Free NEET PG & INI-CET Anaesthesia MCQs

Explanation

The ASA (American Society of Anesthesiologists) physical status classification, I to VI, grades a patient's overall fitness and perioperative risk. ASA I is a normal healthy patient; higher classes reflect increasing systemic disease.

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Standard '6-4-2' fasting rules allow no solids for 6 hours, breast milk up to 4 hours, and clear fluids up to 2 hours before anaesthesia. Fasting reduces the risk of aspiration of gastric contents during induction.

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Mendelson's syndrome is a chemical, acid, aspiration pneumonitis caused by inhaling acidic gastric contents. Fasting, and rapid sequence induction with cricoid pressure in at-risk patients, reduce this risk.

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The Mallampati classification assesses the visibility of the oropharyngeal structures — soft palate, uvula, and pillars — with the mouth open, helping predict difficult laryngoscopy and intubation. A higher class, III or IV, suggests a potentially difficult airway.

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Benzodiazepines such as midazolam are commonly used for anxiolysis and amnesia as premedication. Other premedicants may target secretions with antimuscarinics, aspiration risk with antacids or H2 blockers, or pain with analgesics.

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Predictors of difficult intubation include reduced mouth opening, limited neck extension, a short thyromental distance, a high Mallampati class, a receding mandible, and a large tongue. Anticipating difficulty allows preparation of appropriate equipment and plans.

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A sustained end-tidal CO2 waveform on capnography is the gold standard for confirming tracheal rather than oesophageal intubation, as continued CO2 return indicates ventilation of the lungs. Auscultation and chest movement are supportive but less reliable.

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Rapid sequence induction aims to secure the airway quickly and minimise aspiration risk, using a rapid-onset induction agent and a fast-acting muscle relaxant — suxamethonium or high-dose rocuronium — traditionally with cricoid pressure and minimal bag-mask ventilation.

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An LMA is a supraglottic device sitting over the laryngeal inlet, providing a hands-free airway without tracheal intubation. It is useful for suitable elective cases and as a rescue device in difficult airways, but offers less protection against aspiration than a cuffed tracheal tube.

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In a 'cannot intubate, cannot oxygenate' situation, after failed intubation, supraglottic airway, and bag-mask ventilation, emergency front-of-neck access by cricothyroidotomy is the final life-saving step to restore oxygenation.

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Laryngospasm, reflex vocal cord closure, is first managed with 100% oxygen, gentle positive pressure, and a jaw thrust, removing any stimulus. If it persists and causes hypoxia, a small dose of suxamethonium relaxes the cords.

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Preoxygenation, or denitrogenation, fills the lungs' functional residual capacity with oxygen, extending the time a patient can tolerate apnoea during intubation before desaturating. It is especially important in rapid sequence induction and difficult airways.

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An over-advanced endotracheal tube usually enters the right main bronchus, which is wider, shorter, and more vertical, leading to ventilation of only the right lung and collapse or hypoventilation of the left. Auscultation and capnography help detect this.

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The triad of general anaesthesia is hypnosis, meaning unconsciousness and amnesia, analgesia, and muscle relaxation. Balanced anaesthesia combines agents to achieve each component while minimising side effects.

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Propofol is the most widely used IV induction agent, giving rapid, smooth induction and quick recovery with antiemetic properties. It can cause hypotension and pain on injection. Ketamine, thiopental, and etomidate suit specific situations.

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Ketamine causes sympathetic stimulation, tending to maintain or raise blood pressure and heart rate, making it useful in hypotensive or shocked trauma patients. It also provides analgesia and bronchodilation, though it can cause emergence phenomena.

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MAC is the alveolar concentration of an inhalational agent that prevents movement in response to a surgical stimulus in 50% of patients. A lower MAC indicates a more potent agent. MAC is reduced by opioids, age, and hypothermia.

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Suxamethonium has a rapid onset and short duration, ideal for rapid sequence induction, but can cause hyperkalaemia — dangerous in burns, crush injury, and neuromuscular disease — as well as muscle pains and bradycardia, and it is a trigger for malignant hyperthermia.

Explanation

Neostigmine, an acetylcholinesterase inhibitor, reverses non-depolarising muscle relaxants by increasing acetylcholine at the neuromuscular junction. It is given with an antimuscarinic such as glycopyrrolate or atropine to prevent bradycardia. Sugammadex is a newer specific reversal agent for rocuronium and vecuronium.

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Accidental awareness is most likely when muscle relaxants paralyse the patient but the depth of anaesthesia is inadequate, so the patient cannot move to signal wakefulness. Depth-of-anaesthesia monitoring and careful technique reduce this risk.

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Spinal anaesthesia injects local anaesthetic directly into the CSF in the subarachnoid space, producing rapid, dense sensory and motor block of the lower body. It is commonly used for lower-limb, pelvic, and caesarean surgery.

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The spinal cord usually ends, at the conus medullaris, around L1 to L2 in adults, so spinal anaesthesia is given below this level, commonly L3-L4, to avoid cord injury, entering the CSF where only the cauda equina nerve roots lie.

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Spinal anaesthesia blocks sympathetic fibres, causing vasodilation and hypotension, sometimes with bradycardia. It is managed with IV fluids and vasopressors such as phenylephrine or ephedrine. A high block can also impair breathing.

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Epidural anaesthesia deposits local anaesthetic in the epidural space, outside the dura, giving a slower onset than spinal but allowing a catheter for continuous or repeated dosing — useful for labour analgesia and postoperative pain. It uses larger drug volumes than spinal.

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A post-dural puncture headache results from ongoing CSF leakage through the dural hole, lowering CSF pressure; it is classically postural, worse upright. Management ranges from conservative measures to an epidural blood patch for severe or persistent cases.

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Ultrasound guidance lets the anaesthetist visualise the target nerve, the needle, and the spread of local anaesthetic in real time, improving the success and safety of peripheral nerve blocks compared with landmark or nerve-stimulator techniques alone.

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Local anaesthetics reversibly block voltage-gated sodium channels in nerve membranes, preventing depolarisation and impulse conduction. Smaller, myelinated pain fibres are blocked before larger motor fibres.

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Adrenaline causes local vasoconstriction, which prolongs the anaesthetic's duration, reduces systemic absorption and toxicity, and lessens bleeding. It is avoided at end-artery sites — fingers, toes, penis, nose, and ears — where it could cause ischaemia.

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Local anaesthetic systemic toxicity begins with perioral numbness and tingling, tinnitus, a metallic taste, and light-headedness, and can progress to seizures, arrhythmias, and cardiovascular collapse. Treatment includes stopping the injection, supportive care, and intravenous lipid emulsion.

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Intravenous 20% lipid emulsion, 'intralipid', is the specific antidote for severe local anaesthetic systemic toxicity, thought to act as a 'lipid sink' that sequesters the lipophilic anaesthetic. It is given alongside standard resuscitation.

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Local anaesthetic toxicity is dose-related, so the maximum safe dose is calculated per kilogram of body weight — lignocaine roughly 3 mg/kg plain, more with adrenaline — to avoid systemic toxicity. Weight-based dosing is especially important in children.

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Pulse oximetry non-invasively measures peripheral arterial oxygen saturation using differential light absorption by oxygenated and deoxygenated haemoglobin. It is a standard minimum monitor during anaesthesia.

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A sudden loss of the capnography waveform is an emergency sign that may indicate oesophageal intubation, circuit disconnection, airway obstruction, or cardiac arrest, where there is no cardiac output to deliver CO2 to the lungs. It demands immediate assessment.

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Minimum monitoring during general anaesthesia includes continuous pulse oximetry, capnography, ECG, non-invasive blood pressure, and measurement of inspired oxygen, with agent and airway pressure monitoring. These allow early detection of problems.

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A nerve stimulator delivering a 'train-of-four' assesses the degree of neuromuscular blockade and the adequacy of reversal, helping avoid residual paralysis after surgery. The ratio of the fourth twitch to the first guides recovery.

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Anaesthesia impairs thermoregulation, so patients are prone to perioperative hypothermia, which increases bleeding, wound infection, and cardiac events, and prolongs drug effects. Warming devices and temperature monitoring help maintain normothermia.

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Malignant hyperthermia is a rare inherited reaction to volatile agents and suxamethonium, causing a hypermetabolic crisis with rising CO2, temperature, rigidity, and tachycardia. The specific treatment is dantrolene, plus stopping triggers, cooling, and supportive care.

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Adrenaline is the first-line, life-saving treatment for anaphylaxis, counteracting vasodilation and bronchospasm. Stopping the trigger, giving oxygen and IV fluids, and adjunct steroids and antihistamines follow. Muscle relaxants and antibiotics are common triggers during anaesthesia.

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5-HT3 antagonists such as ondansetron are widely used for preventing and treating PONV, often combined with dexamethasone. Identifying high-risk patients, for example with the Apfel score, guides prophylaxis.

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Suxamethonium apnoea results from a genetic deficiency or abnormality of plasma pseudocholinesterase (butyrylcholinesterase), so suxamethonium is metabolised slowly, causing prolonged paralysis. Management is continued ventilation and sedation until the block wears off.

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Intraoperative bronchospasm is managed with 100% oxygen, deepening anaesthesia — volatile agents are bronchodilators — and bronchodilators such as salbutamol; adrenaline is used if severe or anaphylactic. The trigger, such as light anaesthesia or a drug, should be addressed.

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A Venturi mask delivers a fixed, precise FiO2, such as 24% or 28%, regardless of the patient's breathing pattern, making it useful when controlled oxygen is needed, as in COPD patients at risk of CO2 retention.

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Isotonic crystalloids such as Ringer lactate and normal saline are first-line for hypovolaemic shock, restoring intravascular volume. In haemorrhagic shock, blood products are given for ongoing blood loss; dextrose solutions are poor volume expanders.

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Acute respiratory distress syndrome is managed with lung-protective ventilation — low tidal volumes of about 6 mL/kg predicted body weight, limited plateau pressures, and appropriate PEEP — to reduce ventilator-induced lung injury and improve outcomes.

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Early sepsis management, the 'sepsis six', includes oxygen, blood cultures, early broad-spectrum IV antibiotics, IV fluids, lactate measurement, and monitoring urine output. Prompt antibiotics markedly improve survival.

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The recovery, or lateral, position helps keep the airway open and allows secretions or vomit to drain, reducing aspiration risk in an unconscious but breathing patient without suspected spinal injury. Airway, breathing, and circulation are reassessed continually.

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The WHO analgesic ladder starts with non-opioids such as paracetamol and NSAIDs for mild pain at step 1, adds weak opioids for moderate pain at step 2, and strong opioids for severe pain at step 3, with adjuvants at any step.

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Respiratory depression is the most dangerous opioid side effect, potentially fatal in overdose, and is reversed by naloxone. Other effects include sedation, nausea, constipation, pruritus, and miosis.

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PCA allows the patient to self-administer small, preset opioid boluses on demand, with a lockout interval and dose limits for safety. It gives better pain control and satisfaction than intermittent nurse-administered dosing.

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Neuropathic pain responds poorly to standard analgesics; first-line agents include tricyclic antidepressants such as amitriptyline, SNRIs such as duloxetine, and anticonvulsants such as gabapentin and pregabalin, which modulate abnormal nerve signalling.