The patient is most likely to have Postpartum thyroiditis which goes through 2 phases; hypothyroid and a hyperthyroid phase.
The hyperthyroid phase of postpartum thyroiditis occurs between 2 and 10 months postpartum. Most commonly, it presents at 3 months. Symptoms more common in women with hyperthyroid postpartum thyroiditis include palpitations, fatigue, heat intolerance, and irritability/nervousness. The frequency of asymptomatic hyperthyroidism is 33%.
Untreated, the hyperthyroidism resolves spontaneously within 2–3 months. This phase is diagnosed by the combination of a low serum TSH concentration in the presence of thyroid peroxidase antibodies, in women who are TSH receptor antibody-negative. Free T4 levels are typically elevated but may be normal.
Treatment of hyperthyroidism, when necessary, is based on symptom severity and should be a joint decision of patient and physician. Beta-blockers such as propranolol are given to alleviate palpitations, irritability, and nervousness. The morbidity associated with treatment is the side effects of beta-blockade. The downside of withholding treatment is allowing the woman to remain symptomatic. Antithyroid medicines (thioureas) are not a potential treatment alternative, because the hyperthyroidism is caused by destructive thyroiditis resulting in the release of preformed thyroid hormone.

Hypocalcaemia occurs in patients with impaired function of the parathyroid glands. This is most common after thyroid or parathyroid surgery, but it can be idiopathic—mostly in young adults and less often as part of a genetic syndrome, such as autoimmune polyglandular syndrome type 1. Usually, the first and most useful test to perform in such cases is the measurement of the parathyroid hormone.

This scenario is suggestive of a pancreatic head mass with obstructive jaundice and US showing a ‘double duct’ sign. A CT Scan would be recommended to evaluate for a pancreatic head mass. If a mass was found, the next step would then be to do an ERCP with EUS to obtain a biopsy of the mass for tissue diagnosis. Laparoscopy would not be recommended. CA19-9 would not be diagnostic.

A single dose of intravenous magnesium sulphate is safe and may improve lung function and reduce intubation rates in patients with acute severe asthma. Intravenous magnesium sulphate may also reduce hospital admissions in adults with acute asthma who have had little or no response to standard treatment.

Consider giving a single dose of intravenous magnesium sulphate to patients with acute severe asthma (PEF <50% best or predicted) who have not had a good initial response to inhaled bronchodilator therapy. Magnesium sulphate (1.2–2 g IV infusion over 20 minutes) should only be used following consultation with senior medical staff.

Achondroplasia is a common cause of dwarfism. It is caused by a mutation in fibroblast growth factor receptor 3 (FGFR3). In normal development FGFR3 has a negative regulatory effect on bone growth. In achondroplasia, the mutated form of the receptor is constitutively active and this leads to severely shortened bones. The effect is genetically dominant, with one mutant copy of the FGFR3 gene being sufficient to cause achondroplasia, while two copies of the mutant gene are invariably fatal. A person with achondroplasia thus has a 50% chance of passing dwarfism to each of their offspring. People with achondroplasia can be born to parents that do not have the condition due to spontaneous mutation. It occurs as a sporadic mutation in approximately 80% of cases (associated with advanced paternal age) or it may be inherited as an autosomal dominant genetic disorder.
People with achondroplasia have short stature, with an average adult height of 131 centimeters (52 inches) for males and 123 centimeters (48 inches) for females.

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.

Sunlight, especially its ultraviolet radiation component, can cause increased or additional types of damage in predisposed individuals, such as those taking certain phototoxic drugs, or those with certain conditions associated with photosensitivity, including:
– Psoriasis
– Atopic eczema
– Erythema multiforme
– Seborrheic dermatitis
– Autoimmune bullous diseases (immunobullous diseases)
– Mycosis fungoides
– Smith–Lemli–Opitz syndrome
– Porphyria cutanea tarda
Also, many conditions are aggravated by strong light, including:
– Systemic lupus erythematosus
– Sjögren’s syndrome
– Sinear Usher syndrome
– Rosacea
– Dermatomyositis
– Darier’s disease
– Kindler-Weary syndrome
Acute intermittent porphyria (AIP) belongs to the group inborn errors of metabolism and most patients with AIP are not light sensitive.

Clozapine can cause neutropenia or agranulocytosis.

Clozapine is an atypical antipsychotic used in the treatment of schizophrenia, and in patients who are intolerant to, or unresponsive to other antipsychotics.

It is a weak D2-receptor and D1-receptor blocking activity, with noradrenolytic, anticholinergic, and antihistaminic properties.

Many antipsychotic drugs can occasionally cause bone marrow depression, but agranulocytosis is particularly associated with clozapine.

Other side effects include:
Hypotension, tachycardia
Fever, sedation, seizures (with high doses)
Appetite increase
Constipation
Heartburn
Weight gain
Extrapyramidal symptoms
Agranulocytosis
Neuroleptic malignant syndrome

Inclusion body myositis (IBM) is a progressive muscle disorder characterized by muscle inflammation, weakness, and atrophy (wasting). It is a type of inflammatory myopathy. IBM develops in adulthood, usually after age 50. The symptoms and rate of progression vary from person to person. The most common symptoms include progressive weakness of the legs, arms, fingers, and wrists. Some people also have weakness of the facial muscles (especially muscles controlling eye closure), or difficulty swallowing (dysphagia). Muscle cramping and pain are uncommon, but have been reported in some people. The underlying cause of IBM is poorly understood and likely involves the interaction of genetic, immune-related, and environmental factors. Some people may have a genetic predisposition to developing IBM, but the condition itself typically is not inherited. Elevated creatine kinase (CK) levels in the blood (at most ,10 times normal) are typical in IBM. Muscle biopsy may display several common findings including; inflammatory cells invading muscle cells, vacuolar degeneration, inclusions or plaques of abnormal proteins.

In the PCR, DNA amplification is performed by thermostable enzymes; invariably either family A DNA polymerases from thermophilic and hyperthermophilic Bacteria or family B DNA polymerases from hyperthermophilic Archaea. Family Y DNA polymerase from the hyperthermophilic archaeon Sulfolobus solfataricus, Sso-polY, is also an enzyme marketed for PCR, but with specialist applications. Each thermostable DNA polymerases has different characteristics and to achieve optimal results, the choice of a PCR enzyme depends on the application itself.

Permanent pacing is not indicated as the bradycardia is reversible. Temporary pacing is the definite treatment. Isoprenaline can be used until temporary pacing is available.

Polycythaemia vera (PV) is associated with a low ESR.

PV, also known as polycythaemia rubra vera, is a myeloproliferative disorder caused by clonal proliferation of marrow stem cells leading to an increase in red cell volume, often accompanied by overproduction of neutrophils and platelets. It has peak incidence in the sixth decade of life, with typical features including hyperviscosity, pruritus, splenomegaly, haemorrhage (secondary to abnormal platelet function), and plethoric appearance. PV is associated with a low ESR.

Some management options of PV include lose-dose aspirin, venesection (first-line treatment), hydroxyurea (slightly increased risk of secondary leukaemia), and radioactive phosphorus (P-32) therapy.

In PV, thrombotic events are a significant cause of morbidity and mortality. 5–15% of the cases progress to myelofibrosis or acute myeloid leukaemia (AML). The risk of having AML is increased with chemotherapy treatment.

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.

Bulimia nervosa is a serious, potentially life-threatening eating disorder characterized by a cycle of bingeing and compensatory behaviours such as self-induced vomiting designed to undo or compensate for the effects of binge eating.

According to the DSM-5, the official diagnostic criteria for bulimia nervosa are:
Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following:
Eating, in a discrete period of time (e.g. within any 2-hour period), an amount of food that is definitely larger than most people would eat during a similar period of time and under similar circumstances.
A sense of lack of control over eating during the episode (e.g. a feeling that one cannot stop eating or control what or how much one is eating).
Recurrent inappropriate compensatory behaviour in order to prevent weight gain, such as self-induced vomiting, misuse of laxatives, diuretics, or other medications, fasting, or excessive exercise.
The binge eating and inappropriate compensatory behaviours both occur, on average, at least once a week for three months.
Self-evaluation is unduly influenced by body shape and weight.
The disturbance does not occur exclusively during episodes of anorexia nervosa.

Antidepressants as a group – particularly selective serotonin reuptake inhibitors (SSRIs) – are the mainstay of pharmacotherapy for bulimia nervosa. These may be helpful for patients with substantial concurrent symptoms of depression, anxiety, obsessions, or certain impulse disorder symptoms. They may be particularly good for patients who have not benefited from or had suboptimal response to suitable psychosocial therapy or who have a chronic, difficult course in combination with other treatments.

Food and Drug Administration (FDA) approved treatments
Fluoxetine (Prozac): Initial dose 20 mg/d with advance over 1–2 weeks to 60 mg/d in the morning as tolerated. Some patients may need to begin at a lower dose if side effects are intolerable. A maximum dose of 80 mg/d may be used in some cases.

Excessive sweating points towards a morphine overdose.

Morphine is considered the classic opioid analgesic with which other painkillers are compared. Like other medications in this class, morphine has an affinity for delta, kappa, and mu-opioid receptors.
Most commonly used in pain management, morphine provides major relief to patients afflicted with pain.

Among the more common adverse effects of morphine use is constipation. Other side effects include nausea, vomiting, drowsiness, and confusion. Psychological and physical dependence may occur.

Other side effects include bronchospasm, angioedema, urinary retention, ureteric or biliary spasm, dry mouth, sweating, rash, facial flushing, vertigo, tachycardia, bradycardia, palpitations, orthostatic hypotension, hypothermia, restlessness, mood change, hallucinations, seizures (adults and children) and miosis, headache and allergic reactions (including anaphylaxis) and decreased libido or potency.

Raised intracranial pressure occurs in some patients. Muscle rigidity may occur with high doses. Elevated liver enzymes may occur due to biliary sphincter constriction. Large doses can lead to respiratory depression, circulatory failure, and coma.

Treatment of opioid overdose:
Initial treatment of overdose begins with supportive care.
Naloxone is a pure competitive antagonist of opiate receptors and has no agonistic activity. The drug is relatively safe and can be administered intravenous, intramuscular, subcutaneous or via the endotracheal tube.
Alternatively, nalmefene and naltrexone maybe considered.

Among the options provided, hypothermia is not a symptom of opioid withdrawal.

Symptoms of opioid withdrawal include dysphoric mood, yawning, insomnia, muscle aches, lacrimation/rhinorrhoea, papillary dilatation, piloerection, fever, sweating, nausea/vomiting, diarrhoea.
If the patient is having an opioid withdrawal reaction, then give 10 mg of methadone syrup and wait about 60 min to determine its effect.

COWS (Clinical Opioid Withdrawal Scale) assessment for opioid withdrawal is commonly used to determine the severity of opioid withdrawal.

The history is consistent with carpal tunnel syndrome (CTS) arising as a result of pressure on the median nerve in the carpal tunnel. The median nerve supplies the muscles of the thenar eminence: the abductor pollicis (C7, C8), flexor pollicis brevis and opponens pollicis, and the lateral two lumbricals. The nerve conduction studies confirm marked denervation and absent sensory potentials within the median nerve territory.

Lesions in the optic radiation can cause a homonymous hemianopia with macular sparing, as a result of collateral circulation offered to macular tracts by the middle cerebral artery.
Lesions in the optic tract also cause a homonymous hemianopia, but without macular sparing.
Lesions in the optic chiasm, optic nerve, and temporal lobe cause bitemporal hemianopia, ipsilateral complete blindness, and superior homonymous quadrantanopia respectively.

Temazepam is a medication that is often prescribed for the treatment of short-term insomnia. It belongs to the benzodiazepine family of drugs and is classed as intermediate-acting, meaning that it can take between six and twenty-four hours for the drug to take effect.

Although it is known that shorter-acting benzodiazepines are more harmful and more likely to cause addiction, temazepam is, nevertheless, a highly addictive drug. It should not be taken for longer than four weeks.

-Adverse effects associated with the use of benzodiazepine hypnotics (to which the elderly are most vulnerable) include confusion, over sedation, increased risks of falls and consequent fractures

-Withdrawal from a benzodiazepine hypnotic must be agreed between the clinician and the patient – patients should never be forced or threatened. The risks of continued benzodiazepine use should be explained. An agreed schedule for reduction of and gradual withdrawal from the benzodiazepine hypnotic should also be agreed. This will involve substitution of the hypnotic with a long-acting benzodiazepine (e.g. diazepam) and a subsequent gradual reduction in dose of the substituted benzodiazepine -the substituted benzodiazepine can then be withdrawn in steps of about one-eighth to one-tenth every fortnight
Example: withdrawal schedule for patient on temazepam 20mg nocte
week 1 – temazepam 10mg, diazepam 5mg
week 2 – stop temazepam, diazepam 10mg
week 4 – diazepam 9mg
week 6 – diazepam 8mg
continue reducing dose of diazepam by 1mg every fortnight – tapering of dose may be slower if necessary

Poor prognostic factors for breast cancer include:
1. Young age (<40 years)
2. Premenopausal at the time of diagnosis
3. Increased tumour size
4. High-grade tumour
5. Oestrogen and progesterone receptor-negative tumour
6. Positive lymph node status

Diagnosis of RA is mainly based on clinical features (e.g., morning stiffness, symmetrical joint swelling) and laboratory tests (e.g., anti-CCP). Rheumatoid factor is not very specific for this disease and hence has low reliability. X-ray findings (e.g., soft tissue swelling or joint space narrowing) occur late in the disease and are therefore not typically used for diagnosis.

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.

Primary rubella infection during pregnancy, particularly during the first trimester, can affect several organs and cause birth defects that are responsible for congenital rubella syndrome (CRS). The most common defects of CRS are hearing impairment (unilateral or bilateral sensorineural), eye defects (e.g., cataracts, congenital glaucoma, or pigmentary retinopathy), and cardiac defects (e.g., patent ductus arteriosus or peripheral pulmonic stenosis). Congenital hearing loss is the most common sequela, occurring in approximately 60% of cases, especially when infection occurs in the 4th month of pregnancy.

In patients with polycystic ovarian syndrome (PCOS), FSH levels are within the reference range or low. Luteinizing hormone (LH) levels are elevated for Tanner stage, sex, and age. The LH-to-FSH ratio is usually greater than 3.

Women with PCOS have abnormalities in the metabolism of androgens and oestrogen and in the control of androgen production. PCOS can result from abnormal function of the hypothalamic-pituitary-ovarian (HPO) axis.
The major features of PCOS include menstrual dysfunction, anovulation, and signs of hyperandrogenism. Other signs and symptoms of PCOS may include the following:
– Hirsutism
– Infertility
– Obesity and metabolic syndrome
– Diabetes
– Obstructive sleep apnoea

Androgen excess can be tested by measuring total and free testosterone levels or a free androgen index. An elevated free testosterone level is a sensitive indicator of androgen excess. Other androgens, such as dehydroepiandrosterone sulphate (DHEA-S), may be normal or slightly above the normal range in patients with polycystic ovarian syndrome (PCOS). Levels of sex hormone-binding globulin (SHBG) are usually low in patients with PCOS.

Some women with PCOS have insulin resistance and an abnormal lipid profile (cholesterol >200 mg/dL; LDL >160 mg/dL). Approximately one-third of women with PCOS who are overweight have impaired glucose tolerance or type 2 diabetes mellitus by 30 years of age.

Bicarbonate therapy is not indicated in mild and moderate forms of DKA because metabolic acidosis will correct with insulin therapy. The use of bicarbonate in severe DKA is controversial due to a lack of prospective randomized studies. It is thought that the administration of bicarbonate may actually result in peripheral hypoxemia, worsening of hypokalaemia, paradoxical central nervous system acidosis, cerebral oedema in children and young adults, and an increase in intracellular acidosis. Because severe acidosis is associated with worse clinical outcomes and can lead to impairment in sensorium and deterioration of myocardial contractility, bicarbonate therapy may be indicated if the pH is 6.9 or less.

Beta blockers and calcium channel blockers have proven prognostic benefits. Nitrates don’t have any proven prognostic benefits. A statin is indicated for a patient with angina and cholesterol level of 5.5 to 8.5 to prevent risk of myocardial infarction. So the preferred combination from the given answers is beta blocker + statin.

The blood investigations in this patient reveal hyponatremia as well as hypokalaemia. Among the options provided, Bendroflumethiazide therapy can cause the above presentation with the electrolyte disturbances.
Note:
– Spironolactone is a potassium-sparing diuretic that is associated with hyperkalaemia.
– Enalapril therapy can cause side effects of dizziness, hypotension, cough, and rarely a rash.
– Felodipine therapy can cause side effects of dizziness, headache, cough, and palpitations.

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.

Loss of vision after consumption of antifreeze is a characteristic presentation of methanol poisoning.

Pathophysiology of methanol toxicity:
When ingested, methanol is absorbed rapidly via the gastrointestinal tract in less than 10 minutes. Methanol is not protein-bound and is absorbed directly into the total body water compartment.
Metabolism occurs mainly in the liver through serial oxidation via alcohol dehydrogenase and aldehyde dehydrogenase but begins with alcohol dehydrogenase present in the gastric mucosa.
Alcohol dehydrogenase oxidizes methanol to formaldehyde, and aldehyde dehydrogenase subsequently oxidizes formaldehyde to formic acid.
Formic acid is the primary toxic metabolite that accounts for the associated anion gap metabolic acidosis and end-organ damage.

Clinical presentation:
Patients who present within the first 12 to 24 hours following ingestion may appear normal, and this is described as the latent period.
Nausea, vomiting, and abdominal pain subsequently ensue, followed by CNS depression and hyperventilation due to metabolic acidosis.
Ocular symptoms associated with retinal toxicity are often evident in the form of blurry vision, decreased visual acuity, photophobia, and “halo vision.”

Treatment:
Treatment options for methanol toxicity include supportive care, fomepizole (Antizole, 4-Methylpyrazole or 4MP), ethanol, dialysis, and folate.

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.