Elevated haemoglobin A2 level is seen in beta thalassaemia trait, whereas, it is typically low in iron deficiency anaemia unless the patient has received a recent blood transfusion.

Low mean corpuscular volume (MCV) and reduced haematocrit (Ht) are encountered in both conditions. Peripheral blood smear is grossly abnormal in both beta thalassaemia and severe iron deficiency anaemia, showing bizarre morphology, target cells, and a small number of nucleated red blood cells.

The question describes an alcohol abusing man with chronic epigastric discomfort, radiating into his back, worse with meals, and foul-smelling stools, weight loss, as well as chronic nausea. This is likely, thus chronic pancreatitis due to alcohol abuse. Hepatomegaly and peripheral neuropathy secondary to anaemia support the diagnosis of long term alcohol abuse. Bacterial overgrowth may present with diarrhoea and is a less likely diagnosis than pancreatitis. Celiac disease is a less likely diagnosis than pancreatitis, and you would also expect mention of diarrhoea. VIPoma would also likely present with diarrhoea. Cecal carcinoma would more than likely present with blood in the stool.

The most probable diagnosis in this patient is serotonin syndrome.

The serotonin syndrome is a cluster of symptoms and signs (range from barely perceptible tremor to life-threatening hyperthermia and shock).
It may occur when SSRIs such as citalopram, escitalopram, fluoxetine, fluoxetine, paroxetine, and sertraline that impair the reuptake of serotonin from the synaptic cleft into the presynaptic neuron are taken in combination with monoamine oxidase inhibitors or tricyclic antidepressants. It has also been reported following an overdose of selective serotonin reuptake inhibitors (SSRIs) alone.

Treatment:
Most cases of serotonin syndrome are mild and will resolve with removal of the offending drug alone.
After stopping all serotonergic drugs, management is largely supportive and aimed at preventing complications.
Patients frequently require sedation, which is best facilitated with benzodiazepines.
Antipsychotics should be avoided because of their anticholinergic properties, which may inhibit sweating and heat dissipation.

Liver flap is pathognomonic for liver failure. Paracetamol (also known as acetaminophen) overdose usually presents with symptoms including liver failure, resulting in confusion, jaundice, and coagulopathy a few days after overdose. The first 24 hours, people usually have minimal symptoms. Diagnosis is based on blood levels of acetaminophen at specific times after it was taken (see reference). If she took it a few days ago, levels may indeed be undetectable. The hepatitis B serology suggests prior vaccination. Wilson’s disease is not the most likely diagnosis given her presentation. The AST:ALT ratio would be expected to be reversed in alcohol induced liver failure.

5-ASA is not an acute treatment; it is for maintenance therapy for ulcerative colitis and/or Crohn’s. The most benefit is seen in patients with ulcerative colitis.

Urinary porphobilinogen is increased between attacks of acute intermittent porphyria (AIP) and even more so, between acute attacks.

AIP is a rare autosomal dominant condition caused by a defect in porphobilinogen deaminase, an enzyme involved in the biosynthesis of haem. This results in the toxic accumulation of delta-aminolaevulinic acid and porphobilinogen.

Abdominal and neuropsychiatric symptoms are characteristic of AIP especially in people between the ages of 20–40 years. The disease is more common in females than in males (5:1). Major signs and symptoms of AIP include abdominal pain, vomiting, motor neuropathy, hypertension, tachycardia, and depression.

Diagnosis:
1. Urine turns deep red on standing (classical picture of AIP)
2. Raised urinary porphobilinogen (elevated between attacks and to a greater extent, between acute attacks)
3. Raised serum levels of delta-aminolaevulinic acid and porphobilinogen
4. Assay of red blood cells for porphobilinogen deaminase

All the above side-effects, with the exception of alopecia, may be seen in patients taking lithium.

Common lithium side effects may include:
– dizziness, drowsiness;
– tremors in your hands;
– trouble walking;
– dry mouth, increased thirst or urination;
– nausea, vomiting, loss of appetite, stomach pain;
– cold feeling or discoloration in your fingers or toes;
– rash; or.
– blurred vision.

The patient has a non-functioning pituitary tumour as her hormone profile is normal.
Non-functioning pituitary tumours are relatively common. A large number of these tumours are incidentally found pituitary microadenomas (<1 cm) and are usually of no clinical importance.

A couple of papers written by the same authors indicate that children and adolescents taking an SSRI definitely experience discontinuation reactions that can be mild, moderate or severe when the medication is stopped suddenly or high doses are reduced substantially. Among the SSRIs paroxetine seems to be the worst offender and fluoxetine the least while sertraline and fluvoxamine tend to be intermediate. The rate of discontinuation syndrome varies with the particular SSRI involved. It is generally quoted as 25% but is higher for SSRIs with shorter half-lives. Paroxetine has been associated with more frequent discontinuation symptoms than the other SSRIs.

The use of fluoxetine with its long half-life appears safer in this respect than paroxetine and venlafaxine causing the most concerns.

Paroxetine has the shortest half-life with 21 hours of all listed SSRIs and as such it would be expected to have a higher incidence or severity (greater number of symptoms) and fluoxetine would have the least since it has a half life of 96 hours. Citalopram has a half-life of 35 hours while escitalopram has a half-life of 30 hours.

The most common symptoms reported are: dizziness, light-headedness, drowsiness, poor concentration, nausea, headache and fatigue.
Another common symptom in adults is paraesthesia described as burning, tingling, numbness or electric shock feelings usually in the upper half of the body or proximal lower limbs.

Alveolar haemorrhage (AH) is a rare, but serious manifestation of SLE. It may occur early or late in disease evolution. Extrapulmonary disease may be minimal and may be masked in patients who are already receiving immunosuppressants for other symptoms of SLE.

DLCO or TLCO (diffusing capacity or transfer factor of the lung for carbon monoxide (CO)) is the extent to which oxygen passes from the air sacs of the lungs into the blood.
Factors that can increase the DLCO include polycythaemia, asthma (can also have normal DLCO) and increased pulmonary blood volume as occurs in exercise. Other factors are left to right intracardiac shunting, mild left heart failure (increased blood volume) and alveolar haemorrhage (increased blood available for which CO does not have to cross a barrier to enter).

Alpha1-antitrypsin (AAT) deficiency, first described in 1963, is one of the most common inherited disorders amongst white Caucasians. Its primary manifestation is early-onset of pan acinar emphysema. In adults, alpha1-antitrypsin deficiency leads to chronic liver disease in the fifth decade. As a cause of emphysema, it is seen in non-smokers in the fifth decade of life and during the fourth decade of life in smokers.

Symptoms of alpha1-antitrypsin (AAT) deficiency emphysema are limited to the respiratory system. Dyspnoea is the symptom that eventually dominates alpha1-antitrypsin deficiency. Similar to other forms of emphysema, the dyspnoea of alpha1-antitrypsin deficiency is initially evident only with strenuous exertion. Over several years, it eventually limits even mild activities.
The serum levels of some of the common genotypes are:
•PiMM: 100% (normal)
•PiMS: 80% of normal serum level of A1AT
•PiSS: 60% of normal serum level of A1AT
•PiMZ: 60% of normal serum level of A1AT, mild deficiency
•PiSZ: 40% of normal serum level of A1AT, moderate deficiency
•PiZZ: 10–15% (severe alpha 1-antitrypsin deficiency)

Infections of the superficial skin around the eyes are called periorbital, or preseptal, cellulitis. It is predominantly a paediatric disease. Erysipelas is a bacterial skin infection involving the upper dermis which extends into the superficial cutaneous lymphatics. Sinusitis is in sinuses. Orbital infections and conjunctivitis are within the eye.

Cyanide poisoning:
Aetiology:
Smoke inhalation, suicidal ingestion, and industrial exposure (specific industrial processes involving cyanide include metal cleaning, reclaiming, or hardening; fumigation; electroplating; and photo processing) are the most frequent sources of cyanide poisoning. Treatment with sodium nitroprusside or long-term consumption of cyanide-containing foods is a possible source.
Cyanide exposure most often occurs via inhalation or ingestion, but liquid cyanide can be absorbed through the skin or eyes. Once absorbed, cyanide enters the blood stream and is distributed rapidly to all organs and tissues in the body. 

Pathophysiology:
Inside cells, cyanide attaches itself to ubiquitous metalloenzymes, rendering them inactive. Its principal toxicity results from inactivation of cytochrome oxidase (at cytochrome a3), thus uncoupling mitochondrial oxidative phosphorylation and inhibiting cellular respiration, even in the presence of adequate oxygen stores.

Presentation:
• ‘Classical’ features: brick-red skin, smell of bitter almonds
• Acute: hypoxia, hypotension, headache, confusion
• Chronic: ataxia, peripheral neuropathy, dermatitis

Management:
• Supportive measures: 100% oxygen, ventilatory assistance in the form of intubation if required.
• Definitive: Hydroxocobalamin (iv) is considered the drug of choice and is approved by the FDA for treating known or suspected cyanide poisoning.
• Coadministration of sodium thiosulfate (through a separate line or sequentially) has been suggested to have a synergistic effect on detoxification.
Mechanism of action of hydroxocobalamin:
• Hydroxocobalamin combines with cyanide to form cyanocobalamin (vitamin B-12), which is renally cleared.
• Alternatively, cyanocobalamin may dissociate from cyanide at a slow enough rate to allow for cyanide detoxification by the mitochondrial enzyme rhodanese.

It should be noted that as a general rule 5-HT receptor agonists are used in the acute treatment of migraine whilst 5-HT receptor antagonists are used in prophylaxis. NICE produced guidelines in 2012 on the management of headache, including migraines. Prophylaxis should be given if patients are experiencing 2 or more attacks per month. Modern treatment is effective in about 60% of patients. NICE advises either topiramate or propranolol ‘according to the person’s preference, comorbidities and risk of adverse events’. Propranolol should be used in preference to topiramate in women of child bearing age as it may be teratogenic and it can reduce the effectiveness of hormonal contraceptives.

Weight gain is an extremely common (5-40%) adverse effect of atypical antipsychotics such as olanzapine (dose dependent). Olanzapine causes orthostatic hypotension ≥20% of reported cases. Parkinsonism reactions occurs in 4% of people.

Goserelin (Zoladex) is usually prescribed to treat hormone-sensitive cancers of the breast and prostate not for BPH. All other statements are correct.

Hypopyon can be seen in anterior uveitis, however the combination of a normal pupillary reaction and contact lens use make a diagnosis of keratitis more likely. Keratitis describes inflammation of the cornea, and features include red eye with pain and erythema, photophobia, and foreign body/gritty sensation.

Reactive arthritis, (formerly known as Reiter’s syndrome), is an autoimmune condition that occurs after a bacterial infection of the gastrointestinal or urinary tract. It is categorized as a seronegative spondylarthritis because of its association with HLA-B27. Reactive arthritis primarily affects young men and usually presents with musculoskeletal or extra‑articular symptoms. The characteristic triad consists of arthritis, conjunctivitis, and urethritis. Symmetric lower limb arthropathy and a sterile joint aspirate points towards reactive arthropathy.

The question describes a patient who has had an ileal resection. Bile acids are reabsorbed in the distal ileum. Since this has been resected in this patient, one would expect her to have malabsorption of bile acids, causing her diarrhoea. This is a more likely correct answer than a Crohn’s flare, bacterial overgrowth, gastroenteritis, or tropical sprue, given the details included in the question prompt.

Streptococcus pneumonia is the chief causative organism for lobar pneumonia in this age group patients. Typically patients present with rusty coloured sputum and a cough. Pneumocystis jiroveci is responsible for causing pneumocystis pneumonia among immunocompromised patients.

The most likely organism is enterohemorrhagic verotoxin-producing E.coli. It usually causes haemolytic uremic syndrome.
Crohn’s disease rarely manifests in an acute manner.
Polio and giardiasis usually manifest with non-bloody diarrhoea.

Ezetimibe is a cholesterol-lowering agent that acts to prevent cholesterol absorption by directly inhibiting cholesterol receptors on enterocytes.
It does not affect the absorption of drugs (e.g. digoxin, thyroxine) or fat-soluble vitamins (A, D and K) as the anion-exchange resins do. It does not affect the cytochrome P450 enzyme system.
The increased risk of myositis associated with the statins is not seen with ezetimibe.
The most common adverse effects include headache, runny nose, and sore throat.
Less common reactions include body aches, back pain, chest pain, diarrhoea, joint pain, fatigue, and weakness.

The most COMMON site of inflammation from ulcerative colitis is the rectum, making this the correct answer. This is simply a fact you need to memorize. In general, ulcerative colitis only occurs in colorectal regions– nothing in the small bowel (unless there is backwash into the terminal ileum) and nothing further up the GI tract. In Crohn’s it can affect the entire GI tract from mouth to anus.

Insulinoma is associated with LOW fasting glucose, HIGH insulin level, and HIGH C peptide. Insulin-abuse or overdose will cause HGH insulin levels and a LOW C peptide. If the C peptide is low, be suspicious.

Staph. aureus is the most likely cause. It is found in foods like dairy products, cold meats, or mayonnaise. It produces a heat-stable ENDOTOXIN (remember this) that causes nausea, vomiting, and diarrhoea 1-6 hours after ingestion of contaminated food. B. cereus is classically associated with fried rice being reheated. Salmonella is typical with raw eggs and undercooked poultry. Campylobacter which is most commonly associated with food poisoning, is seen with poultry 50% of the time. Yersinia enterocolitica is seen with raw or undercooked pork, and may be a case presenting with mesenteric adenitis.

Dacryocystitis is an infection of the lacrimal sac, secondary to obstruction of the nasolacrimal duct at the junction of lacrimal sac. It causes pain, redness, a watering eye (epiphora), and swelling and erythema at the inner canthus of the eye. Management is with systemic antibiotics. IV antibiotics are indicated if there is associated periorbital cellulitis.

The patient has small cell lung cancer presented by paraneoplastic syndrome; Ectopic ACTH secretion.

Small cell lung cancer (SCLC), previously known as oat cell carcinoma is a neuroendocrine carcinoma that exhibits aggressive behaviour, rapid growth, early spread to distant sites, exquisite sensitivity to chemotherapy and radiation, and a frequent association with distinct paraneoplastic syndromes.
Common presenting signs and symptoms of the disease, which very often occur in advanced-stage disease, include the following:
– Shortness of breath
– Cough
– Bone pain
– Weight loss
– Fatigue
– Neurologic dysfunction
Most patients with this disease present with a short duration of symptoms, usually only 8-12 weeks before presentation. The clinical manifestations of SCLC can result from local tumour growth, intrathoracic spread, distant spread, and/or paraneoplastic syndromes.
SIADH is present in 15% of the patients and Ectopic secretion of ACTH is present in 2-5% of the patients leading to ectopic Cushing’s syndrome.

This patient has a dendritic corneal ulcer. Herpes simplex keratitis most commonly presents with a dendritic corneal ulcer. Topical acyclovir and ophthalmology review is required. Giving a topical steroid in this situation could be disastrous as it may worsen the infection.

The presence of tinnitus, fever and hyperventilation are clues for aspirin (salicylate) toxicity.
Clinical Presentation of salicylate toxicity can include:
• Pulmonary manifestations include: Hyperventilation, hyperpnea, severe dyspnoea due to noncardiogenic pulmonary oedema, fever and dyspnoea due to aspiration pneumonitis
• Auditory symptoms caused by the ototoxicity of salicylate poisoning include: Hard of hearing and deafness, and tinnitus (commonly encountered when serum salicylate concentrations exceed 30 mg/dL).
• Cardiovascular manifestations include: Tachycardia, hypotension, dysrhythmias – E.g., ventricular tachycardia, ventricular fibrillation, multiple premature ventricular contractions, asystole – with severe intoxication, Electrocardiogram (ECG) abnormalities – E.g., U waves, flattened T waves, QT prolongation may reflect hypokalaemia.
• Neurologic manifestations include: CNS depression, with manifestations ranging from somnolence and lethargy to seizures and coma, tremors, blurring of vision, seizures, cerebral oedema – With severe intoxication, encephalopathy
• GI manifestations include: Nausea and vomiting, which are very common with acute toxicity, epigastric pain, GI haemorrhage – More common with chronic intoxication, intestinal perforation, pancreatitis, hepatitis – Generally in chronic toxicity; rare in acute toxicity, Oesophageal strictures – Reported as a very rare delayed complication
• Genitourinary manifestations include: Acute kidney injury (NSAID induced Nephropathy) is an uncommon complication of salicylate toxicity, renal failure may be secondary to multisystem organ failure.
• Hematologic effects may include prolongation of the prothrombin and bleeding times and decreased platelet adhesiveness. Disseminated intravascular coagulation (DIC) may be noted with multisystem organ failure in association with chronic salicylate toxicity.
• Electrolyte imbalances like: Dehydration, hypocalcaemia, acidaemia, Syndrome of inappropriate antidiuretic hormone secretion (SIADH), hypokalaemia
Management of these patients should be done in the following manner:
• Secure Airway, Breathing, and Circulation
• Supportive therapy
• GI decontamination
• Urinary excretion and alkalization
• Haemodialysis

The correct answer is patchy inflammation. Superficial ulceration as well as non-patchy inflammation are seen in ulcerative colitis (UC) in the colon and rectum; you would expect to see transmural inflammation in Crohn’s disease and it can be patchy and located anywhere from mouth to anus. Crypt distortion and crypt abscesses are seen in both UC and Crohn’s, however they are more common in ulcerative colitis.