Sildenafil (Viagra) is a phosphodiesterase type V inhibitor used in the treatment of impotence.Contraindications:- Patients taking nitrates and related drugs such as nicorandil- Hypotension- Recent stroke or myocardial infarction (NICE recommend waiting 6 months)Side-effects:Visual disturbances e.g. cyanopsia, non-arthritic anterior ischaemic NeuropathyNasal congestionFlushingGastrointestinal side-effectsHeadache

Tricyclic compounds can’t be cleared by haemodialysis.Drugs that can be cleared with haemodialysis include: (BLAST)- Barbiturate- Lithium- Alcohol (inc methanol, ethylene glycol)- Salicylates- Theophyllines (charcoal hemoperfusion is preferable)Drugs which cannot be cleared with haemodialysis include:- Tricyclics- Benzodiazepines- Dextropropoxyphene (Co-proxamol)- Digoxin- Beta-blockers

Desmopressin test (done to differentiate nephrogenic diabetes insipidus from central diabetes insipidus), and serum lithium levels can together confirm a diagnosis of lithium-induced nephrogenic diabetes insipidus.Bipolar disease is most often managed with mood stabilizers like lithium. This patient develops gastrointestinal symptoms followed by an acute confusional state associated with polyuria and polydipsia. These symptoms are suggestive of diabetes insipidus.In a case where these symptoms occur in a bipolar patient under treatment, lithium-induced nephrogenic diabetes insipidus should be considered as the most probable cause.Lithium intoxication can present with symptoms of nausea, vomiting, mental dullness, action tremor, weakness, ataxia, slurred speech, blurred vision, dizziness, especially vertical nystagmus and stupor or coma. Diffuse myoclonic twitching and nephrogenic diabetes insipidus can also occur. Such a clinical syndrome occurs above the serum level of lithium of 1.5–2.0 mEq/L.Management: – Correcting electrolyte abnormalities in patients with acute disease is critical and often life-saving.- Treatment should be initiated with parenteral fluids to replete hypovolemia (normal saline at 200-250 mL/h), followed by administration of hypotonic fluid (0.5% normal saline). – On the restoration of the volume status of the patient forced diuresis should be initiated by the administration of parenteral furosemide or bumetanide accompanied by continued intravenous hypotonic fluid administration to maintain volume status.- Polyuria is managed with hydrochlorothiazide combined with amiloride, acetazolamide.

The statement that fits the characteristics of doxapram is, epilepsy is a contraindication for doxapram use. Concurrent use with theophylline may increase agitation not relaxation.Doxapram is a central respiratory stimulant. In clinical practice, doxapram is usually used for patients who have an acute exacerbation of chronic obstructive pulmonary disease (COPD) who are unsuitable for admission to the intensive therapy unit for ventilatory support. Doxapram infusion may buy an extra 24 h to allow for recovery.Contraindications include: ischaemic heart disease, epilepsy, cerebral oedema, acute stroke, asthma, hypertension, hyperthyroidism, and pheochromocytoma. The infusion may worsen agitation and dyspnoea and lead to hypertension, nausea, vomiting and urinary retention.Drug interactions:Concomitant administration of doxapram and aminophylline (theophylline) can cause increased skeletal muscle activity, agitation, and hyperactivity.

Confusion and pink mucosae are typical features of CO poisoning.The patient often presents, most commonly with headaches, and other symptoms like malaise, nausea, and dizziness.Carbon monoxide (CO) poisoning, considered as the great imitator of other diseases as the patients present with a myriad of symptoms. The carbon monoxide diffuses rapidly across the pulmonary capillary membrane binding to the haem molecule with a very high affinity (240 times that of oxygen) forming carboxy-haemoglobin (COHb). Non-smokers have a baseline COHb of ,3% while smokers have a baseline COHb of 10-15%.Features of carbon monoxide toxicity- Headache: 90% of cases- Nausea and vomiting: 50%- Vertigo: 50%- Confusion: 30%- Subjective weakness: 20%- Severe toxicity: ‘pink’ skin and mucosae, hyperpyrexia, arrhythmias, extrapyramidal features, coma, deathTreatment:Use of Hyperbaric oxygen therapy (HBOT) for treating mild to moderate CO poisoning is not routine.The selection criteria for HBOT in cases of CO poisoning include:• COHb levels > 20-25%• COHb levels > 20% in pregnant patient • Loss of consciousness• Severe metabolic acidosis (pH <7.1)• Evidence of end-organ ischemia (e.g., ECG changes, chest pain, or altered mental status)

Anticholinergic syndrome results from the inhibition of muscarinic cholinergic neurotransmission. Clinical manifestations can be remembered by the mnemonic, red as a beet, dry as a bone, blind as a bat, mad as a hatter, hot as a hare, and full as a flask. The mnemonic refers to the symptoms of flushing, dry skin and mucous membranes, mydriasis (dilated pupil) with loss of accommodation, altered mental status, fever, and urinary retention, respectively.

Mechanism of action of low molecular weight heparin (LMWH): It inhibits coagulation by activating antithrombin III. Antithrombin III binds to and inhibits factor Xa. In doing so it prevents activation of the final common path; Xa inactivation means that prothrombin is not activated to thrombin, thereby not converting fibrinogen into fibrin for the formation of a clot. LMHW is a small fragment of a larger mucopolysaccharide, heparin. Heparin works similarly, by binding antithrombin III and activating it. Heparin also has a binding site for thrombin, so thrombin can interact with antithrombin III and heparin, thus inhibiting coagulation. Heparin has a faster onset of anticoagulant action as it will inhibit not only Xa but also thrombin, while LMWH acts only on Xa inhibition.Compared to heparin, LMWHs have a longer half-life, so dosing is more predictable and can be less frequent, most commonly once per day.Dosage and uses:LMWH is administered via subcutaneous injection. This has long-term implications on the choice of anticoagulant for prophylaxis, for example, in orthopaedic patients recovering from joint replacement surgery, or in the treatment of DVT/PE.Adverse effects:The main risk of LMWH will be bleeding. The specific antidote for heparin-induced bleeding is protamine sulphate.Less commonly it can cause:Heparin-induced thrombocytopenia (HIT)Osteoporosis and spontaneous fracturesHypoaldosteronismHypersensitivity reactions

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.

Renal elimination of a drug has no role in altering the bioavailability of a drug.The bioavailability of a drug is the proportion of the drug which reaches systemic circulation. Mathematically, bioavailability is the AUCoral/AUCiv x 100%, where AUC = area under the concentration-time curve following a single (oral or iv) dose. Other options are true:By definition, the bioavailability of a drug given intravenously is 100%.Drugs given orally that undergo high pre-systemic (first-pass) metabolism in the liver or gut wall have a low bioavailability e.g. lidocaine. Bioavailability is also affected by the degree of absorption from the gut and this can change depending on gut motility and administration of other drugs.

Lidocaine is an example of class IB antiarrhythmics.The Vaughan-Williams classification of antiarrhythmicsI: Membrane stabilizing agentsIA: Quinidine, Procainamide, DisopyramideIB: Lidocaine, MexiletineIC: Propafenone, Flecainide II: β blockers – Propranolol, EsmololIII: Agents widening AP – Amiodarone, Dronedarone, Dofetilide, Ibutilide, SotalolIV: Calcium channel blockers – Verapamil, DiltiazemV: Miscellaneous – Digoxin, adenosine, magnesium

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, tachycardiaFever, sedation, seizures (with high doses)Appetite increaseConstipationHeartburnWeight gainExtrapyramidal symptomsAgranulocytosisNeuroleptic malignant syndrome

Carbimazole is used to treat hyperthyroidism. Carbimazole is a pro-drug as after absorption it is converted to the active form, methimazole. Methimazole prevents thyroid peroxidase enzyme from coupling and iodinating the tyrosine residues on thyroglobulin, hence reducing the production of the thyroid hormones T3 and T4 (thyroxine).

In such a clinical scenario, NICE guidelines support initiating treatment with bisphosphonates without waiting for a DEXA scan.Osteoporosis is defined as low bone mineral density caused by altered bone microstructure ultimately predisposing patients to low-impact, fragility fractures.Management:Vitamin D and calcium supplementation should be offered to all women unless the clinician is confident they have adequate calcium intake and are vitamin D repleteAlendronate is the first-line treatment. Around 25% of patients cannot tolerate alendronate, usually due to upper gastrointestinal problems. These patients should be offered risedronate or etidronate.Strontium ranelate and raloxifene are recommended if patients cannot tolerate bisphosphonates.Other medications that are useful in the treatment of osteoporosis are denosumab, teriparatide, raloxifene, etc.

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.

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.

MDMA commonly known as ecstasy or molly, is a psychoactive drug primarily used as a recreational drug. The desired effects include altered sensations, increased energy, empathy, and pleasure. Features of MDMA abuse include hyponatraemia, tachycardia, hyperventilation, and hyperthermia.

Among the given options the most appropriate management in this patient would be ethanol and haemodialysis.Ethanol competes with ethylene glycol for alcohol dehydrogenase and thus, helps manage a patient with ethylene glycol toxicity.Ethylene glycol is a type of alcohol used as a coolant or antifreezeFeatures of toxicity are divided into 3 stages:Stage 1: (30 min to 12 hours after exposure) Symptoms similar to alcohol intoxication: confusion, slurred speech, dizziness (CNS depression)Stage 2: (12 – 48 hours after exposure) Metabolic acidosis with a high anion gap and high osmolar gap. Also tachycardia, hypertensionStage 3: (24 – 72 hours after exposure) Acute renal failureManagement has changed in recent times:Fomepizole, an inhibitor of alcohol dehydrogenase, is now used first-line in preference to ethanol.Ethanol has been used for many years works by competing with ethylene glycol for the enzyme alcohol dehydrogenase this limits the formation of toxic metabolites (e.g. glycolaldehyde and glycolic acid) which are responsible for the hemodynamic/metabolic features of poisoning.Haemodialysis has a role in refractory cases.

Before the initiation of trastuzumab, an echocardiography is a must to rule out any pre-existing cardiac abnormalities as trastuzumab is cardiotoxic.Trastuzumab (Herceptin) is a monoclonal antibody directed against the HER2/neu receptor. It is used mainly in metastatic breast cancer although some patients with early disease are now also given trastuzumab.Adverse effects include:Flu-like symptoms and diarrhoea are common.Cardiotoxicity: – Risk increases when anthracyclines are used concomitantly. – Trastuzumab-induced cardiac dysfunctions are regarded as less severe and largely reversible because primary cardiomyocyte do not show ultrastructure changes unlike those associated with anthracycline-induced cardiotoxicity. – Primary myocyte injury does not occur in patients who were treated with trastuzumab.

Bisphosphonates are analogues of pyrophosphate, a molecule which decreases demineralisation in bone. They inhibit osteoclasts by reducing recruitment and promoting apoptosis.

Tiotropium is a specific long-acting antimuscarinic agent indicated as maintenance therapy for patients with COPD (chronic obstructive pulmonary disease). It should be used cautiously in patients with narrow-angle glaucoma, prostatic hyperplasia or bladder neck obstruction.The most frequently encountered adverse effects of tiotropium include pharyngitis, bronchitis, sinusitis, dry mouth, cough, and headaches. Paradoxical bronchospasm may also occur as a rare side-effect. Dry mouth occurs in up to 14% of patients taking tiotropium, in keeping with its anticholinergic profile. Rarer side-effects include tachycardia, blurred vision, urinary retention, and constipation.

The principal action of organophosphates is the inhibition of acetylcholinesterase’s, therefore leading to the accumulation of acetylcholine at muscarinic receptors (miosis, hypersalivation, sweating, diarrhoea, excessive bronchial secretions), nicotinic receptors (muscle fasciculations and tremor) and in the central nervous system (anxiety, loss of memory, headache, coma). Removal from the source of the organophosphate, adequate decontamination, supplemental oxygen and atropine are the initial treatment measures. Pralidoxime, an activator of cholinesterase, should be given to all symptomatic patients.

Both fibrates and nicotinic acid have been associated with myositis, especially when combined with a statin. However, the Committee on Safety of Medicines has produced guidance which specifically warns about the concomitant prescription of fibrates with statins concerning muscle toxicity.Bezafibrate: It is a fibric acid derivative (fibrate) that has been used as a class of agents known to decrease triglyceride levels while substantially increasing HDL-C levels.Pharmacological effects:- Increases VLDL catabolism by increasing lipoprotein and hepatic triglyceride lipase.- Decreases triglyceride synthesis by inhibiting acetyl-CoA reductase.- Decreases cholesterol synthesis by inhibiting HMG-CoA reductase.Side effects:- Hypersensitivity- Primary biliary cirrhosis- Pre-existing gallbladder disease- Concurrent use with HMG-CoA inhibitors (statins) can produce myopathy- Hepatic/renal impairment in a patient warrants dose adjustment as this drug is primarily excreted via the renal mechanism.Contraindications: Concurrent use of MAO inhibitors, hypersensitivity, pre-existing cholestasis, and pregnancy.Use: It can be used to treat Barth syndrome (characterized by dilated cardiomyopathy, neutropenia (presenting with recurrent infections), skeletal myopathy and short stature)

The two statements that fit the characteristics of doxapram are, epilepsy is a contraindication for doxapram use and concurrent use with theophylline may increase agitation.Doxapram is a central respiratory stimulant. In clinical practice, doxapram is usually used for patients who have an acute exacerbation of chronic obstructive pulmonary disease (COPD) who are unsuitable for admission to the intensive therapy unit for ventilatory support. Doxapram infusion may buy an extra 24 h to allow for recovery.Contraindications include: ischaemic heart disease, epilepsy, cerebral oedema, acute stroke, asthma, hypertension, hyperthyroidism, and pheochromocytoma. The infusion may worsen agitation and dyspnoea and lead to hypertension, nausea, vomiting and urinary retention.Drug interactions:Concomitant administration of doxapram and aminophylline (theophylline) can cause increased skeletal muscle activity, agitation, and hyperactivity.

All patients require plasma-vancomycin measurement (after 3 or 4 doses if renal function normal, earlier if renal impairment). There is a risk of nephrotoxicity including renal failure, interstitial nephritis and ototoxicity.

The patient’s symptoms and lab results are indicative of ethylene glycol poisoning, commonly found in engine coolant. Ethylene glycol is metabolized to toxic metabolites, including glycolic acid and oxalic acid, which can cause metabolic acidosis (evidenced by the low pH and low bicarbonate levels) and can bind calcium, leading to hypocalcemia.

Fomepizole is an antidote that inhibits alcohol dehydrogenase, the enzyme that converts ethylene glycol into its toxic metabolites. This prevents further formation of the harmful substances, allowing time for the ethylene glycol to be excreted unchanged in the urine.

While haemodialysis is also an important treatment for severe ethylene glycol poisoning, especially in cases of significant acidosis or renal failure, the immediate administration of fomepizole is the most urgent intervention to prevent further toxicity. Haemodialysis can be considered if the patient does not respond adequately to fomepizole or if there are signs of severe toxicity.

The most likely complaint of this patient would be hot flushes.

Alopecia and cataracts are listed as possible side-effects, however they are not as prevalent as hot flushes, which are very common in pre-menopausal women.

Tamoxifen is a Selective Oestrogen Receptor Modulator (SERM) which acts as an oestrogen receptor antagonist and partial agonist. It is used in the management of oestrogen receptor-positive breast cancer

Adverse effects:

• Menstrual disturbance: vaginal bleeding, amenorrhoea
• Hot flushes – 3% of patients stop taking tamoxifen due to climacteric side-effects.
• Venous thromboembolism.
• Endometrial cancer (although antagonistic with respects to breast tissue, tamoxifen may serve as an agonist at other sites. Therefore the risk of endometrial cancer is increased). Raloxifene is a pure oestrogen receptor antagonist and carries a lower risk of endometrial cancer.

Tamoxifen is typically used for 5 years following the removal of the tumour.

Anticholinergic syndrome occurs following overdose with drugs that have prominent anticholinergic activity including tricyclic antidepressants, antihistamines and atropine. Features include dry, warm, flushed skin, urinary retention, tachycardia, mydriasis (dilated pupils) and agitation.

The next step in managing this patient is to give 10 mg and continue administering in 10 mg increments each hour until symptoms are under control.Methadone alleviates opioid withdrawal symptoms and reduces cravings. Methadone is useful for detoxification from longer-acting opioids such as morphine or methadone itself.Methadone should be used with caution if the patient has:Respiratory deficiencyAcute alcohol dependenceHead injuryTreatment with monoamine oxidase inhibitors (MAOIs)Ulcerating colitis or Crohn’s diseaseSevere hepatic impairmentThe dose must be reviewed on a daily basis and adjusted based upon how well the symptoms are controlled and the presence of side effects. The greater the dose of opioids used by the patient, the greater the dose of methadone required to control withdrawal symptoms. To avoid the risk of overdose in the first days of treatment The recommended dosing of methadone is 30mg in two doses of 15mg morning and evening.It is important to note that a methadone dose equivalent to what the patient reports they are taking should never be given. It is rare to need more than 40 mg per 24 hours: beware of overdosing which can lead to respiratory arrest.

Among the give options, reactivation of tuberculosis may occur in a patient under treatment with etanercept.Etanercept is a biological TNF inhibit commonly used to control ankylosing spondylitis, juvenile idiopathic arthritis, plaque psoriasis, psoriatic arthritis, and rheumatoid arthritis.Etanercept is a soluble receptor that binds both TNF-alpha and TNF-beta to inhibit the inflammatory response in joints and skin that is characteristic of these autoimmune disorders.The most common adverse effects include infections (viral, bacterial, and fungal – mostly upper respiratory tract infections) and injection site reaction (erythema, itching, pain, swelling, bleeding, bruising).Rarely it can also cause, reactivation of hepatitis B and TB, pneumocystis pneumonia, congestive cardiac failure, Steven-Johnson syndrome, toxic epidermal necrolysis, etc.

Acetazolamide is in the diuretic and carbonic anhydrase inhibitor families of medication. It works by decreasing the amount of hydrogen ions and bicarbonate in the body and can thus cause metabolic acidosis and electrolyte changes (hypokalaemia, hyponatremia).

The patient (known case of acromegaly) seems to have developed cholelithiasis (presenting with right upper quadrant pain) probably due to octreotide.It is a long-acting analogue of somatostatin which is released from D cells of the pancreas and inhibits the release of growth hormone, glucagon, and insulin.Uses- Acute treatment of variceal haemorrhage- Acromegaly- Carcinoid syndrome- Prevent complications following pancreatic surgery- VIPomas- Refractory diarrhoeaAdverse effectsGallstones (secondary to biliary stasis)Other options:- Bromocriptine – a dopamine agonist with side effects arising from its stimulation of the brain vomiting centre.- Desmopressin – predominantly used in patients with diabetes insipidus by increasing the presence of aquaporin channels in the distal collecting duct to increase water reabsorption from the kidneys. The main side effects include headache and facial flushing due to hypertension.- Metformin – mainly reduces hepatic gluconeogenesis in patients with type 2 diabetes, common side effects include diarrhoea, vomiting, and lactic acidosis- Levothyroxine – synthetic thyroxine used in patients with hypothyroidism, common side effects result from incorrect dosing and mimic the symptoms of hyperthyroidism.

Drug metabolism can be broadly classified into:Phase I (functionalization) reactions: also termed non-synthetic reactions, they include oxidation, reduction, hydrolysis, cyclization and de-cyclization. The most common and vital reactions are oxidation reactions. (Of the given enzymes only Alcohol dehydrogenase is involved in phase I drug metabolism. Succinate dehydrogenase, is a vital enzyme involved in the Kreb’s cycle and the mitochondrial electron transport chain). They are mainly catalysed by Cytochrome P-450 enzyme.Phase II (conjugation) reactions: occur following phase I reactions, they include reactions: glucuronidation and sulphate conjugation, etc. They are mostly catalysed by UDP-glucuronosyltransferase enzyme. Other phase II enzymes include: sulfotransferases, N-acetyltransferases, glutathione S-transferases and methyltransferases.

Spironolactone is an aldosterone antagonist which acts in the distal convoluted tubule. It is a potassium-sparing diuretic that prevents the body from absorbing too much salt and keeps the potassium levels from getting too low. Spironolactone is used to treat heart failure, high blood pressure (hypertension), or hypokalaemia (low potassium levels in the blood).

The most likely cause for these results is delayed paracetamol nephrotoxicity.The blood investigations of this patient are highly suggestive of acute kidney injury. Paracetamol overdose is well known to cause hepatotoxicity, but not for its delayed nephrotoxicity, especially in significant overdose. Appropriate monitoring of a patient’s blood tests is important.Management:NAC (N-Acetyl cysteine) has a clear role in preventing acetaminophen-induced liver necrosis. Although NAC has not been proven to be harmful to the kidney, its role in patients without hepatoxicity and only isolated renal dysfunction is uncertain.Other options:-There are no features in the history that are suggestive of dehydration and pre-renal AKI presenting in this manner in a 25-year-old would be very unusual.- Minimal change nephropathy typically presents with a nephrotic picture of kidney injury.- Berger’s more commonly presents with isolated haematuria.

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.

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) there is increased 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.

Agitation, hypomania and suicidal intent within a few days after initiating corticosteroid therapy is highly suggestive of a diagnosis of corticosteroid-induced psychosis.In some patients corticosteroid related psychosis has been diagnosed up to 12 weeks or more after commencing therapy.Euphoria and hypomania are considered to be the most common psychiatric symptoms reported during short courses of steroids.During long-term treatment, depressive symptoms were the most common. Higher steroid doses appear to carry an increased risk for such adverse effects; however, there is no significant relationship between dose and time to onset, duration, and severity of symptoms. Management: Reduction or cessation of corticosteroids is the mainstay of treatment for steroid psychosis. For those patients who cannot tolerate this reduction/cessation of steroids, mood stabilizers may be of some benefit.

Among the given anti-epileptics the best drug that can be given in this patient is lamotrigine.Topiramate, carbamazepine, phenytoin, and phenobarbital are all hepatic enzyme inducers and are associated with decreased effectiveness of the oral contraceptive (OCP) due to acceleration of the metabolism of oestrogens and progestogens.If she is planning on pregnancy then registry studies suggest that lamotrigine would also be the best choice.Other hepatic enzyme inducers include rifampicin, spironolactone, griseofulvin, etc.

Carbon monoxide (CO) poisoning:It is considered as the great imitator of other diseases as the patients present with a myriad of symptoms. The carbon monoxide diffuses rapidly across the pulmonary capillary membrane binding to the haem molecule with a very high affinity (240 times that of oxygen) forming carboxy-haemoglobin (COHb). Non-smokers have a baseline COHb of ,3% while smokers have a baseline COHb of 10-15%.Clinical features of carbon monoxide toxicity:Headache: 90% of cases (most common clinical feature)Nausea and vomiting: 50%Vertigo: 50%Confusion: 30%Subjective weakness: 20%Severe toxicity: ‘pink’ skin and mucosa, hyperpyrexia, arrhythmias, extrapyramidal features, coma, deathCherry red skin is a sign of severe toxicity and is usually a post-mortem finding.Management• 100% oxygen• Hyperbaric oxygen therapy (HBOT)The use of Hyperbaric oxygen therapy (HBOT) for treatment mild to moderate CO poisoning is not routine.The selection criteria for HBOT in cases of CO poisoning include:• COHb levels > 20-25%• COHb levels > 20% in pregnant patient • Loss of consciousness• Severe metabolic acidosis (pH <7.1)• Evidence of end-organ ischemia (e.g., ECG changes, chest pain, or altered mental status)

Hormone replacement therapy (HRT) involves the use of a small dose of oestrogen, combined with a progestogen (in women with a uterus), to help alleviate menopausal symptoms. The main indication is the control of vasomotor symptoms. The other indications, such as reversal of vaginal atrophy and prevention of osteoporosis, should be treated with other agents as first-line therapies.