnosis:
A 35-year-old lady suffers of severe menorrhagia and pelvic pain. O/E she has tender, enlarged uterus. She underwent a total hysterectomy, pathology report confirmed diffuse fibromyomatous reaction with endometrial tissue within the myometrium.

A

Adenomyosis

Adenomyosis, as you can probably figure out from the name, is the presence of ectopic glandular tissue in muscle. The first test to order is a pelvic USS which shows a normal or enlarged uterus. It is of minimal diagnostic value, especially if the clinical history and examination findings are suggestive, but can be used to rule out endometriosis, where the USS may show the presence of ovarian endometriomas. Examination may reveal an enlarged globular uterus and uterine tenderness on palpation, particularly during the menses. The history is usually of a parous woman, symptoms commonly occuring after childbirth, with heavy menstrual flow or an abnormal bleeding pattern being seen. Adenomyosis is a condition which can be diagnosed clinically, although if a costly MRI pelvis is done, then abnormal signal intensities within the myometrium can be seen.

28
Q

Diagnosis:
An 18 year old student has just returned from holiday in Africa. He is jaundiced and has moderate hepatomegaly. His blood tests reveal increased serum transaminases and elevated bilirubin. He also has specific IgM antibodies.

A

Hepatitis A

gM anti-hepatitis A virus is positive here which is highly sensitive and specific combined with the typical symptoms this student displays. IgM antibodies are detectable typically 5-10 days before symptom onset and remain raised for 4-6 months. It can be ordered alongside IgG anti-HAV and is a cheap and simple test. IgG rises soon after IgM and stays elevated for life so a positive IgG can mean prior infection or recent disease. Again, a cheap and simple to carry out test.
Hepatitis A 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.

29
Q

Mgx:
A 23 year old woman presents with a cough and SOB for 24 hours. O/E she is distressed tahycardicc and resp raet of 25/min. She has a widespread bilateral expiratory wheeze.

A

Nebulised salbutamol

This patient is having an asthma attack. The best option here is nebulised salbutamol initially. Early systemic corticosteroids and supplemental oxygen should be considered and the patient’s status needs to be monitored regularly.

30
Q

Mgx:
A 30 year old teacher presents to her GP with a couch and SOB worsening over 24 hours. O/E she is pyrexial with no abnormal breath sounds. Her CXr shows bilateral shadowing. Her WCC is normal but she has abnormal liver function tests.

A

Oral clarithromycin

This is a CAP which is confirmed by CXR shadowing, which would show airspace shadowing with air bronchograms. The history is also consistent with respiratory symptoms and pyrexia. The most sensitive test for CAP is a CXR. The treatment is initially empirical with antibiotics and management would be guided by this patient’s CURB-65 score. A macrolide is the first choice in adults with no contra-indications without a recent cours eof antibiotics or risk of drug resistance, but always check local prescribing policies. Azithromycin, clarithromycin or erythromycin are all valid choices here.

31
Q

Mgx:
A 43 year old businessman, who has a history of alcohol dependence but has managed to stop drinking. He is afraid of relapsing during a forthcoming business trip and wants help to remain abstinent from alcohol.

A

Disulfiram

Disulfiram is used as an adjunct in the treatment of alcohol dependence. It leads to an unpleasant systemic reaction after taking even the smallest amount of alcohol as it causes acetaldehyde to accumulate in the body. Disulfiram blocks the metabolism of alcohol. It is only effective if taken daily and symptoms can occur within 10 minutes of ingesting any alcohol and include facial flushing, throbbing headache, palpitations, tachycardia, N&V and possible arrhythmias, hypotension and collapse with large doses of alcohol. These reactions can last several hours. Even the smallest amounts of alcohol in medications and even mouthwash can lead to a reaction. After stopping treatment, alcohol still should be avoided for at least a week. Other medications that can be used to prevent relapse and support abstinence include acamprosate (which stabilises glutamate and GABA systems) and naltrexone which is an opioid antagonist.

32
Q

Mgx:
A 25 year old male student drinks about 4 pints of beer a day, every day. He has no symptoms of alcohol dependency or physical problems. He is concerned his level of drinking may be harmful.

A

Physician advice

This (likely medical) student is not dependent nor does he have any physical symptoms but is concerned and aware that his drinking is harmful. At this stage he needs advice on the dangers of excessive alcohol consumption which is the first line intervention for those with patterns of problematic alcohol use but are not dependent (as well as those with mild dependence). The consultations can consist of one or more sessions with a doctor during which feedback can be given about the patient’s alcohol use and the consequences in a supportive and empathic manner. The doctor and patient can work together to develop an action plan for cutting down or eliminating alcohol use and then assessing how effective this is with subsequent visits. Motivational interviewing is a technique which can also be deployed in this situation.

33
Q

Diagnosis:
A 40 year old unmarried actor has noticed recent weight loss. Although he attributed this to stress you are concerned when you detect generalised lymphandenopathy. Blood count shows neutropenia and thrombocytopenia.

A

HIV

HIV is a retrovirus and there are two types, HIV 1 which is the main virus responsible and HIV 2 which is restricted to parts of West Africa. Weight loss is common in HIV and if more than 10% body weight is lost of BMI reduces to 18.5, this is an indication of more severe immunocompromise. Weight loss in HIV may result from malnutrition, co-existent TB infection or HIV wasting syndrome, the latter being an AIDS defining illness. Generalised lymphadenopathy is also common and is characterised by the painless enlargement of 2 more more non-contiguous sites of >1cm for >3 months. Neutropenia is also seen due to CD4 deficiency and thrombocytopenia may also be seen along with an anaemic picture.
There are WHO (stage 1-4) and CDC criteria used in clinical staging. This patient needs to have a CD4 count, HBV and HCV screen, VDRL (syphilis), tuberculin skin test (TB) and CXR. HIV viral load will also be assessed. Prophylaxis and immunisations should be considered against infections such as hepatitis, influenza, PCP and TB. When to initiate HAART depends on the clinical stage, CD4 and co-morbidities. This patient will need to be started on HAART. Classes of antiretrovirals include NRTIs, NNRTIs, protease inhibitors, fusion inhibitors and integrase inhibitors.

34
Q

Diagnosis:
A 70 year old man with a history of 10kg weight loss over the previous 3 months. More recently he developed acute lower back pain. Presents to A&E with coughing & sputum. CXR shows left lower lobe pneumonia.

A

Malignancy

This person likely has lung cancer which has resulted in the significant weight loss of 10kg. This is post-obstructive pneymonia which is common in lung cancer patients and is caused, most of the time, by a large and centrally obstructing tumour. It is essential to relieve this obstruction in this case and many techniques can be tried. There is also bone pain here in the lower spinal column which is due to metastases. The prognosis here is not good.

35
Q

Diagnosis:
The parents noticed that their 7-week baby has a lump in her neck. The swelling seems to come and go. O/E the lump is located in the posterior triangle of the neck, it transilluminates

A

Cystic hygroma

A cystic hygroma is a cystic lymphatic lesion which occurs as a congenital birth defect. It can arise anywhere but is classically found in the left posterior triangle of the neck and is the most common lymphangioma. There are large cyst like cavities in this lesion containing a watery fluid and as such it transilluminates. They are a benign lesion but can be disfiguring and is a condition which very rarely presents in adulthood, and tends to affect children. It can be seen as part of Noonan’s syndrome, which is an autosomal dominant disorder characteristically with short stature, chest deformity, congenital heart defects and unusual facial features.

36
Q

Diagnosis:
A 69-year-old lady noticed hard and painless lumps in her neck. She says it is slowly growing. She also mentions that her voice changed recently. The lumps are located mainly in the anterior triangle, deep to upper third of sternocleidomastoid.

A

Metastatic carcinoma

The voice change here suggests a primary laryngeal carcinoma which we assume here has metastasized locally and to lymph nodes in the deep cervical chain. The hard nature of the lumps, the fact they are painless and firm suggests cervical metastases which are more common in supraglottic cancer (glottic cancer has a much lower rate of cervical metastases). Cervical lymphadenopathy is common and the size, location, mobility and degree of firmness indicate the degree of progression of laryngeal malignancy. Hoarseness, dysphonia, sore throat, dysphagia, referred otalgia, vocal cord lesions and persistent neck mass/adenopathy for >3 weeks are sentinel signs of laryngeal cancer, which is frequently associated with smoking and alcohol use. An MDT approach is taken with the aim of treatment with organ preservation, with salvage surgical resection offered in advanced stage disease. The rate of organ preservation has significantly improved in the last 30 or so years.

37
Q

Diagnosis:
A 75-year-old gentleman complains of dyspnoea and orthopnoea. He has been increasingly tired and lethargic past few weeks.

A

Left heart failure

There are no expressed signs or symptoms of RVF here such as peripheral oedema, ascites, elevated JVP and hepatomegaly. Nocturia may be a symptom as fluid returns from the legs when the patient lies down flat. RVF leads to a backlog of blood and congestion of the systemic capillaries. LVF, on the other hand, causes congestion in the pulmonary circulation so the symptoms are respiratory. As seen in this patient, there is SOB and there may be the classic cough productive of frothy sputum – a sign of pulmonary oedema. On respiratory examination, pulmonary oedema due to LVF may give audible fine late inspiratory crepitations at the bases. 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’.
Initial investigations should include ECG, CXR, TTE and bloods including BNP levels. First line treatment is with an ACE inhibitor which reduces morbidity and mortality. Salt and fluid restriction is also beneficial. All patients with chronic heart failure will also receive a beta blocker such as carvedilol. Other adjuncts include spironolactone, diuretics, hydralazine and a nitrate, and digoxin. The NYHA classification criteria can be used based on symptoms to describe functional limitations and ranges from Class I to Class IV with symptoms occuring at rest. Many patients are asymptomatic for long periods of time because mild cardiac impairment is balanced by compensation.

38
Q

Diagnosis:

A pansystolic murmur in a 53-year-old gentleman with a drinking problem. There is a systolic thrill at the apex.

A

Mitral regurgitation

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. Mitral valve prolapse is a strong risk factor for development of MR. The alcohol history here is hinting at dilated cardiomyopathy as a possible cause.

39
Q

Diagnosis:
A 48 year old male presents with bruising, infections and fatigue. Lab findings indicate a pancytopenia with low reticulocyte count. Bone marrow biopsy is done on which a definitive diagnosis is made.

A

Aplastic anaemia

This is aplastic anaemia characterised here with the pancytopenia (which is common, but diagnosis requires 2 cytopenias out of 3) and the presentation with infections (neutropenia), fatigue (anaemia) and bruising (thrombocytopenia). Risk factors include paroxysmal noctural haemoglobinuria, hepatitis and NSAIDs. If macrocytosis is seen, this may suggest an inherited syndrome such as Fanconi’s anaemia. The reticulocyte count here rules out haemolytic anaemia. The definitive diagnosis is made on biopsy of bone marrow which shows a hypocellular marrow with no abnormal cell populations and no fibrosis. Which conditions would there be abnormal cell populations or fibrosis on bone marrow biopsy?

40
Q

Diagnosis:
A 50 year old man presents with weight loss, tiredness, fever, night sweats and abdominal pain. On examination his spleen was palpably enlarged and there were multiple bruises on his body. Investigations showed low Hb, WBC 150 x 109/L.

A

Chronic myeloid leukaemia

This is CML which tends to present in the 30-60 age group. At presentation 1/3 may be asymptomatic though if symptomatic, it presents with symptoms including fever, weight loss and night sweats. There is myeloid stem cell proliferation and presents with raised neutrophils, metamyelocytes and basophils. The patient may also describe LUQ discomfort or fullness due to the feeling of a mass due to splenomegaly. There are also symptoms of anaemia here due to BM infiltration of leukaemic cells. Bruises are common and are either spontaneous or from minor trauma. All patients have raised WCC.
CML is associated with the philadelphia chromosome characterised by t(9;22) of bcr-abl. There tends to be massive splenomegaly which is the most common physical finding on examination. This conditon may transform to AML or ALL in what is known as a ‘blast crisis’. CML responds to imatinib, which is an anti-bcr-abl antibody and gives long term remission in most patients.

41
Q

Causative organism:
A 30-year-old man presents jaundiced. He tells you he has recently completed a triathlon. He has been suffering from flu-like symptoms for the last week, he complains of severe headache, myalgia, anorexia. O/E he has tender hepatosplenomegaly and a rash over the lower limbs.

A

Leptospira interrogans

Leptospirosis is a zoonosis, which is transmitted by contact with urine of infected animals (also possible sources include blood and fluids). The history may reveal someone swimming in rat infested canal water, for instance, or in this case, a triathlon – which involves some swimming in perhaps not too clean water. Outbreaks of this are associated with flooding and natural disasters, as can be expected. Affected patients can present with an extensive spectrum of clinical manifestations ranging from subclinical illness in 90% to renal and hepatic failure and pulmonary haemorrhage. The important factor in diagnosis is a high index of suspicion based on epidemiological exposure. There is an acute phase with fever, headaches, myalgia and then an immune phase with additional pulmonary symptoms and potential organ damage (leading to the symptoms seen here such as jaundice). The rash is maculopapular and non-pruritic, lasting 1 or 2 days, present during the acute phase. It is rarely seen. Treatment is with benzylpenicillin or amoxicillion and/or doxycycline and supportive care. Those with severe disease carry a poor prognosis.

42
Q

Causative organism:
A 42-year-old presents with crampy abdominal pain, nausea and profuse diarrhoea a couple of days after eating grilled chicken in a newly opened restaurant. A gram stain of the faeces shows Gram-negative, motile, spiral-shaped rods.

A

Campylobacter jejuni

This is what we colloquially refer to as ‘food poisoning’ – infective gastroenteritis. The most common bacterial cause in the UK is Campylobactor jejuni. This organism is also a major cause of traveller’s diarrhoea. The second most common cause of acute enteritis is an organism known as Campylobacter coli. There is also Campylobacter fetus which is a rare cause of extra-intestinal infection mainly in immunocompromised patients. Campylobacters are small, gram negative rods with a curved spiral shape. 11 Campylobacters are pathogenic to humans. Most Campylobacter jejuni infections come from infected poultry. The diarrhoea is usually self limiting and resolves in a week – bacteraemia is very rare. Fluid and electrolyte replacement is essential. Only a small number of patients will benefit from antimicrobials. Note that C. jejuni is a commonly identified organism in the aetiology of Guillain-Barre syndrome.

43
Q

Diagnosis:
A 27-year-old with severe headaches and hypertension is found to have phaeochromocytoma. Further investigations reveal he has hypercalcaemia secondary to hyperparathyroidism. The alarmed clinician orders a thyroid biopsy which confirms his suspicions.

A

MEN II

MEN (Multiple Endocrine Neoplasia) syndromes are hereditary autosomal dominant tumour syndromes with distinct patterns of organ involvement. At this stage, the purely simplified patterns (classification is actually more complicated) you need to be familiar with are: MEN1 consists of parathyroid adenomas, pancreatic tumours and pituitary adenomas. MEN2A consists of parathyroid, medullary thyroid cancer and phaeochromocytoma. And MEN2B or 3 consists of what is seen in 2A plus the addition of a marfanoid phenotype and ganglioneuromas (intestinal and visceral).
Prophylactic thyroidectomy in childhood is indicated in MEN2. Medical management is aimed at controlling hormone hypersecretion. Surgery is often done on tumours. If you’re really interest, you can look MEN syndromes up in more detail. MEN1 is typically caused by mutations in the MEN1 gene whereas MEN2 is typically caused by mutations in the RET proto-oncogene.

44
Q

Diagnosis:
A 55-year-old lady has centripetal obesity, plethoric moon-shaped face, proximal muscle wasting. Her daughter says she is very lethargic and seems depressed lately. Blood show macrocytosis and raised gamma-GT. The serum cortisol is elevated and fails to suppress on low-dose-dexamethasone test. MRI of the head and CT of the body are normal

A

Pseudo-Cushing’s syndrome

Pseudo-Cushing’s syndrome is where a patient has all of the signs and symptoms and even abnormal hormone levels seen in Cushing’s syndrome however there is no problem to be found with the hypothalamo-pituitary-adrenal axis. It is hence idiopathic. Whole body CT here is normal so rules out causes from organs such as the lungs (ectopic ACTH), adrenals and MRI has also ruled out a pituitary cause.

45
Q

Diagnosis:
Previously well, 17-year-old girl presents with 3-months history of swelling of her right leg. There is no pain or other associated features. O/E you confirm pitting oedema of the shin, blood tests normal. Her mother also suffers from swollen legs.

A

Milroy’s disease

Milroy’s is primary lymphoedema with a familial autosomal dominant pattern of inheritance. It often presents in infancy. There is unfortunately no cure and treatment involves compression, with surgery reserved for those refractive to conservative measures and/or with major morbidity.

46
Q

Diagnosis:
A 27-year-old gentleman has a long history of frequent nose-bleeds. O/E of his nose you notice red spots on muous membrane. on his face and skin you can also notice some red spots.

A

Osler-Weber-Rendu Syndrome

This man has the facial telangiectasia of OWR, also called hereditary haemorrhagic telangiectasia. This causes abnormal blod vessels pretty much everywhere which are prone to bleed. It is an autosomal dominant condition so a positive FH can often be found.

47
Q

Diagnosis:
A 62-year-old diabetic lady presents with recurrent ulceration of the gaiter area of the left leg. The ulcer is well circumscribed, irregular in shape and of partial thickness. There is a brown discolouration and ‘eczema’ over both calves.

A

Venous Ulcer

Venous ulcers occur on a background of deep venous insufficiency. There is oedema and a brown skin discolouration due to leaching of pigments and haemosiderin deposition. In addition there may be lipodermatosclerosis and an inflammatory response, which is seen as an eczema-like thickening and hardening of the skin. The skin can also be drawn tightly around the ankle. Ulceration usually follows trauma and is usually on the medial gaiter region. The base has granulation tissue and is sloughy in nature and there is a sloping edge to the ulcer. The shape is often irregular. Look up some photos to help you remember. Once significant arterial disease is excluded (ulcers can have mixed components), the mainstay of treatment is with compression bandaging, appropriate dressings and treatment of any infection with antibiotics. Maggots can also be used and varicose veins should be treated where possible to reduce recurrence. If the ulcer is not healing, a biopsy should be considered (Marjolin’s ulcer).

48
Q

Diagnosis:
A 24-year-old lady from sub-Saharan Africa presents with a painful ulcer over the anterior shin of the left leg. ABPI is normal.

A

Sickle cell anaemia

Adults with sickle cell anaemia may present with leg ulcers although it has to be said that it is very unusual for a person with sickle cell disease to reach adulthood without being aware of their diagnosis. The adult patient could present with unexplained haemolysis, possible intermittent episodes of pain due to vaso-occlusive crises, avascular necrosis and retinal haemorrhage too. The doppler derived ankle-brachial pressure index is normal here which points away from peripheral arterial disease, which in this relatively young person is unlikely in any case. The typical constellation of findings of venous ulcers are not seen (oedema, lipodermatosclerosis).
In real medicine, as it is rare for sickle cell anaemia to present this late, I would consider other possibilities like pyoderma gangrenosum (which is arguably more likely in this case, given the location of the ulcer and age of the patient, so if this was your answer then you can give yourself a ‘real life medicine’ mark), but this is an EMQ (key point!) and the fact this lady is from the sub-Saharan Africa is a key fact. From an epidemiological perspective, the prevalence is 10-30% in sub-Saharan Africa. Between 25 and 30% of newborns in western Africa are carriers of sickle cell trait. This patient here will need to have their peripheral blood film reviewed following by haemoglobin electrophoresis and HPLC. Sickle solubility is a rapid test which can also be done but will not differentiate sickle trait from sickle disease.

49
Q

Diagnosis:
A 41-year-old man has a slowly growing circular ulcer over his right shin for a year now. The ulcers edges are raised and there is contact bleeding along one edge.

A

Squamous cell carcinoma

SCC is a malignant tumour of keratinocytes arising in the epidermis of the skin. Risk factors include UV exposure, older age, immunosuppression, fair skin, HPV and exposure to ionising radiation. The skin changes here are characteristic. Most frequently however, SCC often presents with multiple actinic keratoses, with a change in the lesion such as bleeding, induration, change in size and shape or inflammation. Aks and SCCs lie on a spectrum so it may be difficult to clinically differentiate the two. Skin biopsy will confirm the diagnosis. This can either be a shave biopsy, punch biopsy, incisional biopsy or excisional biopsy depending on the size and location.

50
Q

Diagnosis:
A 17-year-old girl recently started OCP. She presents with abdominal pain and, vomiting and tachycardia. She has developed left foot drop.

A

Porphyria

There are many types of porphyria. This patient has acute intermittent porphyria, which is characterised by symptoms like the ones this patient describes – abdominal pain, peripheral motor neuropathy, mental symptoms like confusion. These symptoms, certainly in EMQs, can be trigged by the use of certain drugs which are known to provoke AIP attacks. In reality, the list of drugs is pretty vast and include most CYP450 inducers, but in EMQs, alcohol and the OCP are common. It is worth noting that alcohol also induces an enzyme called delta-aminolevulinic acid synthase, which can exacerbate AIP. It is probably not worth learning the pathways unless you plan on sitting USMLE. AIP is a genetic disorder where there is a partial deficiency of PBGD (the third enzyme in the haem biosynthetic pathway). Treatment of acute attacks involves IV haem arginate with adjunctive dextrose IV. The pain is thought to be neuropathic in origin. The patient may complain of red/browny urine due to increased urinary excretion of intermediates in the haem pathway.

51
Q

Diagnosis:
A disabled 60 year-old lady lives on her own and rarely leaves her flat. She called an ambulance after becoming SOB while walking upstairs to her bedroom. O/E she has peripheral oedema up to the groin. She has painful feet and calves with mixed motor and sensory neuropathy. She is tachycardic, hypotensive, with raised JVP.

A

Beri-beri

Beriberi is vitamin B1 (thaimine) deficiency. Deficiency is the cause of several clinical syndromes including wet and dry beriberi and Wenicke’s encephalopathy. The presentation depends on the chronicity of B1 deficiency. Dry beriberi is a distal peripheral polyneuropathy characterised by parasthesia, reduced knee jerks and other tendon reflexes, and progressive severe weakness with muscle wasting secondary to chronic deficiency. Wet beriberi, which this person also has is secondary to either acute or chronic deficiency and is characterised by high-output heart failure with peripheral vasodilation, peripheral oedema and orthopnoea or low-output heart failure with lactic acidosis and peripheral cyanosis. The latter is also referred to as Shosin beriberi.
Remember that Wernicke’s is an acute neuropsychiatric syndrome which classically presents with the triad of acute confusion, ataxia and ocular abnormalities (such as nystagmus and strabismus) secondary to acute B1 deficiency.

52
Q

Diagnosis:
A 37-year-old man presents with 4-week history of progressive numbness and pain in his hands. O/E you notice multiple violaceous patches and evidence of peripheral sensory neuropathy.

A

HIV

HIV is a retrovirus and there are two types, HIV 1 which is the main virus responsible and HIV 2 which is restricted to parts of West Africa. Strong risk factors include needle sharing with IVDU, unprotected receptive intercourse, needle stick injury and high maternal viral load (mother to child). Kaposi’s sarcoma may present as a pink or violaceous patch on the skin or in the mouth and it is an AIDS-defining condition. Peripheral neuropathy is common and may be related either to HIV or some other medicine or toxin (some HAART can cause PN).
There are WHO (stage 1-4) and CDC criteria used in clinical staging. This patient needs to have a CD4 count, HBV and HCV screen, VDRL (syphilis), tuberculin skin test (TB) and CXR. HIV viral load will also be assessed. Prophylaxis and immunisations should be considered against infections such as hepatitis, influenza, PCP and TB. When to initiate HAART depends on the clinical stage, CD4 and co-morbidities. This patient will need to be started on HAART if he has not already. Classes of antiretrovirals include NRTIs, NNRTIs, protease inhibitors, fusion inhibitors and integrase inhibitors.

53
Q

Diagnosis:
A 31-year-old stuntman sustains a displaced spinal fracture with cord transaction at T12/L1 while performing a new trick. He also broken his left humerus and radius. He is stable but his BP remains 100/60 despite fluid resuscitation and his pulse is 55bpm.

A

Neurogenic shock

This is a thoracolumbar spine fracture. Neurogenic shock is not to be confused with spinal shock which is not circulatory in nature ( and is characterised by hypotonia or flaccidity that resolves within 24 hours). Neurogenic shock is a form of distributive shock due to spine or braintem injury and there is resulting failure of vasoregulation. As a result there is a fall in systemic vascular resistance with vasodilation, leading to low BP as blood pools in the extremeties where sympathetic tone is low. This is occasionally associated with bradycardia which is due to autonomic disruption

54
Q

Diagnosis:
A 72-year-old man underwent hip replacement surgery. 8 hours post-op his urine output has been 30ml, 20ml and 5ml over last 3hours. He is now anuric and seems lethargic. Other vital signs remain normal.

A

Urinary retention

This is clearly urinary retention. Urine output is gradually deteriorating in a step-wise manner and he is now anuric

55
Q

Diagnosis:
A 66-year old obese, smoker with T2DM presents drowsy to A&E. He has central abdominal pain radiating to the back that started around 5 hours before. He is tachycardic, tacypnoeic and his BP is 90/40 mmHg. Femoral pulses are faintly palpable and you can’t feel any pulses distally. His wife says his pulses are not palpable because of his peripheral vascular disease.

A

Haemorrhagic shock

This is a history of a ruptured AAA. He has key risk factors of obesity, smoking and T2DM. There is abdominal pain radiating to the back here and the low BP and compensatory tachycardia is due to the blood loss. This patient is in haemorrhagic shock. As this AAA has ruptured, this man will need urgent surgical repair, with of course standard resuscitation measures. The airway will needed to be managed with supplemental oxygen and ET intubation, a central venous catheter will need to be inserted, an arterial catheter and urinary catheter will also be needed for monitoring, and the target systolic BP is 50-70. Infusing too many gluids may increase the risk of death. The most effective form of surgical repair is an EVAR (endovascular AAA repair), anatomy permitting, otherwise traditional open repair is performed. Open repair has a mortality of 48%. Antibiotics will also be needed to cover bacteria to prevent graft infection. This will be prescribed in line with local protocols.

56
Q

Diagnosis:

Mr A.L is a 69-year-old who had oesophageal cancer underwent oesophagectomy.What kind of feed does he require?

A

Percutaneous jejunostomy

This patient needs nutritional support to prevent malnutrition and starvation. Enteral nutrition here is not possible as a chunk of the oesophagus has just been removed and we have to wait for an intact anastomosis. During surgery, a percutaneous jejunostomy can be placed to provide a temporary route of nutrition until oral feeding can resume. A surgeon at operation cannot place a percutaneous gastrostomy, and it is more suitable for prolonged feeding. Furthermore, in the immediate post-operative period, there may be gastric stasis so it is preferred to deliver the feed via a post-pyloric placement. If you have seen a PEG tube (percutaneous gastrostomy), you will know why it is not preferred. It is not a pleasant sight (and I don’t mean cosmetically – just have a look at the needle). Some younger people may ask for it to be converted to a button gastrostomy for cosmetic reasons. A PEG tube is placed laparoscopically.
A percutaneous jejunostomy is an alternative to parenteral (IV) nutrition in this post-operative patient. Parenteral nutrition is really a last resort and this is not an indication for it. Only when the GIT is either unavailable or function is indequate should you consider it. This can be delivered via a venflon, PICC line or centrally. There are a host of complications, both nutritionally, related to the catheter e.g. infection, thrombosis and the effect on organ systems e.g. biliary disease. Note that you should also be aware of the phenomenon known as refeeding syndrome.

57
Q

Diagnosis:
46-year-old woman with Crohn’s disease presents with oliguria for 3 days. She has also recently suffered from lower back pain.O/E she is hypertensive, the kidneys are palpable.

A

Retroperitoneal fibrosis

Retroperitoneal fibrosis is a rare disorder where there is proliferation of fibrous tissue in the retroperitoneum which here has caused the ureters to become obstructed. This has led to oliguria, back pain and the palpable kidneys. The cause could be an effect of antihypertensives, or due to malignancy or some other cause. A CT scan is the test to order here and treatment depends on severity and can be either surgical or medical, the latter generally with glucocorticoids followed by DMARDs.