The rationale behind the use of sodium bicarbonate is that it increases the alkalinity of the urine promoting lithium excretion. The preferred treatment in severe cases would be haemodialysis.Lithium is a mood-stabilizing drug used most commonly prophylactically in bipolar disorder but also as an adjunct in refractory depression. It has a very narrow therapeutic range (0.4-1.0 mmol/L) and a long plasma half-life being excreted primarily by the kidneys. Lithium toxicity generally occurs following concentrations > 1.5 mmol/L.Toxicity may be precipitated by dehydration, renal failure, diuretics (especially Bendroflumethiazide), ACE inhibitors, NSAIDs and metronidazole.Features of toxicityCoarse tremor (a fine tremor is seen in therapeutic levels)HyperreflexiaAcute confusionSeizureComaManagementMild-moderate toxicity may respond to volume resuscitation with normal salineHaemodialysis may be needed in severe toxicitySodium bicarbonate is sometimes used but there is limited evidence to support this. By increasing the alkalinity of the urine it promotes lithium excretion.

The most probable diagnosis for this patient is delirium tremens due to alcohol withdrawal, which should be treated as a medical emergency. Delirium tremens is a hyperadrenergic state and is often associated with tachycardia, hyperthermia, hypertension, tachypnoea, tremor, and mydriasis.Treatment:- The most common and validated treatment for alcohol withdrawal is benzodiazepine: first-line treatment includes oral lorazepam. – If the symptoms persist, or the medication is refused, parenteral lorazepam, haloperidol or olanzapine should be given.- Central-acting, alpha-2 agonists such as clonidine and dexmedetomidine should not be used alone for the treatment of alcohol withdrawal.- It is also recommended to avoid using alcohol, antipsychotics, anticonvulsants, beta-adrenergic receptor blockers, and baclofen for the treatment of alcohol withdrawal as there are not enough studies to support the safety of these.

Finasteride inhibits the formation of dihydrotestosterone.Finasteride is a 5α-reductase inhibitor and thus, inhibits the conversion of testosterone to dihydrotestosterone (DHT). DHT is much more active than testosterone and binds more avidly to cytoplasmic receptors. DHT stimulates prostate growth and may be responsible for benign prostatic hyperplasia in the elderly. Thus, finasteride can cause a reduction in prostatic volume and help in managing a patient with benign prostatic hyperplasia.

Vestibular damage is a neurological side effect of streptomycin.Streptomycin is an aminoglycoside bactericidal antibiotic. It is used in the treatment of tularaemia and resistant mycobacterial infections.The most common neurological side-effect is vestibular damage leading to vertigo and vomiting. Cochlear damage is less frequent and results in deafness. Other side-effects include rashes, angioneurotic oedema, and nephrotoxicity.

The cause for bone marrow suppression in this patient is most probably mercaptopurine toxicity.Azathioprine is metabolized to 6-mercaptopurine (6-MP), which itself is metabolized by xanthine oxidase. Xanthine oxidase inhibition by allopurinol leads to the accumulation of 6-MP which then precipitates bone marrow failure. This may be potentially fatal if unrecognized.Clinical presentation:Toxicity symptoms include gastrointestinal symptoms, bradycardia, hepatotoxicity, myelosuppression.

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%.Use of Hyperbaric oxygen therapy (HBOT) for treatment of 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)Principle of HBOT:Exposing patients to 100 percent oxygen under supra-atmospheric conditions results in a decrease in the half-life (t1/2) of COHb, from , 90 min in atmospheric air to , 30 minutes. The amount of oxygen dissolved in the blood also rises from , 0.3 to 6 mL/dL, increasing the delivery of non-haemoglobin-bound oxygen to the tissues.

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 most appropriate steps of initial management include iv glucagon and iv isoprenaline.The most likely diagnosis in the above scenario (decreased conscious level, profound hypertension, and bradycardia) is β-blocker toxicity/overdose. Bronchospasm rarely occurs in an overdose of β-blockers, except where there is a history of asthma.Immediate management is to give iv glucagons (50–150μg/kg) followed by infusion to treat hypotension and isoprenaline or atropine to treat bradycardia. Where patients fail to respond to these measures, temporary pacing may be required. If the patient is seen within the first 4 hours of the overdose, gastric lavage may be of value.

Moxonidine and alpha-methyl dopa are centrally acting antihypertensives and modify blood pressure through modifying sympathetic activity.Other options:Verapamil is a calcium antagonist.Minoxidil and hydralazine are both vasodilators.Phenoxybenzamine is an alpha-blocker.Adverse effects:Dry mouth and somnolence were the most frequently reported adverse events, followed by headache, dizziness, nausea and allergic skin reactions.

The symptoms of ataxia, slurred speech and blurred vision are all suggestive of phenytoin toxicity. Cimetidine increases the efficacy of phenytoin by reducing its hepatic metabolism.Phenytoin has a narrow therapeutic index (10-20 mg/L) and its levels are monitored by measuring the total phenytoin concentration.Cimetidine is an H2 receptor antagonist used in the treatment of peptic ulcers. It acts by decreasing gastric acid secretion.Cimetidine also has an inhibitory effect on several isoforms of the cytochrome enzyme system including the CYP450 enzymatic pathway. Phenytoin is metabolized by the same cytochrome P450 enzyme system in the liver. Thus, the simultaneous administration of both these medications leads to an inhibition of phenytoin metabolism and thus increases its circulating levels leading to phenytoin toxicity.

The most probable diagnosis in this patient is serotonin syndrome.The serotonin syndrome is a cluster of symptoms and signs (range from barely perceptible tremor to life-threatening hyperthermia and shock). It may occur when SSRIs such as citalopram, escitalopram, fluoxetine, fluoxetine, paroxetine, and sertraline that impair the reuptake of serotonin from the synaptic cleft into the presynaptic neuron are taken in combination with monoamine oxidase inhibitors or tricyclic antidepressants. It has also been reported following an overdose of selective serotonin reuptake inhibitors (SSRIs) alone.Treatment:Most cases of serotonin syndrome are mild and will resolve with removal of the offending drug alone. After stopping all serotonergic drugs, management is largely supportive and aimed at preventing complications. Patients frequently require sedation, which is best facilitated with benzodiazepines.Antipsychotics should be avoided because of their anticholinergic properties, which may inhibit sweating and heat dissipation.

Blue tinge of vision/cyanopsia is caused due to the intake of sildenafil citrate.Sildenafil citrate (Viagra) is the first oral drug to be widely approved for the treatment of erectile dysfunction. It is a potent and selective inhibitor of type-V phosphodiesterase, the primary form of the enzyme found in human penile erectile tissue, thereby preventing the breakdown of cyclic guanosine monophosphate (cGMP), the intracellular second messenger of nitric oxide.Uses:It is used for the treatment of erectile dysfunction, idiopathic pulmonary hypertension, premature ejaculation, high altitude illness, penile rehabilitation after radical prostatectomy, angina pectoris, and lower urinary tract symptoms.Adverse effects:Mild headache, flushing, dyspepsia, cyanopsia, back pain, and myalgias – due to a high concentration of PDE11 enzyme in skeletal muscle, which shows significant cross-reactivity with the use of tadalafil.It can also cause hypotension, dizziness, and rhinitis.Note: Xanthopsia (yellow-green vision) may occur secondary to treatment with digoxin.

Ethanol reduces the calcium-dependent secretion of anti-diuretic hormone (ADH) by blocking channels in the neurohypophyseal nerve terminal.Thus, ethanol’s inhibitory effect helps to explain the increased diuresis experienced during intoxicated states as well as increased free water loss; without appropriate ADH secretion, more water is excreted by the kidneys.Nausea associated with hangovers is mainly due to vagal stimulation to the vomiting centre. Following a particularly severe episode of alcohol excess, people may experience tremors due to increased glutamate production by neurons to compensate for the previous inhibition by ethanol.Management of alcoholism:Nutritional support: – Alcoholic patients should receive oral thiamine if their ‘diet may be deficient’.Pharmacological management:- Benzodiazepines for acute withdrawal- Disulfiram promotes abstinence – alcohol intake causes a severe reaction due to inhibition of acetaldehyde dehydrogenase. Patients should be aware that even small amounts of alcohol (e.g. In perfumes, foods, mouthwashes) can produce severe symptoms. Contraindications include ischaemic heart disease and psychosis.- Acamprosate reduces craving, known to be a weak antagonist of NMDA receptors, improves abstinence in placebo-controlled trials.

1mg Prednisolone = 4mg hydrocortisone, so the actual equivalent daily dose is 7mg.

The given clinical scenario is suggestive of myo-neuropathy and is most likely to be caused by colchicine toxicity. It gives rise to subacute proximal muscle weakness and on occasions can lead to an acute necrotizing myopathy. Creatine phosphokinase may be normal or may be elevated.Weakness resolves when the drug is discontinued but the neuropathic features remain.Death is usually a result of respiratory depression and cardiovascular collapse.Treatment is symptomatic and supportive, and the treatment for colchicine poisoning includes lavage and measures to prevent shock.

Dilation of systemic veins is a beneficial effect of nitro-glycerine.Administration of nitro-glycerine results in the dilation of systemic veins and decrease of myocardial wall tension and oxygen demand. Dilatation of systemic veins can cause reduced systemic vascular resistance leading to reduced cardiac workload thus reducing anginal symptoms secondary to demand ischemia.This is accompanied by vasodilation of large and medium-sized coronary arteries with increased coronary blood flow to the sub endocardium.

The cardiovascular effects of β-adrenoceptor block result from reduction of the sympathetic drive which includes reduced heart rate (automaticity) and reduced myocardial contractility (rate of rise of pressure in the ventricle). This will lead to reduced cardiac output and an overall fall in oxygen consumption.

The most appropriate intervention in this patient is intravenous hydroxocobalamin.The clinical scenario provided is suggestive of acute cyanide toxicity secondary to burning plastics in the house fire. Cyanide ions inhibit mitochondrial cytochrome oxidase, preventing aerobic respiration. This manifests in normal oxygen saturations, a high pO2 and flushing (or ‘brick red’ skin) brought on by the excess oxygenation of venous blood. In the question above it is important to note that the blood gas sample given is venous rather than arterial. His blood gas also demonstrates an increased anion gap, consistent with his high lactate (generated by anaerobic respiration due to the inability to use available oxygen).The recommended treatment for moderate cyanide toxicity in the UK is one of three options: sodium thiosulfate, hydroxocobalamin or dicobalt edetate. Among the options given is hydroxocobalamin and this is, therefore, the correct answer. Hydroxocobalamin additionally has the best side-effect profile and speed of onset compared with other treatments for cyanide poisoning.Other options:- Intubation would be appropriate treatment in the context of airway burns but this patient has no evidence of these, although close monitoring would be advised. – High-flow oxygen is the treatment for carbon monoxide poisoning – a sensible differential, but this man’s very high lactate and high venous pO2 fit better with cyanide toxicity. Intravenous dexamethasone would be another treatment for airway oedema once an endotracheal tube had been placed. – Intravenous sodium nitroprusside is a treatment for high blood pressure that can cause cyanide poisoning, and would, therefore, be inappropriate.Note:Cyanide may be used in insecticides, photograph development and the production of certain metals. Toxicity results from reversible inhibition of cellular oxidizing enzymesClinical presentation:Classical features: brick-red skin, the smell of bitter almondsAcute: hypoxia, hypotension, headache, confusionChronic: ataxia, peripheral neuropathy, dermatitisManagement:Supportive measures: 100% oxygenDefinitive: hydroxocobalamin (intravenously), also a combination of amyl nitrite (inhaled), sodium nitrite (intravenously), and sodium thiosulfate (intravenously).

Among the following hypertensives, lisinopril (an ACE inhibitor) is contraindicated in patients who are planning for pregnancy.Per the NICE guidelines, when treating the woman in question, she should be treated as if she were pregnant given the absence of effective contraception. ACE inhibitors such as lisinopril are known teratogens and most be avoided.Drugs contraindicated in pregnancy:AntibioticsTetracyclinesAminoglycosidesSulphonamides and trimethoprimQuinolonesOther drugs:ACE inhibitors, angiotensin II receptor antagonistsStatinsWarfarinSulfonylureasRetinoids (including topical)Cytotoxic agentsThe majority of antiepileptics including valproate, carbamazepine, and phenytoin are known to be potentially harmful.

Sodium cromoglycate principally acts by inhibiting the degranulation of mast cells triggered by the interaction of antigen and IgE. The inhibitory effect on mast cells appears to be cell-type specific since cromoglycate has little inhibitory effect on mediator release from human basophils.Thus, it inhibits the release of histamine, leukotrienes, and slow-reacting substance of anaphylaxis from mast cells by inhibiting degranulation following exposure to reactive antigens.Adverse effects include cough, flushing, palpitation, chest pain, nasal congestion, nausea, fatigue, migraine, etc.

Hyperthermia (Temperature 39.5 C) points towards the use of ecstasy.MDMA (3,4 – methylenedioxymethamphetamine), or more commonly known as Molly or Ecstasy, is a synthetic psychoactive substance.Patients who consumed MDMA may present in a tachycardic, hypertensive, hyperthermic, and agitated state. Adverse effects, even at minor recreational doses, include increased muscle activity (such as bruxism, restless legs, and jaw clenching), hyperactivity, insomnia, difficulty concentrating and feelings of restlessness.Treatment of MDMA overdose:Emphasis should be on maintaining the airway along with the stabilization of breathing and circulation.Patients may present obtunded due to hyponatremia requiring endotracheal intubation.For the hyperthermic patient, evaporative cooling along with ice packs to the groin and axilla are beneficial.Patients who present in severe toxicity within one hour of ingestion can receive activated charcoal PO or via an NG tube. Antipyretics, such as acetaminophen, should be avoided as they have no role and can worsen an already compromised liver.

Lead can be absorbed through the skin and by inhalation. It is associated with iron deficiency and a microcytic anaemia. The most common gastrointestinal symptoms are abdominal colic and constipation.

1. Normal saline (N saline) should be started IV: Intravenous normal saline is recommended to enhance renal excretion of lithium. Adequate hydration is crucial because lithium is primarily excreted by the kidneys, and maintaining good urine output can help reduce lithium levels.
2. Dialysis: This is considered the most effective treatment for severe lithium toxicity, especially when serum levels are significantly elevated (typically >2.5 mmol/L) and the patient presents with severe symptoms such as seizures, altered mental status, or renal impairment. Given the patient’s lithium level of 3.2 mmol/L and her critical condition, dialysis is necessary to rapidly reduce lithium levels.

The other options are less appropriate or ineffective in this context:

• Gastric lavage should be considered: This is not typically recommended for lithium poisoning because lithium is rapidly absorbed and lavage is unlikely to be effective several hours post-ingestion.
• Activated charcoal is likely to be effective: Activated charcoal does not effectively bind lithium and is not recommended for lithium poisoning.
• 5% dextrose should be started IV: While maintaining hydration is important, normal saline is preferred over dextrose solutions in this context to promote renal excretion of lithium.
• Dialysis is not normally required unless levels are above 5 mmol/L: This statement is incorrect. Dialysis is often required at lower levels, particularly in cases of severe toxicity or if the patient is symptomatic, as seen in this case.

The most probable diagnosis in this patient is an oculogyric crisis, that is most appropriately managed with procyclidine or benztropine (antimuscarinic). An oculogyric crisis is a dystonic reaction to certain drugs or medical conditions.Features include:Restlessness, agitationInvoluntary upward deviation of the eyesCauses:PhenothiazinesHaloperidolMetoclopramidePostencephalitic Parkinson’s diseaseManagement:Intravenous antimuscarinic agents like benztropine or procyclidine, alternatively diphenhydramine or ethopropazine maybe used.

Acute dystonic reactions (extrapyramidal symptoms) such as spasmodic torticollis, trismus, and oculogyric crises can occur following the administration of metoclopramide or stemetil and thus, neither is recommended for the treatment of nausea in young women.

Such reactions respond well to treatment with benztropine or procyclidine.

– Benztropine: It is an anticholinergic medication with significant CNS penetration. A single dose of benztropine 1 to 2 mg IV followed by 1 to 2 mg p.o twice a day for up to 7 days to prevent a recurrence. Subsequently, both the offending agent and those from the same group should be avoided.

– Alternatively, diphenhydramine can be used intravenously (up to a dose of 50mg) or intramuscularly followed by p.o therapy every 6 hours for 1 to 2 to prevent a recurrence.- Second-line therapy with IV benzodiazepines is reserved for those patients who do not respond to anticholinergics.

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.

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 phosphateSigns and symptoms of Organophosphorus Poisoning (OPP) can be classified as:• Muscarinic effects:o Cardiovascular – Bradycardia, hypotensiono Respiratory – Rhinorrhoea, bronchorrhea, bronchospasm, cough, severe respiratory distresso Gastrointestinal – Hypersalivation, nausea and vomiting, abdominal pain, diarrhoea, faecal incontinenceo Genitourinary – Incontinenceo Ocular – Blurred vision, miosiso 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, apnoeaMainstay Treatment:• Decontamination• Securing Airway, Breathing and Circulation• Atropine• Pralidoxime• Benzodiazepines

The principal mechanism by which strontium inhibits osteoclast activity is by enhancing the secretion of osteoprotegerin (OPG) and by reducing the expression of the receptor activator of nuclear factor κB ligand (RANKL) in osteoblasts.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 true statement among the given options is that she will still be protected against pregnancy if she takes amoxicillin for a lower respiratory tract infection while on the combined pill.Other than enzyme-inducing antibiotics such as rifampicin, antibiotics do not reduce the efficacy of the combined oral contraceptive pill.It was previously advised that barrier methods of contraception should be used if taking an antibiotic while using the contraceptive pill, due to concerns that antibiotics might reduce the absorption of the pill. This is now known to be untrue. However, if the absorptive ability of the gut is compromised for another reason, such as severe diarrhoea or vomiting, or bowel disease, this may affect the efficacy of the pill.The exception to the antibiotic rule is that hepatic enzyme-inducing antibiotics such as rifampicin and rifaximin do reduce the efficacy of the pill. Other enzyme-inducing drugs, such as phenytoin, phenobarbital, carbamazepine or St John’s Wort can also reduce the effectiveness of the pill.Other options:The combined pill is often prescribed for women with heavy periods as it can make them lighter and less painful. There is no evidence that women on the combined pill put on any significant weight, although they may experience bloating at certain times in the course. Women on the pill require monitoring of their blood pressure. There are multiple different types of combined pills.

Here, the patient seems to be intolerant to standard metformin. In such cases, modified-release preparations is considered as the most appropriate next step. There is some evidence that these produce fewer gastrointestinal side-effects in patients intolerant of standard-release metformin.Metformin is a biguanide and reduces blood glucose levels by decreasing the production of glucose in the liver, decreasing intestinal absorption and increasing insulin sensitivity. Metformin decreases both the basal and postprandial blood glucose.Other uses: In Polycystic Ovarian Syndrome (PCOS), Metformin decreases insulin levels, which then decreases luteinizing hormone and androgen levels. Thus acting to normalize the menstruation cycle.Note:Metformin is contraindicated in patients with severe renal dysfunction, which is defined as a glomerular filtration rate (GFR) less than 30 ml/min/1.732m2. Metformin overdose has been associated with hypoglycaemia and lactic acidosis, for this reason, it has a black box warning for lactic acidosis.