IM25.1-22 | Geriatrics — Graded Quiz

Correct. Haloperidol (and all antipsychotics) prolongs the QTc interval via potassium channel blockade. In an elderly patient with AF, CKD, and an active infection (which causes electrolyte disturbance — hypokalaemia, hypomagnesaemia from poor intake and catecholamine release), the combined QTc-prolonging effect dramatically increases the risk of Torsades de Pointes — a polymorphic ventricular tachycardia that can degenerate to ventricular fibrillation. This is the most immediate life-threatening risk. In DLB specifically, haloperidol is absolutely contraindicated due to neuroleptic sensitivity.

Delirium management: first-line = non-pharmacological (HELP protocol: reorientation, hydration, early mobilisation, vision/hearing aids, sleep protocol, family presence). Pharmacological intervention only for severe agitation threatening safety — lowest effective dose of haloperidol, monitoring QTc, electrolytes. Haloperidol ABSOLUTELY CONTRAINDICATED in Lewy body dementia.

The immediate life-threatening risk of IV haloperidol in this elderly patient is QTc prolongation leading to Torsades de Pointes, especially in the context of infection-related electrolyte disturbance (hypokalaemia) and AF. Antipsychotic use in elderly patients with dementia also increases 30-day mortality from cardiovascular events. Non-pharmacological de-escalation (reorientation, familiar voice, low lighting, therapeutic presence) is the first-line management of delirium-related agitation.

Correct. This is a classic presentation of Alzheimer disease: insidious onset, progressive course, early episodic memory loss (repeating questions), followed by apraxia (difficulty dressing in correct sequence — a parietal lobe sign), with MRI showing medial temporal lobe (hippocampal) atrophy. The primary neurochemical deficit in Alzheimer disease is acetylcholine deficiency due to neuronal loss in the nucleus basalis of Meynert — this is the rationale for cholinesterase inhibitor therapy (donepezil, rivastigmine). Vascular dementia has a stepwise progression with vascular risk factors and white matter changes; FTD has early personality change; NPH has the Hakim triad (gait, urinary incontinence, dementia).

Dementia type differentiation: Alzheimer = insidious + hippocampal atrophy + ACh deficit. Vascular = stepwise + cerebrovascular risk factors + white matter changes. DLB = hallucinations + parkinsonism + fluctuating. FTD = early personality/behaviour change + frontal atrophy. NPH = Hakim triad (wet-wobbly-wacky). Reversible causes: hypothyroidism, B12 deficiency, normal pressure hydrocephalus, subdural haematoma — investigate with TFT, B12, CT head.

Alzheimer disease: most common dementia (50-70%); insidious onset; early episodic memory loss then semantic memory, language, and visuospatial/parietal (apraxia, agnosia); MMSE declines 3-4 points/year untreated. Neurochemical deficit: acetylcholine (nucleus basalis of Meynert) → rationale for cholinesterase inhibitors. MRI: hippocampal and medial temporal lobe atrophy. Treatment: donepezil/rivastigmine/galantamine (mild-moderate), memantine (moderate-severe, NMDA antagonist).

Correct. Frailty — a state of reduced physiological reserve across multiple organ systems — is an independent predictor of adverse surgical outcomes including post-operative delirium, prolonged hospital stay, complications, new functional dependence (inability to return to pre-operative ADL status), and 30-day and 90-day mortality. Frailty risk is relevant for both elective and emergency surgery. Detection of frailty should trigger prehabilitation (nutritional optimisation, exercise, medication review), informed consent discussion about risk, and a clear post-operative rehabilitation plan — not automatic cancellation.

Perioperative geriatric assessment: frailty, functional status (ADL/IADL), cognition (MMSE), nutritional status (albumin, MNA), polypharmacy review. Prehabilitation: nutrition + exercise for 4-8 weeks pre-operatively improves outcomes. Post-operative: early mobilisation within 24h, avoid bladder catheters beyond 24h, DVT prophylaxis, pain control avoiding opioids where possible, delirium prevention protocol.

Frailty independently predicts post-operative delirium, prolonged hospitalisation, new functional dependence, and mortality in both elective and emergency surgery. A high frailty score should trigger prehabilitation and informed consent about elevated risk — not automatic cancellation. Frailty markers include slow gait speed (TUG >12s), low grip strength, exhaustion, weight loss, low physical activity, and low albumin (malnutrition).

Correct. Capacity assessment is decision-specific (a patient may lack capacity for one decision but retain it for another) and time-specific (capacity can fluctuate, especially in delirium). The four functional criteria for capacity are: (1) understanding the relevant information, (2) retaining it long enough to make the decision, (3) weighing up the information to arrive at a choice, and (4) communicating that choice. Age alone, diagnosis of dementia or depression, or a treatment refusal that clinicians disagree with do NOT automatically establish incapacity. The Mental Healthcare Act 2017 in India establishes the right of persons with mental illness to make decisions about their own treatment.

Ethical principles in geriatric care: autonomy (most commonly violated by ageism), beneficence, non-maleficence, justice. Capacity is decision-specific and time-specific — must be assessed freshly for each significant decision. Mental Healthcare Act 2017 (India): rights of persons with mental illness; advance directives recognised. Do not conflate age, cognitive impairment, or treatment refusal with incapacity.

Capacity is decision-specific and time-specific. The four criteria: understand + retain + weigh + communicate. Age and diagnosis do not automatically remove capacity. The Mental Healthcare Act 2017 (India) enshrines the right of persons with mental illness to make treatment decisions. If capacity is confirmed, a competent refusal must be respected. Only a formal capacity assessment showing failure of one or more of the four criteria justifies overriding a decision in the patient's best interests.

Correct. The combination of unexplained bruising, malnutrition, unkempt appearance, and paranoid accusations raises a significant safeguarding concern for elder abuse. The FIRST step is to interview the patient alone (privately, without the potential perpetrator present) to create a safe space for disclosure. Elder abuse occurs in 4-10% of elderly Indians, is perpetrated most often by family caregivers, and takes the form of physical, financial, emotional, sexual abuse, or neglect. The Maintenance and Welfare of Parents and Senior Citizens Act 2007 provides legal recourse in India. Prescribing an antipsychotic without assessment, assuming benign explanations, or discharging without safety assessment would all be errors.

Elder abuse: affects 4-10% of elderly; types: physical, emotional, financial, sexual, neglect. Risk factors: cognitive impairment, social isolation, caregiver stress, substance abuse, financial dependence. Indian law: Maintenance and Welfare of Parents and Senior Citizens Act 2007. Screen privately; document injuries with photo; involve social work; Maintenance Tribunals can order care and protection.

Unexplained bruising + malnutrition + unkempt appearance = screen for elder abuse. The first step is always to interview the patient PRIVATELY — remove the potential abuser from the room. Elder abuse (physical, financial, emotional, neglect) is perpetrated most often by family members or caregivers. Indian law: Maintenance and Welfare of Parents and Senior Citizens Act 2007. Screen with tools like EASI (Elder Abuse Suspicion Index). Document carefully; involve social work; do not discharge to an unsafe home without a safety plan.

Correct. SSRI-induced SIADH (syndrome of inappropriate antidiuretic hormone secretion) is a well-recognised complication of SSRIs in elderly patients, typically presenting within the first 4-6 weeks of treatment. Hyponatraemia (serum sodium <135 mEq/L, here severely low at 126) causes confusion, lethargy, nausea, and increased fall risk. Elderly patients have reduced renal concentrating ability and are more susceptible to this complication. Sertraline is the preferred SSRI in the elderly (least drug interactions, not anticholinergic), but sodium should be checked at baseline and after 4 weeks. The management is to stop or hold the SSRI and correct the sodium.

Depression in elderly: SSRIs first-line (sertraline, escitalopram preferred). Avoid paroxetine (anticholinergic), tricyclics (anticholinergic, cardiac arrhythmia, falls). SSRI monitoring: serum sodium at baseline and 4 weeks (SIADH risk). GDS-15 score: 5-8 mild, 9-11 moderate, 12-15 severe. Treat 6-12 months; relapse risk high if stopped early in elderly.

SSRI-induced SIADH causing hyponatraemia is a common and under-recognised complication in elderly patients, typically occurring within 4-6 weeks of starting therapy. Sodium 126 mEq/L = severe hyponatraemia → confusion + falls. Action: hold the SSRI, correct sodium, recheck before restarting at lower dose. Sertraline/escitalopram are preferred SSRIs in elderly (not contraindicated). Always check sodium at baseline and 4 weeks after SSRI initiation in the elderly.

Correct. Intrinsic fall risk factors are patient-related: peripheral neuropathy (impaired sensory feedback from feet), orthostatic hypotension (lying-to-standing systolic BP fall ≥20 mmHg or diastolic ≥10 mmHg), and joint disease (impaired proprioception from knee OA). These arise from the patient's physiology. Extrinsic factors are environmental (loose rugs, poor lighting, absence of grab rails, wet floors). Medications are often considered a separate modifiable category. Effective falls prevention must address intrinsic, extrinsic, AND medication-related factors simultaneously — single-component interventions are less effective than multifactorial programmes.

Falls assessment: TUG test >12 sec = fall risk. Orthostatic hypotension: systolic drop ≥20 mmHg or diastolic ≥10 mmHg on standing after 3 minutes. Multifactorial intervention = most effective: exercise (balance/strength), medication review (stop benzodiazepines, review antihypertensives), vision correction, home modification, vitamin D if deficient.

Intrinsic fall risk factors = patient physiology: sensory impairment (peripheral neuropathy, visual loss), balance disorders, muscle weakness, orthostatic hypotension (systolic drop ≥20 mmHg on standing), joint disease, cognitive impairment, incontinence (rushing to toilet). Extrinsic = environment: loose rugs, poor lighting, no grab rails. Medications = modifiable: benzodiazepines, antihypertensives, diuretics, sedatives. Multifactorial fall prevention addresses all three simultaneously.

Correct. Neuroplasticity — the biological basis of rehabilitation — is maximally exploited by early, high-intensity, task-specific, interdisciplinary rehabilitation. Post-stroke rehabilitation should begin within 24-48 hours of medical stability. High-intensity training (e.g., constraint-induced movement therapy, repetitive task training) drives cortical reorganisation. Left neglect is addressable through specific neglect rehabilitation strategies. AF with embolic stroke requires anticoagulation (INR 2-3 for VKA, or a DOAC) — this should be started within 2 weeks of ischaemic stroke (not deferred until rehabilitation is complete).

Geriatric rehabilitation principles: early, high-intensity, task-specific, interdisciplinary, goal-directed. Team: geriatrician, physiotherapist, OT, speech therapist, neuropsychologist, social worker. Outcome measures: FIM (Functional Independence Measure), Barthel Index, MRS (Modified Rankin Scale). Neuroplasticity basis: use-dependent cortical reorganisation maximised by high-repetition, task-specific training within the critical window post-injury.

Post-stroke rehabilitation principles: early (24-48h after medical stability), high-intensity, task-specific, interdisciplinary (physiotherapy + OT + speech therapy + neuropsychology). Neuroplasticity drives recovery — more practice = more cortical reorganisation. Left neglect requires specific rehabilitation (visual scanning training, prism adaptation). AF post-stroke: anticoagulate within 2 weeks (DOAC or warfarin INR 2-3) — do NOT defer for rehabilitation.

Correct. Refeeding syndrome is caused by the rapid reintroduction of carbohydrates after prolonged starvation. Insulin release drives phosphate (and potassium and magnesium) into cells — in a severely phosphate-depleted patient, serum phosphate falls catastrophically (hypophosphataemia <0.5 mmol/L). Phosphate is critical for ATP production; profound ATP deficit causes: (1) respiratory muscle weakness and respiratory failure, (2) cardiac arrhythmia and heart failure, (3) rhabdomyolysis, (4) haemolytic anaemia, and (5) neurological dysfunction. Prevention: correct electrolytes first, start feeding slowly (50% of target calories), monitor electrolytes daily, supplement thiamine.

Refeeding syndrome: risk groups (BMI <16, minimal intake >10 days, massive weight loss). Mechanism: insulin-driven cellular phosphate uptake → hypophosphataemia → ATP deficit. Manifestations: respiratory failure, cardiac arrhythmia, haemolytic anaemia, rhabdomyolysis, seizures. Prevention: NICE refeeding guidelines — correct electrolytes first, start at 10 kcal/kg/day, supplement thiamine + multivitamins, daily electrolyte monitoring.

Refeeding syndrome: rapid carbohydrate refeeding in a severely malnourished patient → insulin surge → cellular uptake of phosphate (and K+ and Mg2+) → acute hypophosphataemia → ATP depletion → respiratory failure, cardiac arrhythmia, rhabdomyolysis. Prevention: start feeding slowly (25-50% target), correct electrolytes before starting, supplement thiamine, monitor phosphate/K+/Mg2+ daily for 1 week. High-risk: BMI <16, weight loss >15% in 3-6 months, minimal intake >10 days.

Correct. NSAIDs (ibuprofen) are on both the STOPP criteria and the Beers Criteria as potentially inappropriate medications in elderly patients with heart failure and CKD. Mechanism: NSAIDs inhibit prostaglandin-mediated renal afferent arteriolar dilation → acute deterioration of GFR; they cause sodium and water retention → volume overload → worsening heart failure; they antagonise the effects of ACE inhibitors and diuretics. NSAIDs in a patient on spironolactone + ramipril + furosemide also increases the risk of hyperkalaemia. Paracetamol is the analgesic of choice for osteoarthritis in elderly patients with CKD and heart failure.

STOPP criteria highlights: NSAIDs (contraindicated in heart failure, CKD ≥stage 3, on anticoagulants); benzodiazepines (falls, cognitive impairment); long-acting sulfonylureas (hypoglycaemia); PPIs >8 weeks without clear indication (C. difficile, hypomagnesaemia). START criteria highlights: ACE inhibitor in systolic HF, bisphosphonate in long-term corticosteroid users, anticoagulation in AF.

NSAIDs (ibuprofen) are STOPP criteria-listed as inappropriate in elderly patients with heart failure (sodium/water retention worsens cardiac function) and CKD (afferent arteriolar constriction reduces GFR). Additionally, NSAIDs + ACE inhibitor + diuretic = 'triple whammy' combination causing acute kidney injury. Substitute paracetamol (maximum 3 g/day in elderly, avoid 4 g/day) for osteoarthritis analgesia. If NSAIDs are unavoidable, use lowest dose, shortest duration, with a PPI.

Correct. The CGA is a multidimensional assessment that covers: (1) medical domain (comorbidities, medications, disease-specific problems), (2) functional domain (ADL — activities of daily living such as bathing, dressing, eating; and IADL — instrumental activities such as medication management, cooking, shopping, finances), (3) psychological domain (cognition, mood), (4) social domain (social support, caregiver availability, social isolation, abuse risk), and (5) environmental domain (home safety, accessibility, transport). This patient's primary impairments are: IADL impairment (unable to manage medications), social (living alone, no family support), and environmental (unsafe bathroom, no grab rails) — functional + social + environmental domains.

CGA domains and tools: Medical = problem list + medications (STOPP/START); Functional = ADL (Barthel/Katz), IADL (Lawton); Cognitive = MMSE, MoCA; Psychological = GDS; Social = social history + carer assessment; Environmental = home safety assessment. Outcome: coordinated MDT management plan. CGA evidence base: reduces hospital readmission, nursing home placement, and mortality in acutely hospitalised elderly.

CGA domains: medical, functional (ADL/IADL), psychological (cognition/mood), social (support network, isolation), environmental (home safety). This patient's presenting problems map to: IADL impairment (medication management), social isolation (no family, living alone), and environmental hazards (no grab rails, unsafe home) = functional + social + environmental. The CGA drives the multidisciplinary plan — each impaired domain triggers a specific intervention.

Correct. Recurrent fractures and progressive DEXA decline despite 2 years of oral bisphosphonate adherence represents treatment failure on oral bisphosphonates. The first step is to reassess: confirm adherence (bisphosphonates must be taken correctly — fasting, 30 minutes before food, upright), exclude secondary causes of osteoporosis (hyperparathyroidism, malabsorption, vitamin D insufficiency, corticosteroid use). If true treatment failure, escalation options include: denosumab (RANK-L inhibitor, SC injection every 6 months, can be used with eGFR <30), or teriparatide (PTH analogue, anabolic, indicated for severe osteoporosis or bisphosphonate failure, 18-24 month course). Two bisphosphonates simultaneously is not appropriate.

Osteoporosis treatment escalation: first-line bisphosphonate (alendronate/risedronate oral, zoledronic acid IV). Treatment failure = escalate to denosumab (RANKL inhibitor, works in CKD) or teriparatide (anabolic, severe cases). Bisphosphonate holiday: at 5 years (oral) or 3 years (IV zoledronic) in lower-risk patients — not applicable in treatment failure. Fracture liaison service (FLS) model improves secondary prevention.

Osteoporosis treatment failure: recurrent fractures + progressive DEXA decline despite bisphosphonate adherence. First: check adherence (empty stomach, 30 min before food/medications, stand upright for 30 min) + secondary causes (hyperparathyroidism, Cushing, malabsorption). Then escalate: denosumab (RANKL inhibitor, 60 mg SC every 6 months, safer than bisphosphonate in CKD) or teriparatide (anabolic PTH analogue, severe/refractory osteoporosis). Never combine two bisphosphonates.