Diseases that cause predominantly sensory loss include diabetes, uraemia, leprosy, alcoholism, vitamin B12 deficiency, and amyloidosis.
Those that cause predominantly motor loss include Guillain-Barre syndrome, porphyria, lead poisoning, hereditary sensorimotor neuropathies, chronic inflammatory demyelinating polyneuropathy, and diphtheria.

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.

The major endocrine functions of adrenal gland are to produce catecholamines and steroids. Catecholamine, synthesized by the adrenal medulla, is responsible for blood pressure and blood flow regulation whereas steroids produced by the cortex control energy and water homeostasis and immune responses. Glucocorticoids, a major group of adrenal steroids, have a stimulatory effect on catecholamine synthesis in the medulla.

Hypersegmented neutrophils in the peripheral blood film is suggestive of megaloblastic changes in bone marrow.

The patient has Acromegaly.
Acromegaly is a chronic disorder characterised by growth hormone (GH) hypersecretion, predominantly caused by a pituitary adenoma.

Random GH level testing is not recommended for diagnosis given the pulsatile nature of secretion. Stress, physical exercise, acute critical illness and fasting state can cause a physiological higher peak in GH secretion.

Pegvisomant is a US Food and Drug Administration-approved treatment for use after surgery. In a global non-interventional safety surveillance study, pegvisomant normalised IGF-1 in 67.5% of patients after 5 years (most likely due to lack of dose-up titration), and also improved clinical symptoms. Pegvisomant improves insulin sensitivity, and long-term follow-up showed significantly decreased fasting glucose over time, while the first-generation SRL only have a marginal clinical impact on glucose homeostasis in acromegaly. Pegvisomant does not have any direct anti-proliferative effects on pituitary tumour cells, but tumour growth is rare overall.

Salbutamol stimulates beta-2 adrenergic receptors, which are the predominant receptors in bronchial smooth muscle (beta-2 receptors are also present in the heart in a concentration between 10% and 50%).

Stimulation of beta-2 receptors leads to the activation of enzyme adenyl cyclase that forms cyclic AMP (adenosine-mono-phosphate) from ATP (adenosine-tri-phosphate). This increase of cyclic AMP relaxes bronchial smooth muscle and decrease airway resistance by lowering intracellular ionic calcium concentrations. Salbutamol relaxes the smooth muscles of airways, from trachea to terminal bronchioles.

Increased cyclic AMP concentrations also inhibits the release of bronchoconstrictor mediators such as histamine and leukotriene from the mast cells in the airway.

Thioridazine has a quinidine-like action on the heart and is known to cause cardiac arrhythmias including prolonged PR and QT intervals and widening of QRS complexes. Intravenous magnesium sulphate is regarded as the treatment of choice for this arrhythmia.

The patient most likely has Klinefelter’s syndrome.
Klinefelter syndrome (KS) refers to a group of chromosomal disorders in which the normal male karyotype, 46,XY, has at least one extra X chromosome. XXY aneuploidy, the most common human sex chromosome disorder. It is also the most common chromosomal disorder associated with male hypogonadism and infertility.
Klinefelter syndrome is characterized by hypogonadism (micro-orchidism, oligospermia/azoospermia), gynecomastia in late puberty, hyalinization and fibrosis of the seminiferous tubules, elevated urinary gonadotropin levels, and behavioural concerns.

Mild cases are often not treated at all, or are simply covered up with normal cosmetics and avoiding sun exposure. Therapy for the treatment of rosacea is not curative, and is best measured in terms of reduction in the amount of facial redness and inflammatory lesions. The two primary modalities of rosacea treatment are topical and oral antibiotic agents (including metronidazole and tetracyclines). Laser therapy may be appropriate for patients with prominent telangiectasia.

Of all the listed options, gastric cancer is least likely to be inherited.

The above mentioned tumours are ruled out as explained below:
1. Breast and Ovarian cancers: Between 5%–10% of all breast cancers are thought to be hereditary. Mutation in the BRCA1 and BRCA2 genes also increase the risk of ovarian cancer.

2. Colorectal and Endometrial cancers: About 5% of cases of colorectal cancer are caused by hereditary non-polyposis colorectal carcinoma (HNPCC) and 1% are due to familial adenomatous polyposis. Women who have HNPCC also have a markedly increased risk of developing endometrial cancer—around 5% of endometrial cancers occur in women with this risk factor.

The history is suggestive of hypertrophic obstructive cardiac myopathy. The degree of left ventricular hypertrophy is strongly associated with sudden cardiac death.

Lymphedema is most commonly the result of removal or damage to lymph nodes.

Absolute risk reduction (ARR) – also called risk difference (RD) – is the most useful way of presenting research results to help your decision-making. In this example, the ARR is 8 per cent (20 per cent – 12 per cent = 8 per cent). This means that, if 100 children were treated, 8 would be prevented from developing bad outcomes. Another way of expressing this is the number needed to treat (NNT). If 8 children out of 100 benefit from treatment, the NNT for one child to benefit is about 13 (100 ÷ 8 = 12.5). CER = 20 / 400 = 1 / 20 = 0.05, EER = 10 / 400 = 0.025, ARR =CER – EER = 0.025

Given her history of bowel resections, the most likely answer in this case is short bowel syndrome. IBS is a diagnosis of exclusion and less likely. Bacterial overgrowth does not relate to resection history, so unlikely. Celiac disease or a flare of IBD are also less likely than short bowel syndrome in this case, simply given the history. Also her labs are normal making these unlikely. History, history, history!

A t test is a type of statistical test that is used to compare the means of two groups. It is one of the most widely used statistical hypothesis tests in pain studies. There are two types of statistical inferences: parametric and nonparametric methods. Parametric methods refer to a statistical technique in which one defines the probability distribution of probability variables and makes inferences about the parameters of the distribution. In cases in which the probability distribution cannot be defined, nonparametric methods are employed. T tests are a type of parametric method; they can be used when the samples satisfy the conditions of normality, equal variance, and independence. In this case the data is parametric, comparing two independent samples from the same population.

There are five prognostic factors which indicate poor prognosis in HOCM:
-family history of HOCM-related sudden cardiac death
-unexplained recent syncope
-large left ventricular wall thickness (MLVWT ≥ 30 mm)
-multiple bursts of nsVT on ambulatory electrocardiography
-hypotensive or attenuated blood pressure response to exercise

Type I pneumocyte: The cell responsible for the gas (oxygen and carbon dioxide) exchange that takes place in the alveoli. It is a very thin cell stretched over a very large area. This type of cell is susceptible to a large number of toxic insults and cannot replicate itself.
Type II pneumocyte: The cell responsible for the production and secretion of surfactant (the molecule that reduces the surface tension of pulmonary fluids and contributes to the elastic properties of the lungs). The type 2 pneumocyte is a smaller cell that can replicate in the alveoli and will replicate to replace damaged type 1 pneumocytes. Alveolar macrophages are the primary phagocytes of the innate immune system, clearing the air spaces of infectious, toxic, or allergic particles that have evaded the mechanical defences of the respiratory tract, such as the nasal passages, the glottis, and the mucociliary transport system. The main role of goblet cells is to secrete mucus in order to protect the mucous membranes where they are found. Goblet cells accomplish this by secreting mucins, large glycoproteins formed mostly by carbohydrates.

People with polyarteritis nodosa often exhibit anaemia of chronic disease. Leucocytosis and eosinophilia may also be present. ANCA is only rarely positive. As polyarteritis nodosa affects the kidneys as well, the creatinine is elevated in most cases.

Post-primary pulmonary tuberculosis is a chronic disease commonly caused by either endogenous reactivation of a latent infection or exogenous re-infection by Mycobacterium tuberculosis.
Post-primary pulmonary tuberculosis (also called reactivation tuberculosis) develops in 5%–20% of patients infected with M. tuberculosis.

Found mainly in adults, this form of tuberculosis arises from the reactivation of bacilli that lay dormant within a fibrotic area of the lung. In adults, reinfection with a strain of mycobacterium that differs from that which caused the primary infection is also possible. Predisposing factors include immunosuppression, diabetes, malnutrition and alcoholism.

Infliximab is a monoclonal antibody against tumour necrosis factor α (TNF-α). It is FDA approved for many autoimmune conditions, including rheumatoid arthritis and Crohn’s disease. One of the many known side effects of infliximab therapy is reactivation of latent tuberculosis (TB). Because of the resemblances in clinical and radiological features, tubercular lesions in the lung may mimic malignancy. TB accounts for 27% of all infections initially presumed to be lung cancer on imaging studies.

Memantine is an antagonist of the NMDA (N-Methyl-D-Aspartate)-receptor subtype of glutamate receptor. It is used to slow the neurotoxicity thought to be involved in Alzheimer’s disease and other neurodegenerative diseases.

Drug interactions:
When given concomitantly with other NMDA-receptor antagonists (e.g., ketamine, amantadine) increase the risk of psychosis.
Dopamine agonists, L-dopa, and anticholinergics enhance effects of memantine.
Antispasmodics (e.g., baclofen)  enhance effects, as memantine has some antispasmodic effects.
Drugs excreted by cationic transporters in the kidney (e.g. quinine, cimetidine, ranitidine) reduce excretion.

Common adverse effects include dizziness, headache, confusion, diarrhoea, and constipation.

Acute, symptomatic hypocalcaemia is treated with 10ml of 10% calcium gluconate over 10 minutes.

Fundoscopy findings of cotton wool spots and retinal tears, accompanied by a history of blurred vision, are characteristic of retinitis. Cytomegalovirus is known to cause retinitis.

The right and left lung anatomy are similar but asymmetrical. The right lung consists of three lobes: right upper lobe (RUL), right middle lobe (RML), and right lower lobe (RLL). The left lung consists of two lobes: right upper lobe (RUL) and right lower lobe (RLL). The right lobe is divided by an oblique and horizontal fissure, where the horizontal fissure divides the upper and middle lobe, and the oblique fissure divides the middle and lower lobes. In the left lobe there is only an oblique fissure that separates the upper and lower lobe.

The lobes further divide into segments which are associated with specific segmental bronchi. Segmental bronchi are the third-order branches off the second-order branches (lobar bronchi) that come off the main bronchus.

The right lung consists of ten segments. There are three segments in the RUL (apical, anterior and posterior), two in the RML (medial and lateral), and five in the RLL (superior, medial, anterior, lateral, and posterior). The oblique fissure separates the RUL from the RML, and the horizontal fissure separates the RLL from the RML and RUL.

There are eight to nine segments on the left depending on the division of the lobe. In general, there are four segments in the left upper lobe (anterior, apicoposterior, inferior and superior lingula) and four or five in the left lower lobe (lateral, anteromedial, superior and posterior). The medium sized airways offer the maximum airway resistance, not smaller ones.

Azathioprine therapy can cause acute myelosuppression. Toxicity is in part caused by the incorporation of azathioprine-derived 6-thioguanine nucleotides (6-TGN) into deoxyribonucleic acid (DNA). The enzyme thiopurine methyltransferase (TPMT) plays an important role in azathioprine catabolism.

Anti-TNF-α therapy is effective for patients with arthritis but it can oftentimes lead to the reactivation of latent TB. Hence it should be used with great caution in patients with a past history of TB or current infection.

Drug induced lupus typically presents with pulmonary involvement and no renal or neurological involvement. Hence glomerulonephritis would be highly unlikely in this case. Rash and arthralgias are classic presentations. Pleurisy can be present as pulmonary involvement may occur with DILE.

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 patient’s history points to absence seizures. Carbamazepine has been shown to aggravate generalized seizure types, especially absence seizures, because it acts directly on the ventrobasal complex of the thalamus which is critical to the neurophysiology of absence seizures.

To confirm the diagnosis, especially in patients with negative anti-Ro or anti-La antibodies, labial gland biopsy is done. In performing a labial biopsy, the surgeon typically makes a shallow 1/2 inch wide incision on either side of the inner lip after numbing the area with a local anaesthetic. Schirmer’s test determines whether the eye produces enough tears to keep it moist. This test can be done for ocular symptoms of Sjogren syndrome but is of no diagnostic importance as it can be positive with many other diseases.

Pseudomembranous colitis is caused by a C. difficile infection that causes membranes to form on the colon wall. It is caused most commonly by broad-spectrum antibiotics. This would include cephalosporins, broad-spectrum penicillin, and clindamycin. Macrolides and quinolones have also been reported as potential aetiologies, but much less commonly.