B2-microglobulin is a useful marker of prognosis in multiple myeloma (MM). Raised levels imply a poorer prognosis. Low levels of albumin are also associated with a poor prognosis.

The given clinical scenario warrants urgent admission and psychiatric evaluation as the mother seems to be suffering from puerperal psychosis.

Post-partum mental health problems can range from the ‘baby-blues’ to puerperal psychosis.

The Edinburgh Postnatal Depression Scale may be used to screen for depression:
A 10-item questionnaire, with a maximum score of 30
indicates how the mother has felt over the previous week
score > 13 indicates a ‘depressive illness of varying severity’
sensitivity and specificity > 90%. It includes a question about self-harm

Postpartum psychosis has a complex multifactorial origin. Risk factors include a history of bipolar disorder, history of postpartum psychosis in a previous pregnancy, a family history of psychosis or bipolar disorder, a history of schizoaffective disorder or schizophrenia and discontinuation of psychiatric medications during pregnancy.
Incidence rate: 2.6 per 1000 births.
Onset usually within the first 2-3 weeks following birth
Symptoms of puerperal psychosis include confusion, lack of touch with reality, disorganized thought pattern and behaviour, odd effect, sleep disturbances, delusions, paranoia, appetite disturbances, a noticeable change in the level of functioning from baseline, hallucinations and suicidal or homicidal ideation.
The safety of the patient and new-born is of utmost importance, and thus, immediate hospitalization is warranted if there is a risk of harm to either one.
Cognitive-behavioural therapy may be beneficial. Certain SSRIs such as sertraline and paroxetine may be used if symptoms are severe – whilst they are secreted in breast milk it is not thought to be harmful to the infant
There is around a 20% risk of recurrence following future pregnancies

Only cystine stones are semi-opaque because they contain sulphur. All the other stones will appear either radio-lucent or radio-opaque.

This is a picture of bone marrow failure secondary to acute myeloid leukaemia (AML). AML is the acute expansion of the myeloid stem line, which may occur as a primary disease or follow the secondary transformation of a myeloproliferative disorder. It is more common over the age of 45 and is characterized by signs and symptoms largely related to bone marrow failure such as anaemia (pallor, lethargy), frequent infections due to neutropenia (although the total leucocyte count may be very high), thrombocytopaenia (bleeding), ostealgia, and splenomegaly.

The disease has poor prognosis if:
1. Age of the patient >60 years
2. >20% blasts seen after the first course of chemotherapy
3. Chromosomal aberration with deletion of part of chromosome 5 or 7.

Acute promyelocytic leukaemia (APL) is an aggressive form of AML.

Other listed options are ruled out because:
1. Von Willebrand disease: may present with epistaxis and bleeding gums in severe cases but rarely with abnormalities on blood results.

2. Acute lymphoblastic leukaemia: mostly seen in children.

3. Lymphoma: usually presents with rubbery enlargement of lymph nodes.

4. Warfarin overdose: no bilobed large mononuclear cells seen on blood film.

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.

Retinitis pigmentosa is a genetic disorder of the eyes that causes loss of vision. Symptoms include trouble seeing at night and decreased peripheral vision. Onset of symptoms is generally gradual.
– In keratitis, there will be pain, redness and photophobia but vision is not affected
– In macular degeneration, near blindness does not occur rather the inability to identify faces or read small print
– Cataracts are more common in elderly
– It is not angle closure glaucoma as angle closure glaucoma occurs usually after the age of 50; In open angle glaucoma visual loss is not gradual but rather occurs suddenly following progression

Myc is a family of regulator genes and proto-oncogenes that code for transcription factors.

A tumor suppressor gene, or antioncogene, is a gene that protects a cell from one step on the path to cancer. When this gene mutates to cause a loss or reduction in its function, the cell can progress to cancer, usually in combination with other genetic changes. Tumor suppressor genes can be grouped into categories including caretaker genes, gatekeeper genes, and landscaper genes; the classification schemes are continually evolving.
Examples include:
Gene Associated cancers
p53 Common to many cancers, Li-Fraumeni syndrome
APC Colorectal cancer
BRCA1 Breast and ovarian cancer
BRCA2 Breast and ovarian cancer
NF1 Neurofibromatosis
Rb Retinoblastoma
WT1 Wilm’s tumour

The pons is above the level of decussation of the corticospinal tracts so a pontine lesion would cause a contralateral limb weakness.
The facial motor nucleus is located in the pons and supplies the ipsilateral facial muscles.
A right cerebral lesion would give left upper and lower limb weakness. It would also cause a left sided facial weakness.
A left cerebral lesion would give right upper and lower limb weakness with right facial weakness.
Finally, a cervical spinal cord lesion would not cause a facial weakness.

Pneumococcal meningitis is the most common and severe form of bacterial meningitis. Fatality rates are substantial, and long-term sequelae develop in about half of survivors. Disease outcome has been related to the severity of the proinflammatory response in the subarachnoid space. The complement system, which mediates key inflammatory processes, has been implicated as a modulator of pneumococcal meningitis disease severity in animal studies. C5 fragment levels in cerebrospinal fluid (CSF) of patients with bacterial meningitis correlated with several clinical indicators of poor prognosis. The common terminal pathway consists of complement components C5–C9, and activation forms the anaphylatoxin C5a, a strong proinflammatory mediator, and the membrane attack complex (MAC), which creates pores in the bacterial cell wall (12). Deficiencies in these late complement components have been recognized as a cause of recurrent and familial meningococcal infections.

The farmer has most likely ingested an organophosphate insecticide.
Organophosphorus compounds are used widely as:
• Insecticides – Malathion, parathion, diazinon, dichlorvos
• Nerve gases – Soman, sarin, tabun, VX
• Ophthalmic agents – Echothiophate
• Antihelmintics – Trichlorfon
• Herbicides – merphos
• Industrial chemical (plasticizer) – Tricresyl phosphate
Signs and symptoms of Organophosphorus Poisoning (OPP) can be classified as:
• Muscarinic effects:
o Cardiovascular – Bradycardia, hypotension
o Respiratory – Rhinorrhoea, bronchorrhea, bronchospasm, cough, severe respiratory distress
o Gastrointestinal – Hypersalivation, nausea and vomiting, abdominal pain, diarrhoea, faecal incontinence
o Genitourinary – Incontinence
o Ocular – Blurred vision, miosis
o Glands – Increased lacrimation, diaphoresis
• Nicotinic effects:
o Muscle fasciculation, weakness, cramping, diaphragmatic failure, and autonomic side effects include: hypertension, tachycardia, and mydriasis.
• Central nervous system (CNS) effects:
o Anxiety, emotional lability, restlessness, confusion, ataxia, tremors, seizures, coma, apnoea
Mainstay Treatment:
• Decontamination
• Securing Airway, Breathing and Circulation
• Atropine
• Pralidoxime
• Benzodiazepines

Pacemaker spikes on the ECG indicate that pacemaker is functioning. The most probable cause for this presentation is the change of the position of the tip of the pacing wire. Increasing the voltage will solve the problem. If it works, repositioning of the pacing wire should be done.

Acute angle closure glaucoma is associated with hypermetropia, whereas primary open-angle glaucoma is associated with myopia. Glaucoma is a group of eye disorders characterised by optic neuropathy due, in the majority of patients, to raised intraocular pressure (IOP). It is now recognised that a minority of patients with raised IOP do not have glaucoma and vice versa.

The best option would be the combination of ampicillin and gentamycin. Changing to IV amoxicillin+gentamycin is however the best among the given choices here.

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.

Illness anxiety disorder (IAD) is a recent term for what used to be diagnosed as hypochondriasis, or hypochondrial disorder. People diagnosed with IAD strongly believe they have a serious or life-threatening illness despite having no, or only mild, symptoms.

Symptoms of IAD may include:
-Excessive worry over having or getting a serious illness.
-Physical symptoms are not present or if present, only mild. If another illness is present, or there is a high risk for developing an illness, the person’s concern is out of proportion.
-High level of anxiety and alarm over personal health status.
-Excessive health-related behaviours (e.g., repeatedly checking body for signs of illness) or shows abnormal avoidance (e.g., avoiding doctors’ appointments and hospitals).
-Fear of illness is present for at least six months (but the specific disease that is feared may change over that time).
-Fear of illness is not due to another mental disorder.

Arthritis mutilans is a rare (occurs in only 5% of the patients) and extremely severe form psoriatic arthritis characterized by resorption of bones and the consequent collapse of soft tissue. When this affects the hands, it can cause a phenomenon sometimes referred to as ‘telescoping fingers.’ The associated nail changes are also characteristic of arthritis.

Flashes and floaters are symptoms of vitreous detachment. The patient is at risk of retinal detachment and should be referred urgently to an ophthalmologist.

The most common causes of a sudden painless loss of vision are as follows:
– Ischaemic optic neuropathy (e.g. temporal arteritis or atherosclerosis)
– Occlusion of central retinal vein
– Occlusion of central retinal artery
– Vitreous haemorrhage
– Retinal detachment

Methemoglobinemia is a rare condition in which the haemoglobin iron is in oxidized or ferric state (Fe3+) and cannot reversibly bind oxygen. Normally, the conversion of ferrous form of iron (Fe2+) to its ferric form (Fe3+) is regulated by NADH methaemoglobin reductase, which results in the reduction of methaemoglobin to haemoglobin. Disruption in the enzyme leads to increased methaemoglobin in the blood. There is tissue hypoxia as Fe3+ cannot bind oxygen, and hence the oxygen-haemoglobin dissociation curve is shifted to the left.

Methemoglobinemia can occur due to congenital or acquired causes. Congenital causes include haemoglobin variants such as HbM and HbH, and deficiency of NADH methaemoglobin reductase. Acquired causes are drugs (e.g. sulphonamides, nitrates, dapsone, sodium nitroprusside, and primaquine) and chemicals (such as aniline dyes).

The features of methemoglobinemia are cyanosis, dyspnoea, anxiety, headache, severe acidosis, arrhythmias, seizures, and loss of consciousness. Patients have normal pO2 but oxygen saturation is decreased. Moreover, presence of chocolate-brown coloured arterial blood (colour does not change with addition of O2) and brown urine also point towards the diagnosis of methemoglobinemia.

Aortic dissection is defined as separation of the layers within the aortic wall. Tears in the intimal layer result in the propagation of dissection (proximally or distally) secondary to blood entering the intima-media space. This can be caused as a result of both congenital or acquired factors like chronic uncontrolled hypertension. This patient shows no sign of hypertension but his physical examination hints towards Marfan Syndrome. Marfan syndrome (MFS) is an autosomal dominant connective tissue disorder affecting the microfibrils and elastin in connective tissue throughout the body. MFS is associated with pathological manifestations in the cardiovascular system (e.g., mitral valve prolapse, aortic aneurysm, and dissection), the musculoskeletal system (e.g., tall stature with disproportionately long extremities, joint hypermobility), and the eyes (e.g., subluxation of the lens of the eye). Decreased collagen production occurs in ageing, hydroxylation defects are present in vitamin C deficiency, copper deficiency affecting lysyl oxidase enzyme occurs in Menke’s disease.

Rasburicase is a recombinant version of urate oxidase which is an enzyme that metabolizes uric acid to allantoin.

TLS is a potentially fatal condition occurring as a complication during the treatment of high-grade lymphomas and leukaemias. It occurs from the simultaneous breakdown (lysis) of the tumour cells and subsequent release of chemicals into the bloodstream. This leads to hyperkalaemia and hyperphosphatemia in the presence of hyponatraemia. TLS can occur in the absence of chemotherapy, but it is usually triggered by the introduction of combination chemotherapy. Awareness of the condition is critical for its prophylactic management.

Patients at high risk of TLS should be given IV rasburicase or IV allopurinol immediately prior to and during the first few days of chemotherapy. Allantoin is much more water soluble than uric acid and is therefore more easily excreted by the kidneys. Patients in lower-risk groups should be given oral allopurinol during cycles of chemotherapy in an attempt to avoid the condition.

TLS is graded according to the Cairo-Bishop scoring system as:
1. Laboratory tumour lysis syndrome
2. Clinical tumour lysis syndrome

The likely diagnosis in this case is Haemolytic Uremic Syndrome (HUS), which is generally seen in young children presenting with a triad of symptoms, namely: acute renal failure, microangiopathic haemolytic anaemia, and thrombocytopenia. The typical cause of HUS is ingestion of a strain of Escherichia coli causing diarrhoea in these cases as well.

Angioid retinal streaks are seen on fundoscopy as irregular dark red streaks radiating from the optic nerve head. They are caused by degeneration, calcification and breaks in Bruch’s membrane. They are typically associated with Paget’s disease.

ACE inhibitors are known to cause a dry cough and they should be stopped, to settle the cough. The next drug of choice is an angiotensin receptor blocker such as candesartan.

Annual incidence of DVT in the general population is about 1 per 1000 adults. So the most suitable answer is about 2 per 1000.

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.

Churg-Strauss disease (CSD) is one of three important fibrinoid, necrotizing, inflammatory leukocytoclastic systemic small-vessel vasculitides that are associated with antineutrophil cytoplasm antibodies (ANCAs).
The first (prodromal) phase of Churg-Strauss disease (CSD) consists of asthma usually in association with other typical allergic features, which may include eosinophilia. During the second phase, the eosinophilia is characteristic (see below) and ANCAs with perinuclear staining pattern (pANCAs) are detected. The treatment would therefore be different from asthma. For most patients, especially those patients with evidence of active vasculitis, treatment with corticosteroids and immunosuppressive agents (cyclophosphamide) is considered first-line therapy

Activated charcoal is useful if given within one hour of the paracetamol overdose. Liver function tests, INR and prothrombin time will be normal, as liver damage may not manifest until 24 hours or more after ingestion.

The antidote of choice is intravenous N-acetylcysteine, which provides complete protection against toxicity if given within 10 hours of the overdose.

Scabies is due to an infestation of Sarcoptes scabiei and most commonly presents with these symptoms. The organism resides in burrows in a pattern specifically affecting the interdigital spaces and the skin folds of the arms and legs. The infection spreads from one person to another, especially in populated communities, through close contact.
Henoch-Schönlein purpura is a type of vascular inflammation.
Psoriasis rash is characterised by scaly plaques affecting the extensor surfaces of the body. Pemphigus vulgaris and bullous pemphigoid both are bullous disorders of the skin. They may present as crusted, weeping, diffuse lesions and there may be involvement in other sites; erosions in the mouth are typically involved in pemphigus vulgaris. Bullous pemphigoid involves the flexural areas and may be associated with a new medication.

Classic Kallmann syndrome (KS) is due to isolated hypogonadotropic hypogonadism. Most patients have gonadotropin-releasing hormone (GnRH) deficiency, as suggested by their response to pulsatile GnRH therapy. The hypothalamic-pituitary function is otherwise normal in most patients, and hypothalamic-pituitary imaging reveals no space-occupying lesions. By definition, either anosmia or severe hyposmia is present in patients with Kallmann syndrome.

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.