GC079 Prescribing In Older People
Prescribing in older people involves the careful selection, dosing, and monitoring of medications to account for age-related pharmacokinetic and pharmacodynamic changes, polypharmacy, and increased vulnerability to adverse drug reactions.
Prescribing in Older People
This lecture, delivered by Dr KCP Chiu (Consultant, Division of Geriatrics, QMH), is a cornerstone General Clerkship session that addresses one of the most commonly examined and clinically dangerous areas in geriatric medicine: how ageing fundamentally changes the way drugs behave in the body, and why prescribing in older people demands a different mindset [1].
The core thesis is simple but profound: ageing seldom comes alone — older patients accumulate chronic diseases, episodic illnesses, disability, frailty, and consequently multiple drugs, which in turn cause adverse effects that cascade into further problems [1]. The lecture walks through five interconnected pillars:
- Adverse Drug Reactions (ADRs)
- Drug–Disease Interactions
- Drug–Drug Interactions
- Polypharmacy
- Medication Adherence
Each pillar is illustrated with vivid clinical cases that are classic exam material. The lecture concludes with prescribing principles — the "before / during / after" framework — that examiners love to test in SAQs, minicases, and MCQs.
This lecture is exceptionally high-yield for the Fourth Summative. Past papers repeatedly test ADR classification, the prescribing cascade, drug–disease interactions (especially the classic table), CYP450 interactions with Paxlovid/ritonavir, MALA, and deprescribing. The supplementary STOPP/START v3 and Beers Criteria are also testable.
Learning Objectives (Inferred from Slides)
- Understand pharmacokinetic and pharmacodynamic changes with ageing
- Recognise common ADRs causing hospital admissions in older adults
- Identify drug–disease and drug–drug interactions relevant to geriatric prescribing
- Define polypharmacy, the prescribing cascade, and deprescribing
- Apply principles of safe prescribing in older people
- Know STOPP/START and Beers Criteria at a conceptual level
"Aging seldom comes alone" — chronic diseases, acute illnesses, disability, frailty → multiple drug use → adverse effects from use of drugs [1]
The introductory case is a M/85 with HT, CHF, AF, stroke, PTB, OA knee, and gout [1]. This patient illustrates the vicious cycle:
- Fluid overload → diuretics → gout → colchicine → gastroenteritis → stopped diuretics → fluid overload again
Why this matters from first principles: Each additional drug creates more possible drug–drug and drug–disease pairings, while frailty, organ dysfunction and limited physiological reserve increase the chance that an interaction becomes clinically important. Polypharmacy is therefore a risk marker, not automatically inappropriate treatment: the question is whether every drug still has a worthwhile indication, dose and monitoring plan.
Age-related changes → Increase in plasma & tissue concentration of drugs → Increase in drug effect → ADR [1]
Pharmacokinetic Changes Table
| ADME Phase | Age-Related Change | Clinical Consequence |
|---|---|---|
| Absorption | ↓ gastric acid, ↓ GI motility, ↓ splanchnic blood flow | Usually modest effect; some drugs absorbed more slowly |
| Distribution | ↑ body fat, ↓ lean body mass, ↓ total body water, ↓ serum albumin | Fat-soluble drugs have ↑ Vd and ↑ half-life (e.g. diazepam); water-soluble drugs have ↑ plasma concentration (e.g. digoxin); ↓ albumin → ↑ free fraction of protein-bound drugs (e.g. warfarin, phenytoin) |
| Distribution | ↑ α₁-acid glycoprotein | ↓ free fraction of basic drugs (e.g. lidocaine, propranolol) — partially offsets the albumin effect for basic compounds |
| Metabolism | ↓ liver mass, ↓ hepatic blood flow, ↓ Phase I metabolism (CYP450) | ↓ first-pass metabolism → ↑ bioavailability of drugs with high hepatic extraction (e.g. propranolol, morphine); Phase II (conjugation) relatively preserved |
| Excretion | ↓ GFR, ↓ renal blood flow, ↓ tubular secretion | Accumulation of renally cleared drugs (e.g. digoxin, metformin, lithium, aminoglycosides) |
Read the medication screenshot before blaming age alone: The 79-year-old case has major vascular disease and diabetes complications and is taking aspirin, atorvastatin, basal insulin, linagliptin, metformin and pioglitazone. Several drugs may be appropriate secondary-prevention or glucose-lowering treatments; the task is to reconcile the list against function, renal status, hypoglycaemia risk, heart-failure risk, prior simvastatin rhabdomyolysis, goals and treatment burden. Current diabetes guidance supports simplifying or deintensifying when burdens/harms exceed benefits while retaining therapies with cardiovascular or kidney benefit when indicated [19].
Key clinical case — Metformin-Associated Lactic Acidosis (MALA):
Metformin is eliminated unchanged by the kidneys. When metformin accumulates in plasma, lactic acid increases → lactic acidosis [1]
The deck's incidence estimate (0.03–0.06 per 1000 patient-years) and “mortality approaches 50%” are historical figures. MALA remains rare but is a medical emergency; contemporary risk assessment focuses on metformin exposure plus a precipitating illness that impairs clearance or causes tissue hypoxia.
Conditions increasing risk of MALA: severe dehydration, shock, alcohol use, hypoxic states, sepsis, CHF, advanced age (age-related decline in renal function + increased risk of acute renal failure) [1]
MALA Mechanism (from Lecture Diagram) [1]:
For patients with eGFR < 30 mL/min/1.73m², metformin should NOT be prescribed [1]
Why from first principles: Metformin is cleared unchanged by the kidneys and suppresses hepatic gluconeogenesis from lactate. Acute kidney injury can therefore cause accumulation, while shock, sepsis or hypoxia independently increase lactate production and reduce clearance. MALA is usually a two-hit problem rather than ageing alone.
The lecture case (M/79) shows coffee-ground vomiting, a post-void bladder scan of about 441 mL, and 600 mL drained immediately after catheterisation. The creatinine then normalised. The screenshot therefore supports post-renal AKI from acute urinary retention, with possible concurrent volume depletion, rather than proving a purely pre-renal process. In a patient taking metformin, either mechanism can acutely reduce drug clearance [1].
Exam Trap: MALA
Students often forget that MALA risk isn't just about baseline CKD — any acute illness causing dehydration, sepsis, or hypotension can precipitate MALA in a patient with previously "acceptable" renal function on metformin. Always consider temporarily holding metformin during acute illness ("sick day rules").
Current renal-safety framing [12]:
- Obtain eGFR before treatment and at least annually; check more often in older adults or when renal function may be changing.
- Do not initiate metformin at eGFR 30–44 mL/min/1.73 m²; if eGFR falls below 45 during treatment, reassess benefit, dose and risk.
- Stop metformin if eGFR falls below 30. Temporarily withhold it during significant acute illness/AKI and in the specified iodinated-contrast settings; restart only after renal function is stable.
Pharmacodynamics = Biochemical & physiological effects of drugs. Older people are more sensitive to effects of some drugs, especially those acting on the CNS and CVS [1]
Pharmacodynamic Changes Table (Directly from Lecture Slide)
| Drug Class | Effect of Ageing | ADR |
|---|---|---|
| Antihypertensive agents | Increased risk | Hypotension |
| Benzodiazepines | Increased sensitivity | Drowsiness |
| Beta-adrenergic blockers | Decreased beta-adrenergic responsiveness | Bradycardia |
| Anticoagulants | Increased sensitivity | Bleeding tendency |
| Diuretics | Increased susceptibility to complications | Orthostatic hypotension & electrolyte disturbance |
Why from first principles: Ageing reduces the number and sensitivity of receptors, impairs baroreceptor reflexes (→ orthostatic hypotension), reduces cholinergic neurotransmission (→ increased vulnerability to anticholinergics), and reduces cerebral reserve (→ lower threshold for sedation and confusion).
Impact of ageing: PK changes + PD changes → increase in plasma/tissue drug concentration + increase in drug effect → ADR → necessitating dosage adjustment [1]
High Yield Lecture Framing
Elderly are excluded from clinical trials. Treatment decisions are derived from studies involving younger adults. The benefit-to-risk ratio is different in frail older patients with comorbidities. Applicability of study findings to routine geriatric practice is limited. "Evidence-based medicine" may turn into "evidence-biased medicine." Guidelines derived from such evidence may cause harm to elderly patients. [1]
This is a favourite conceptual exam question, but the slide wording is deliberately provocative. The safe conclusion is not to ignore guidelines: judge whether the trial population, time-to-benefit and outcomes match this person's frailty, cognition, function, comorbidity, life expectancy and goals. Under-treatment can be as harmful as over-treatment.
The four principles to reduce drug-related iatrogenic disease [1]:
- Think carefully before prescribing
- Prescribe with maximum knowledge about the patient and therapeutics
- Monitor the patient for efficacy and side-effects
- Help the patient make better use of their medication
Five Approaches to Optimise Medication Management in Older Adults [1]:
- Avoid adverse drug reactions
- Reduce polypharmacy (overuse)
- Avoid potentially inappropriate medications (misuse)
- Enhance medication adherence
- Avoid clinically important drug interactions
5. Adverse Drug Reactions (ADRs)
ADR: A harmful/unpleasant reaction from use of a medicinal product at normal dose → predicts risk from future use → warrants prevention, specific treatment, altered dose regimen, or withdrawal of drug [1]
| Type | Mnemonic | Features | Examples |
|---|---|---|---|
| A: Dose-related | Augmented | Common, related to pharmacological action, predictable, low mortality | Phenytoin toxicity; anticholinergic effects of TCAs |
| B: Non-dose-related | Bizarre | Uncommon, not related to pharmacological action, unpredictable, HIGH mortality | Penicillin hypersensitivity |
| C: Dose- and time-related | Chronic | Uncommon, related to cumulative dose | HPA axis suppression by corticosteroids |
| D: Time-related | Delayed | Uncommon, usually dose-related, occurs some time after use | Parkinsonism from neuroleptic drugs |
| E: Withdrawal | End of use | Uncommon, occurs soon after withdrawal | Opiate, benzodiazepine withdrawal syndrome |
| F: Unexpected failure of therapy | Failure | Common, dose-related, often caused by drug interactions | Phenytoin + Warfarin → reduced anticoagulation |
Exam Tip
The A–F classification is commonly tested in MCQs. The key discriminator: Type A = common + predictable + low mortality vs. Type B = uncommon + unpredictable + HIGH mortality. Type F (failure) is an underrecognised cause of ADRs — always consider drug interactions causing therapeutic failure (e.g., enzyme inducers reducing warfarin efficacy).
ADRs trigger increased hospitalisation, prolonged hospital stay, additional clinical investigations, and prescription cascades [1].
From Budnitz et al., NEJM 2011 [1]:
Four medication classes implicated alone or in combination in 67% of hospitalisations:
- Warfarin (33.3%)
- Insulins (13.9%)
- Oral antiplatelet agents (13.3%)
- Oral hypoglycaemic agents (10.7%)
From Hong Kong data (Chan et al., Drug Safety 1992) [1]:
4.4% of admissions attributed to ADRs. 84% from sulphonylureas, NSAIDs, insulin, diuretics, aspirin. Most frequent ADRs: hypoglycaemia (43%), GI haemorrhage (29.7%), dehydration/hypoNa/hypoK (5.4%). Old age & impaired renal function = important risk factors.
Key Exam Fact
The top causes of ADR-related hospitalisations are NOT exotic drugs — they are the everyday workhorses: warfarin, insulin, antiplatelets, oral hypoglycaemics, NSAIDs, and diuretics. Examiners test whether you know the common culprits, not rare idiosyncratic reactions.
5.5 Clinical Cases Illustrating ADRs
Admitted for decreased GCS 2 weeks after starting new medications [1]
Diagnosis: Thiazide-induced hyponatraemia
Key laboratory findings on admission [1]: Na 105 mmol/L (↓↓), K 3.4 mmol/L (↓), Cl 68 mmol/L (↓↓), Cr 102 µmol/L (↑), eGFR 43 — consistent with severe dilutional hyponatraemia with hypokalaemia and hypochloraemia.
Indapamide (Natrilix) is a thiazide-like diuretic. Common side effects: hyponatraemia, hypochloraemia, hypokalaemia, dehydration, orthostatic hypotension, hyperuricaemia [1]
Independent predictive factors of thiazide-induced hypoNa: increasing age, low body weight, low serum K level [1]
Mechanism: Thiazide and thiazide-like diuretics impair urinary dilution in the distal convoluted tubule while leaving the medullary concentrating mechanism relatively intact. Volume depletion, low solute intake, hypokalaemia and non-osmotic vasopressin can compound water retention. Older age, female sex and low body mass are common risk factors; the slide does not establish lisinopril as the mechanistic cause.
Immediate safety point: Na 105 mmol/L with reduced consciousness is severe symptomatic hyponatraemia. Stop the offending diuretic, assess tonicity/volume and other causes, and treat urgently in a monitored setting. Contemporary guidance uses 3% hypertonic saline for severe symptoms, aiming for an initial rise of roughly 4–6 mmol/L sufficient to reverse cerebral oedema, then limits further correction to avoid osmotic demyelination; potassium replacement also raises serum sodium and must be counted [13].
Extensive investigations unremarkable. More history: 15 tablets of Zopiclone per night for > 10 years (OTC). Diagnosis: Zopiclone dependence & withdrawal delirium. Treatment: Zopiclone resumed and titrated down → alertness improved [1]
Zopiclone: non-benzodiazepine hypnotic. Licensed for SHORT-TERM treatment of insomnia only. Long-term continuous use is NOT recommended [1]
Why this matters: This is a Type E ADR (withdrawal/end of use). When a patient physically dependent on a sedative-hypnotic is admitted and the drug is abruptly omitted because it was not captured in the medication history, withdrawal delirium may follow. Z-drugs can cause delirium, falls, fractures and dependence in older adults and offer only modest sleep benefit [14]. Stabilisation and a slow, supervised, individualised taper are safer than abrupt cessation; severe withdrawal may need inpatient management. The lesson is to ask non-judgmentally about prescribed, OTC, borrowed, herbal and traditional medicines [20].
A 76-year-old lady developed neck swelling, fever, and skin rash after 1 month of allopurinol → subsequently passed away after 2 months [1]
Allopurinol-induced SJS/TEN: delayed-type immune-mediated reaction. Strong association with HLA-B5801. Risk of SJS/TEN increased 80–97 times in HLA-B5801 carriers. This adverse event could be prevented if genetic information is known a priori [1]
Why this is critical: This is a severe delayed immune-mediated cutaneous adverse reaction. HLA-B*58:01 markedly increases the risk of allopurinol-associated SJS/TEN and DRESS, but the event is not entirely “unpredictable”: ancestry, CKD and starting dose matter. Current ACR guidance conditionally recommends pre-treatment testing in people of Southeast Asian ancestry (including Han Chinese, Korean and Thai people) and African American patients, and recommends against universal testing in lower-prevalence groups [15]. If positive, choose an alternative rather than expose the patient; never rechallenge after allopurinol SCAR.
The patient was admitted for UTI, had GI bleeding, and upon discharge the Calcichew D3 was omitted. She was due for denosumab with CKD (eGFR 30) and no calcium/vitamin D supplementation [1].
Denosumab inhibits osteoclastic bone resorption → reduces calcium mobilisation from bone → hypocalcaemia. Risk factors: renal impairment, vitamin D deficiency, lack of prophylactic calcium/vitamin D supplementation [1]
High risk of hypoCa in CKD and lack of Ca/Vit D supplementation among patients receiving denosumab [1]
Read the laboratory screenshot: Six weeks before the injection, total calcium was 2.06 mmol/L but albumin-adjusted calcium was 2.38 mmol/L. After denosumab, total calcium fell to 1.61 mmol/L, adjusted calcium to 1.93 mmol/L, with phosphate 0.77 mmol/L — genuine, clinically important hypocalcaemia rather than low albumin alone [1].
Current safety update [16]:
- Before each dose, assess kidney function, corrected/ionised calcium, vitamin D and — in advanced CKD — evidence of CKD-mineral and bone disorder (CKD-MBD); correct hypocalcaemia first and ensure an appropriate calcium/vitamin D plan.
- The FDA now carries a boxed warning for severe hypocalcaemia in advanced CKD, especially dialysis or CKD-MBD. Specialist input is appropriate when renal osteodystrophy is possible.
- In advanced CKD, monitor calcium closely after injection: most reported severe events occurred 2–10 weeks later, peaking at weeks 2–5. “Check in two weeks” without first correcting risk factors is not a safe plan.
- Do not casually omit, delay or stop denosumab: rebound bone turnover can cause multiple vertebral fractures. If it must be discontinued, arrange timely alternative antiresorptive therapy rather than simply abandoning treatment.
6. Drug–Disease Interactions
Exacerbations by medications of pre-existing diseases, conditions, or syndromes. More common in older adults (multiple chronic diseases + multiple medications). More adverse impact (less physiologic reserve) [1]
Antihistamines have anticholinergic properties → decrease detrusor tone & impair bladder sensation. Sympathomimetic (decongestant) properties → increase smooth muscle tone in neck of bladder. Combined effect in a patient with underlying BPH → acute urinary retention [1]
These are risk flags, not ten universal absolute contraindications. Judge indication, dose, alternatives and monitoring in context.
| Disease/Condition | Drugs to Avoid | Mechanism/Reason |
|---|---|---|
| BPH | Anticholinergics; TCA | Reduce detrusor tone, impair bladder emptying |
| CRF | NSAIDs | Further ↓ GFR via prostaglandin inhibition |
| Constipation | Anticholinergics; Opioids; TCA | Reduce gut motility |
| DM | Corticosteroids | Hyperglycaemia via gluconeogenesis/insulin resistance |
| Falls | Antipsychotics; Sedative-hypnotics; TCA; Benzodiazepines | Sedation, postural hypotension, impaired balance |
| Heart block | Digoxin; TCA | Worsen AV conduction |
| Narrow-angle glaucoma | Anticholinergics | Pupil dilation → angle closure |
| Parkinson's disease | Metoclopramide | D2 receptor blockade worsens Parkinsonism |
| Peptic ulcer disease | Aspirin; NSAIDs | Mucosal damage via COX-1 inhibition |
| Syncope | Alpha-blockers | Postural hypotension |
Exam Trap: Metoclopramide in Parkinson's
Metoclopramide blocks central D2 receptors and can worsen Parkinsonism. Do not reflexively substitute domperidone: it has dose-, age- and interaction-related QT/arrhythmia risk, and ritonavir can further increase exposure. Choose an antiemetic for the actual indication and individual cardiac/drug-interaction profile.
Learning point: Pay attention to drug–disease interaction when initiating drug treatment in a patient with underlying medical conditions [1]
7. Drug–Drug Interactions
A clinically meaningful alteration in the effect of one drug (object drug) as a result of co-administration of another (precipitant drug). May have potentially life-threatening consequences in older adults [1]
Elderly are more susceptible because of age-related PK/PD changes, increased risk of diseases, and increased medication use. Drug-drug interactions are often PREDICTABLE and therefore AVOIDABLE or MANAGEABLE [1]
The most frequent pharmacokinetic drug–drug interactions involve CYP450 isoenzymes and drug transporters such as P-glycoprotein [1]
CYP450 Inducers and Inhibitors (Lecture List, with an Important Caveat)
| CYP450 Inducers (↑ activity) | CYP450 Inhibitors (↓ activity) |
|---|---|
| Phenobarbitone | Amiodarone |
| Phenytoin | Diltiazem |
| Primidone | Verapamil |
| Carbamazepine | Ciprofloxacin |
| Rifampicin | Clarithromycin |
| Itra-/keto-/fluconazole | |
| Metronidazole | |
| Sulphonamide | |
| Cimetidine | |
| Ritonavir |
Mechanism of enzyme induction:
Enzyme inducers + substrate drugs → Increased clearance → Reduced effects of substrate drugs [1]
Substrates affected: antidepressants, calcium antagonists, corticosteroids, cyclosporin, theophylline, thyroxine, warfarin, nirmatrelvir [1]
Mechanism of enzyme inhibition:
Enzyme inhibitors + substrate drugs → Decreased clearance → Enhanced effects of substrate drugs [1]
Same substrates are affected but in the opposite direction only when the relevant isoenzyme/transporter and exposure actually overlap. “CYP inhibitor” is not a single interchangeable property: ciprofloxacin is mainly a CYP1A2 inhibitor, clarithromycin strongly inhibits CYP3A, fluconazole prominently inhibits CYP2C9/2C19 and ritonavir strongly inhibits CYP3A plus several transporters. Always check the exact drug pair, renal/hepatic function, time course and therapeutic index.
Mnemonic for CYP Inducers
"PC BRAS" — Phenobarbitone, Carbamazepine, Barb(s), Rifampicin, Alcohol (chronic), St John's Wort (though not listed on slide, clinically important). Or remember the anti-epileptic drugs + rifampicin as the core inducers.
Paxlovid = nirmatrelvir (SARS-CoV-2 main protease inhibitor) + ritonavir (inhibits metabolism of nirmatrelvir → increases its plasma concentration). Ritonavir itself is NOT active against SARS-CoV-2 [1]
Ritonavir is a STRONG CYP3A4 inhibitor AND a P-glycoprotein inhibitor → concomitant use of Paxlovid and certain drugs may result in significant drug interactions [1]
Historical context: The slide reproduces a 2022 HA CCIDER pathway and early Omicron-era Hong Kong observational data. Treat those as historical evidence, not a current prescribing algorithm. Current eligibility, preferred antiviral and renal dosing must be checked against the live local guideline. The durable teaching point is medication reconciliation before a time-limited antiviral whose booster has major interactions.
Paxlovid Drug Interaction Table (HIGH YIELD — Directly from Lecture)
| Concomitant medication | Consequence | Current label-level response [17] |
|---|---|---|
| Rivaroxaban | Increased exposure/bleeding | Avoid concomitant use |
| Apixaban | Increased exposure/bleeding | Management depends on the existing apixaban dose; consult its label/specialist rather than applying a blanket rule |
| Dabigatran | Increased exposure/bleeding | Dose-reduce or avoid depending on indication and renal function |
| Warfarin | INR may rise or fall | If coadministration is necessary, monitor INR closely |
| Amiodarone (also dronedarone, flecainide, propafenone, quinidine) | Potential serious arrhythmia | Contraindicated with Paxlovid |
| Digoxin | Increased exposure/toxicity | Use caution and monitor serum concentration/clinical toxicity |
| Simvastatin or lovastatin | Myopathy/rhabdomyolysis | Stop ≥12 h before Paxlovid, throughout the 5-day course and for 5 days after; a permanent statin switch is not automatically required |
| Clonazepam | Increased exposure/sedation | Dose reduction may be needed with clinical monitoring |
| Quetiapine | Increased exposure/toxicity | If unavoidable, reduce dose and monitor according to its label |
| Carbamazepine, phenytoin, phenobarbital or primidone | Marked loss of antiviral exposure/possible resistance | Contraindicated; a brief hold does not solve the interaction because induction persists after stopping |
Management strategies for Paxlovid drug interactions [1]:
- Increasing monitoring for potential adverse reactions
- Adjusting dose of concomitant medication
- Temporarily withholding the concomitant medication
- Using an alternative to the concomitant medication
- Using alternative COVID-19 therapies
Exam Intelligence: Paxlovid
The key teaching point is not that ritonavir “raises everything.” It is a strong CYP3A inhibitor and affects P-gp and other pathways, so consequences are drug-specific: some combinations are contraindicated, some require a temporary hold or dose change, some need monitoring, and strong inducers can make Paxlovid ineffective. Check the current product label plus an authoritative interaction resource for the complete medication list, including OTC/herbal drugs.
Elderly have reduced homeostatic mechanisms → particularly sensitive to combined effects of two drugs. Even additive (not synergistic) effects may be sufficient to cause adverse effects [1]
Dangerous Pharmacodynamic Combinations (Directly from Lecture)
| Combination Category | Drugs | Risk |
|---|---|---|
| Postural hypotension | Nitrates + Ca antagonists + ACEI + Alpha-blockers + Antiparkinsonian agents | Synergistic BP lowering → orthostatic hypotension → falls/syncope |
| Sedative effects and falls | Antihistamines + Hypnotics + Antipsychotics + Anticonvulsants | Additive CNS depression → falls, over-sedation |
Five steps [1]:
- Review all drugs for appropriate indications
- Discontinue the drug causing the interaction, or the drug affected
- Substitute with another drug of similar efficacy but lower interaction potential
- Decrease the dose
- Change the time of administration — useful mainly for absorption/administration interactions; spacing doses does not neutralise most CYP or transporter interactions
8. Polypharmacy
Polypharmacy = use of multiple medications by a patient. The minimum number is variable (generally 5–10). Must also consider OTC drugs and herbal/supplements [1]
For exams, ≥5 medicines is a common operational threshold, but distinguish appropriate polypharmacy (several evidence-based medicines with net benefit) from problematic polypharmacy (no current indication, duplication, unacceptable harm, treatment burden or goals no longer aligned).
The lecture illustrates this with two dramatic cases:
- A patient discharged on 23 drugs — including losartan, aspirin, senna, quetiapine, prednisolone, cyclosporin, diltiazem, metformin, atorvastatin, rabeprazole, gliclazide, frusemide, mycophenolate, lactulose, tramadol, hydralazine, escitalopram, levofloxacin, and Fosamax Plus, among others [1]. The screenshot should trigger indication/duration checks (some entries are explicitly for three days), interaction review and a realistic administration plan rather than an automatic “stop medicines” response.
- Madam Yip, F/72 with 19 diagnoses, 11 specialist clinics, and 33 medications spanning 8 specialty prescribers [1]
Increased risk of: ADRs, drug–drug interactions, drug–disease interactions, non-adherence, inappropriate drug use and medication errors; associated adverse outcomes include disability, cognitive impairment, falls/fractures, malnutrition, hospitalisation, institutionalisation, mortality and greater healthcare cost [1]
Deprescribing = the process of supervised withdrawal of inappropriate medications, for which potential harms outweigh benefits [1]
Through medication review → withdraw medications no longer appropriate or taper to minimum effective dosage → balance benefits & risks according to patient's current health status. Particularly relevant to patients with burden of polypharmacy or changing clinical conditions [1]
The deck states that planned withdrawal may reduce falls and improve cognition/psychomotor function. These benefits are not guaranteed for every drug or patient. Deprescribing is an active, supervised treatment: agree goals, prioritise the highest-harm/lowest-benefit drugs, taper when withdrawal or rebound is possible, monitor for symptom recurrence, and document who will follow up. STOPP/START and Beers identify candidates; they do not replace clinical judgement [14][18].
Common cause of polypharmacy. An adverse effect of one drug is misinterpreted as a new medical condition → prescription of another drug → additional unnecessary medications → increased medication burden [1]
Prescribing Cascade Examples (Directly from Lecture)
Example 1: BPSD → Antipsychotic → Extrapyramidal side effects → Levodopa [1]
- The antipsychotic blocks dopamine receptors → drug-induced Parkinsonism → treated with levodopa, creating a contradictory drug regimen
Example 2: Dihydropyridine CCB → Peripheral oedema → Diuretic → HypoNa/K → Na/K supplements [1]
- The ankle oedema from amlodipine is NOT fluid overload — it's peripheral vasodilation and capillary leak. Adding a diuretic doesn't address the cause and creates electrolyte disturbances.
As a general principle: Prescription of drugs solely for the purpose of treating drug side effects should be avoided in elderly patients [1]
Exam Trap: The Prescribing Cascade
This is a favourite SAQ/minicase stem. The examiner describes a patient on Drug A who develops Symptom X, and Drug B is added. You must recognise that Symptom X is a side effect of Drug A, not a new disease. The correct action is to reassess Drug A (stop, switch, or dose-reduce), NOT add Drug B.
9. Medication Adherence
Stopped all medicines for 3 weeks → admitted with dyspnoea/decompensated heart failure [1]
The 14-item list includes lisinopril, furosemide, potassium, digoxin, aspirin, famotidine, thyroxine, four antituberculous drugs plus pyridoxine, lactulose and senna. The image makes the mechanism visible: pill burden, intermittent TB dosing and several indications are cognitively demanding for a person living alone. “Non-compliance” labels the patient; non-adherence prompts us to find the barrier.
| Factor | Causes |
|---|---|
| Medication factors | Polypharmacy, complex regimens, side effect profiles, inconvenient dosing frequency |
| Patient factors | Poor understanding/disagreeing with plan, memory problems, behavioural factors, poor organisation, difficulty taking (vision, dexterity, pill dysphagia), affordability |
| Disease/condition factors | Asymptomatic disease, mild severity |
| Factor | Solutions |
|---|---|
| Medication | Remove non-beneficial drugs, simplify timing, reduce frequency where pharmacologically appropriate, and use combination products only when they truly reduce burden |
| Patient/system | Use teach-back and accessible written instructions; address cost, swallowing, vision, dexterity and beliefs; offer adherence aids only after checking the person can use them; involve chosen carers, pharmacists or community nurses |
| Disease/condition | Explain the purpose of preventive/asymptomatic treatment and agree a plan that reflects the patient's goals |
10. Principles of Prescribing in Older People
Take thorough history: medical Hx including cognitive Hx, social Hx, medication Hx (hospital records, private doctors, OTC medicines, traditional Chinese medicines) [1]
Prescribe only if necessary. Always look for non-drug alternatives. Avoid over- or under-use. Use the lowest possible effective dose [1]
The right drug → The right dose → The right route → Check allergy → Check RFT → Aware of side effects → START LOW & GO SLOW [1]
“Start low and go slow” is a titration principle, not permission to undertreat severe pain, infection, heart failure or another time-critical illness. Start at an age-/organ-appropriate dose, define the therapeutic target and titrate deliberately while monitoring.
Monitor patient for efficacy → Monitor side-effects → Check compliance → Discontinue unnecessary medications [1]
11. STOPP/START Criteria & Beers Criteria — Supplementary Material
The STOPP (Screening Tool of Older Persons' Prescriptions) identifies potentially inappropriate medications (PIMs) that should be stopped, while START (Screening Tool to Alert to Right Treatment) identifies potential prescribing omissions (PPOs) [4][5].
Key STOPP criteria relevant to this lecture [4]:
| Section | Criterion | Reason |
|---|---|---|
| Renal | Metformin if eGFR < 30 | Risk of lactic acidosis |
| Renal | Digoxin ≥125μg/day if eGFR < 30 (long-term) | Digoxin toxicity |
| Renal | Dabigatran if eGFR < 30 | Bleeding risk |
| Renal | Factor Xa inhibitors if eGFR < 15 | Bleeding risk |
| Renal | NSAIDs if eGFR < 50 | Deterioration of renal function |
| Renal | Bisphosphonates if eGFR < 30 | Acute renal failure |
| Renal | Nitrofurantoin if eGFR < 45 | Nitrofurantoin toxicity |
| GI | Metoclopramide with Parkinsonism | Exacerbates Parkinsonian symptoms |
| CNS | Levodopa for drug-induced Parkinsonism | Inappropriate prescribing cascade |
| Endocrine | Long half-life sulphonylureas (glibenclamide, chlorpropamide, glimepiride) | Prolonged hypoglycaemia |
| Endocrine | TZDs with heart failure | Worsens HF |
| Falls | Benzodiazepines in patients with recurrent falls | Reduced sensorium, impaired balance |
| Falls | Antipsychotics in patients with recurrent falls | May cause Parkinsonism |
| Falls | Hypnotic Z-drugs in patients with recurrent falls | Protracted sedation, ataxia |
Key updates relevant to this lecture [6][7]:
Aspirin for primary prevention of CVD: AVOID initiating in older adults. Consider deprescribing in those already taking it. Risk of major bleeding increases markedly with age. Note: Aspirin IS generally indicated for secondary prevention [6]
Avoid sulfonylureas as first- or second-line monotherapy/add-on when safer effective options are available. If one is used, the US Beers document prefers a short-acting agent such as glipizide over long-acting glimepiride or glyburide (glibenclamide). Gliclazide is commonly used locally but is not the named US Beers example [7][14].
Diphenhydramine (oral): avoid in older adults. Consider total anticholinergic burden during regular medication reviews [6]
Avoid baclofen when eGFR < 60 (risk of encephalopathy in older adults) [7]
STOPP/START vs. Beers
Both tools aim to optimise prescribing in older adults. STOPP/START is European and more systems-based; Beers is American. For HKU exams, you do NOT need to memorise every criterion — understand the principles (avoid PIMs, address PPOs) and know the high-yield examples listed above. The exam tests clinical reasoning, not criterion numbers.
Old age → Chronic diseases + Episodic illnesses → New drug use + Polypharmacy → ADRs + Drug-drug interactions + Drug-disease interactions + Medication non-adherence → All compounded by altered pharmacokinetics and pharmacodynamics → AVOID INAPPROPRIATE PRESCRIPTION [1]
Elderly subjects take more medications than any other age group. Age-related PK & PD changes → reduction in physiologic reserves → increasing risk of ADRs / drug-drug interactions / drug-disease interactions / polypharmacy. Special attention is needed in prescribing among the elderly population to prevent adverse outcomes [1]
13. Integration with Related Material
- Reinforces the systematic approach to checking indications, contraindications, dose adjustment, allergy, and interactions before every prescription
- Emphasises the role of clinical pharmacists in medication reconciliation
- Iatrogenesis (including drug-related harm) is one of the "geriatric giants" alongside immobility, instability, incontinence, and intellectual impairment
- ADRs are a leading cause of hospital admission in the elderly
- Frail patients have even less physiologic reserve → lower thresholds for ADRs
- Deprescribing is a key component of frailty management
- Drug-induced Parkinsonism (from antipsychotics, metoclopramide) is a key differential for Parkinsonism in the elderly
- Falls in the elderly are often multifactorial, with drugs being a modifiable risk factor
| Trap | Correct Reasoning |
|---|---|
| "Metformin is safe in all diabetic patients" | Must check eGFR; contraindicated if < 30; hold during acute illness |
| "Ankle oedema on CCB → give diuretic" | This is the prescribing cascade; switch CCB instead |
| "Antihistamine is safe for URTI in elderly" | Anticholinergic effects → urinary retention (BPH), constipation, glaucoma, sedation/falls |
| "Ignore guidelines because the patient is old" | Apply evidence through frailty, function, goals, time-to-benefit and treatment burden; avoid both over- and under-treatment |
| "Type A ADRs are dangerous" | Type A = common but LOW mortality; Type B = uncommon but HIGH mortality |
| "Aspirin for primary prevention in 80-year-old" | Beers 2023: AVOID. Risk of major bleeding outweighs benefit |
| "Zopiclone is safe for long-term use" | Licensed for short-term only; long-term → dependence and withdrawal delirium |
| "Everyone needs HLA-B*58:01 before allopurinol" | Test high-prevalence/high-risk groups (including Han Chinese in the ACR guideline); if positive, avoid allopurinol. Universal testing is not recommended for every ancestry |
High Yield Summary
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The Five Pillars of Prescribing Problems in Older People
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- ADRs — Top historical culprits include anticoagulants, insulin, antiplatelets, hypoglycaemics, NSAIDs and diuretics. Know the A–F classification. 2. Drug–Disease Interactions — Use the classic table as screening prompts. 3. Drug–Drug Interactions — Check the exact enzyme/transporter, dose, organ function and time course; Paxlovid management is drug-specific. 4. Polypharmacy — ≥5 is a screening threshold, not a diagnosis of inappropriate care. 5. Non-adherence — Find medication, patient, disease and system barriers; simplify and support rather than blame.
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-
Prescribing Principles
- Before (thorough Hx, assess need), During (right drug/dose/route, check RFT, check allergy, START LOW GO SLOW), After (monitor efficacy + side effects, check compliance, deprescribe).
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Key Specifics
- Metformin: do not start at eGFR 30–44; stop below 30 and withhold during relevant AKI/acute illness.
- Denosumab: correct calcium/vitamin D and assess CKD-MBD; monitor high-risk CKD patients after dosing and never stop without a transition plan.
- Allopurinol: test HLA-B*58:01 in high-risk ancestries/populations; avoid if positive and never rechallenge after SCAR.
- Zopiclone: older adults remain at risk of falls, delirium and dependence; avoid abrupt withdrawal after long-term use.
- Paxlovid/ritonavir: strong CYP3A inhibition creates contraindications, dose changes, temporary holds and monitoring needs that differ by drug.
Active Recall - Prescribing in Older People
[1] Lecture slides: GC 079. Prescribing in older people.pdf (all pages) [2] Senior notes: Block A - High white cell count_ acute and chronic leukaemia; bone marrow transplantation; immunogenetics.pdf (allopurinol/HLA-B*5801 section) [3] Senior notes: Block A - Chronic diarrhoea_ irritable bowel syndrome and inflammatory bowel disease.pdf (pharmacogenomics context) [4] GC 079 (supp-2)STOPP-START-V3.pdf (Sections D, E, F, J, K) [5] GC 079 (supp-1)STOPP-START criteria for potentially inappropriate prescribing in older 2023.pdf [6] AOS - Geriatrics.pdf (Beers Criteria pocket guide content) [7] GC 079 (supp-3)AGS Beers Criteria for potentially inappropriate med use_2023.pdf [8] Lecture slides: GC 029. Am I prescribing the right drug.pdf [9] Lecture slides: CFB (MED12) Introduction to Geriatric Medicine.pdf [10] Lecture slides: GC 054. Frailty in the older people.pdf [11] Lecture slides: GC 037. Common neurological problems in older people.pdf [12] US FDA. FDA revises warnings regarding use of metformin in certain patients with reduced kidney function. Current eGFR-based labelling recommendations. https://www.fda.gov/media/96771/download [13] Spasovski G. Hyponatraemia—treatment standard 2024. Nephrology Dialysis Transplantation. https://academic.oup.com/ndt/article/39/10/1583/7713921 [14] American Geriatrics Society Beers Criteria Update Expert Panel. 2023 updated AGS Beers Criteria® for potentially inappropriate medication use in older adults. J Am Geriatr Soc. https://doi.org/10.1111/jgs.18372 [15] FitzGerald JD, et al. 2020 American College of Rheumatology Guideline for the Management of Gout. Arthritis Care Res. https://pmc.ncbi.nlm.nih.gov/articles/PMC10563586/ [16] US FDA. Boxed Warning: severe hypocalcemia in patients with advanced CKD taking Prolia (denosumab). 2024. https://www.fda.gov/drugs/drug-safety-communications/fda-adds-boxed-warning-increased-risk-severe-hypocalcemia-patients-advanced-chronic-kidney-disease [17] US FDA. PAXLOVID (nirmatrelvir/ritonavir) Prescribing Information. 2025 label. https://www.accessdata.fda.gov/drugsatfda_docs/label/2025/217188s010lbl.pdf [18] O'Mahony D, et al. STOPP/START criteria for potentially inappropriate prescribing in older people: version 3. Eur Geriatr Med. 2023. https://pmc.ncbi.nlm.nih.gov/articles/PMC10447584/ [19] American Diabetes Association Professional Practice Committee. Older Adults: Standards of Care in Diabetes—2026. Diabetes Care. https://doi.org/10.2337/dc26-S013 [20] Joint Clinical Practice Guideline on Benzodiazepine Tapering. ASAM and partner societies, 2025. https://www.asam.org/quality-care/clinical-guidelines/benzodiazepine-tapering
GC078 Polyuria And Polydipsia Glucose Metabolism, Diabetes Mellitus, Diabetic Ketoacidosis
Polyuria and polydipsia in the context of disordered glucose metabolism arise from osmotic diuresis due to hyperglycemia, as seen in diabetes mellitus, which can progress to diabetic ketoacidosis when severe insulin deficiency leads to uncontrolled lipolysis, ketonemia, and metabolic acidosis.
GC079 (supp-1)stopp-start Criteria For Potentially Inappropriate Prescribing In Older 2023
The 2023 STOPP/START criteria are evidence-based screening tools designed to identify potentially inappropriate medications (STOPP) and potential prescribing omissions (START) in adults aged 65 years and older to optimize pharmacotherapy and reduce adverse drug events.