Geriatric Medicine

Oliver Hart

Welcome to the Geriatric Medicine podcast! This episode aims to recap all of the important aspects of each topic so that you feel confident in your knowledge.

Alys Davies

We’ve split the episode into two parts. First, we will go through the Geriatric Medicine topic breakdown. Then we will move into our rapid-recall question round, a section where we test your knowledge on the topics we have covered in the episode.

Oliver Hart

There are nine Geriatric Medicine topics to cover, with tips dotted throughout.

Alys Davies

If you are using this podcast as revision for upcoming exams, please always look on official websites for specifics on question weighting and structure. In this episode, we will be explaining each topic through realistic clinical scenarios, like the ones you will encounter in exams and real clinical situations.

Oliver Hart

So, let’s get started!

Alys Davies

The first topic we’ll discuss is frailty. Understanding frailty well means that topics like falls, delirium, and polypharmacy all make more sense, because frailty is the biological context in which those problems occur.

Oliver Hart

At its core, frailty is caused by sarcopenia, the loss of skeletal muscle mass and function. The biological drivers are denervation of fast-twitch muscle fibres, decline of anabolic hormones including IGF-1, testosterone, and DHEA, chronic low-grade inflammation called inflammaging mediated by IL-6 and TNF-alpha, and mitochondrial dysfunction. These processes interact and accelerate each other, which is why frailty tends to progress.

Alys Davies

With muscle loss as the driver, interventions like progressive resistance exercise and adequate protein intake can directly address the cause. Protein intake for at-risk older adults is 1.0 to 1.5 grams per kilogram per day, above the standard RDA, and worth knowing for nutrition-focused questions.

Alys Davies

To assess frailty in practice, there are three tools the exam tests. The first is the Fried Frailty Phenotype, which defines frailty using five measurable clinical criteria. The mnemonic we have created for this is WEAKS. If a patient has 1 or 2 of these criteria, then they are considered pre-frail.

Oliver Hart

The first letter. W, is weight loss, an unintentional weight loss of 4.5killograms, or 5% of body weight in the past year.

Alys Davies

E, exhaustion, a self-reported fatigue.

Oliver Hart

A, activity, a low activity level, usually within the lowest quintile.

Alys Davies

K, kinesis, related to the patient's movement, specific to the patient's sex and height threshold.

Oliver Hart

And S, strength, specific to the patient’s sex and BMI threshold.

Alys Davies

The second tool is the Clinical Frailty Scale, which is used at the bedside to grade overall severity of frailty. It runs from 1: very fit, to 9: terminally ill. Two specific scores come up in exam questions. CFS 5 is mildly frail: the person is dependent for instrumental ADLs, things like managing finances or transport, but still independent for personal care. CFS 7 is severely frail: dependent for all personal care.

Oliver Hart

Remember, CFS is scored on premorbid function two weeks before acute illness. Scoring the acute presentation instead of the premorbid baseline is the most commonly tested frailty error.

Alys Davies

The third tool is the Frailty Index, which uses the cumulative deficit model, the ratio of deficits present to total deficits assessed. A score above 0.25 indicates frailty. It is more sensitive than the Fried Phenotype and better for tracking change over time, but it is better suited to population research than rapid bedside use. In clinical practice, the CFS is more commonly used.

Oliver Hart

Let’s move on to frailty management. There is no licensed pharmacological treatment for frailty itself. The evidence base supports these interventions: progressive resistance exercise, nutritional optimisation including protein supplementation, vitamin D 800 IU daily, and the Comprehensive Geriatric Assessment as the delivery framework.

Alys Davies

The CGA structures care across seven domains: medical, functional, cognitive, psychological, social, environmental, and nutritional. The Barthel Index for functional ADLs, the MoCA out of 30 for cognition, the GDS-15 for depression, and the MUST for nutritional screening.

Oliver Hart

Remember. Distinction between ward-based CGA and CGA consultation models often appears in the exam papers. Ward-based CGA, where the geriatric team is embedded on the ward, increases the likelihood of a patient being alive and at home at 12 months. However, CGA consultation models, where the team reviews a patient from outside the ward, do not show the same benefit. This is from the 2017 Ellis Cochrane review.

Alys Davies

Now, we’re moving on to falls. A fall is usually the result of several risk factors acting together, which is why assessment and management both need to be multifactorial. That multifactorial aetiology is captured in the mnemonic DAME PIVOTS, and knowing it lets you systematically identify every contributing factor.

Oliver Hart

D, drugs, like psychotropics, antihypertensives, opioids, and alpha-blockers.

Alys Davies

A, age-related changes, like baroreceptor sensitivity, muscle mass, and vision.

Oliver Hart

M, musculoskeletal. Issues similar to sarcopenia, arthritis, and foot problems.

Alys Davies

E, environment, with hazards like poor lighting, no grab rails, and ill-fitting footwear.

Oliver Hart

P, postural hypotension.

Alys Davies

I, impaired cognition or vision.

Oliver Hart

V, vestibular dysfunction.

Alys Davies

O, other medical conditions, like Parkinson's, stroke, neuropathy, and hypoglycaemia.

Oliver Hart

T, training deconditioning.

Alys Davies

And S, syncope or near-syncope.

Oliver Hart

Of all the factors in our DAME PIVOTS mnemonic, postural hypotension is one of the most frequently examined because it has a precise definition and a clinically important subtype distinction. Postural hypotension is defined as a sustained drop in systolic BP of 20 mmHg or more, or diastolic 10 mmHg or more within 3 minutes of standing.

Alys Davies

The subtype distinction: neurogenic causes (Parkinson's disease and MSA) show no compensatory heart rate rise on standing, because the autonomic nervous system is damaged and cannot respond. Non-neurogenic causes, such as volume depletion or medication, show tachycardia as a compensatory response. That physiological difference tells you something important about the underlying cause and guides management.

Oliver Hart

Once risk factors are established, assessment focuses on two areas: mobility testing and fracture risk quantification, both of which directly inform management decisions. For mobility, the Timed Up and Go test is the standard bedside measure. Over 12 seconds indicates high fall risk, and over 20 seconds indicates impaired mobility.

Alys Davies

For fracture risk, FRAX calculates 10-year fracture probability and is interpreted using NOGG thresholds to guide treatment decisions. A fragility fracture is a clinical diagnosis of osteoporosis regardless of the DXA T-score.

Oliver Hart

That brings us to bone protection. DXA T-scores for osteoporosis are minus 2.5 or below. For osteopenia, T-scores are minus 1 to minus 2.5. A score which is considered normal is minus 1 or above. First-line bone protection is alendronic acid 70 milligrams weekly, a nitrogen-containing bisphosphonate that inhibits osteoclasts. If oral is not tolerated, use zoledronic acid 4 annually.

Alys Davies

To close the falls topic, we’d like to highlight the evidence base for prevention. NICE NG 249 2025 supports three interventions: the OTAGO and FaME exercise programmes, which improve strength and balance; home hazard modification, which addresses the environmental factors in the DAME PIVOTS mnemonic; and medication review, which is where the STOPP criteria directly apply.

Alys Davies

Remember, stopping denosumab without transitioning to a bisphosphonate causes rebound vertebral fractures. Always plan the exit strategy before starting it.

Oliver Hart

Delirium. This topic carries high clinical stakes. In definition: delirium is an acute disturbance of attention, awareness, and cognition, developing over hours to days, with a fluctuating course, representing a change from baseline. It is a medical emergency.

Alys Davies

To understand why delirium happens, and why it is managed the way it is, you need the three pathophysiological mechanisms. First, cholinergic deficiency: this explains why anticholinergic drugs precipitate delirium, and why patients with dementia are so vulnerable, because they already have reduced cholinergic reserve.

Oliver Hart

Second, relative dopaminergic excess: this is the rationale for haloperidol as a D2 antagonist in severe cases.

Alys Davies

And third, neuroinflammation: peripheral cytokines crossing the blood-brain barrier, which is why systemic illness, surgery, and pain can all trigger delirium.

Oliver Hart

Those mechanisms point directly to the precipitants. We’ve given it the mnemonic PINCH ME. It gives you the full list of delirium precipitants.

Alys Davies

P, pain — undertreated or new.

Oliver Hart

I, infections — like UTI, pneumonia, sepsis, or a surgical wound.

Alys Davies

N, nutrition/dehydration.

Oliver Hart

C, constipation.

Alys Davies

H, hypoxia and metabolic disturbances — like electrolytes, glucose, and uraemia.

Oliver Hart

M, medications. Like opioids, anticholinergics, sedatives, new additions.

Alys Davies

And E, environment — an unfamiliar ward, immobility, sensory deprivation, or night disruption.

Alys Davies

Knowing the precipitants gets you to the cause. The next step is recognising which subtype of delirium you are dealing with, because the subtypes look very different clinically and the hypoactive subtype is the one most commonly missed. Hyperactive delirium accounts for around 25% of cases and is hard to miss. Hypoactive accounts for around 50%, carries the worst prognosis, and is the one most often attributed to tiredness or low mood. In a clinical situation, if a patient is quiet and nobody has flagged them as a concern, think hypoactive delirium.

Oliver Hart

For assessment, there are two validated tools, and you need to know what each is for. The 4AT is the bedside screening tool. It has four components: alertness, Abbreviated Mental Test 4 (or AMT 4), attention, and acute change. A score of 4 or above indicates probable delirium. A score of 1 to 3 suggests possible cognitive impairment.

Alys Davies

The Confusion Assessment Method, or CAM, is the reference standard for trained assessors. It requires: acute onset plus fluctuation, plus inattention, plus either disorganised thinking or altered consciousness. With trained assessors, it gives a sensitivity of 94% and specificity of 89%.

Alys Davies

Management follows directly from the model. First, review the patient using the mnemonic PINCH ME. Then, look at non-pharmacological measures to support recovery: reorientation, sensory optimisation including hearing aids and glasses, sleep hygiene, early mobilisation, nutrition and hydration.

Oliver Hart

The HELP programme — Hospital Elder Life Program — reduces delirium incidence by around 30% through structured delivery of these measures. Pharmacological intervention is reserved for severe agitation that poses a safety risk: haloperidol 0.5 to 1 milligram.

Alys Davies

Remember, haloperidol is contraindicated in Parkinson's disease and Lewy body dementia. The risk of acute neuroleptic sensitivity reactions is significant and can be fatal. If antipsychotic cover is needed in these patients, use quetiapine at the lowest effective dose under specialist guidance.

Oliver Hart

Now, we’ll look at Dementia. The starting point is knowing the four subtypes, their distinguishing features, and how the management differs between them.

Alys Davies

Alzheimer's disease is the first and most common. The pathology is amyloid-beta plaques and tau tangles, the clinical presentation is insidious memory loss, and MRI shows hippocampal atrophy. Vascular dementia is the second and is driven by cerebrovascular disease. The key feature is stepwise deterioration, and prominent executive dysfunction. There are no licensed pharmacological treatments, so management focuses instead on vascular risk factor modification.

Oliver Hart

The third subtype is Lewy body dementia, which has the most specific and the most examined diagnostic features. Alpha-synuclein pathology is the basis.

Alys Davies

The clinical features for this is captured in the mnemonic FLAP. F, fluctuating cognition. L, lewy body pathology on DATscan. A, alerting visual hallucinations. and P, parkinsonism.

Oliver Hart

Remember, REM sleep behaviour disorder can also occur, this is where the patient acts out dreams, a symptom wich predates dementia by years.

Alys Davies

The fourth subtype is frontotemporal dementia and can appear in exams due to its atypical presentation and younger patient age range. The typical age range for patient onset is 45 to 65. The behavioural variant presents with disinhibition, loss of empathy, and personality change; these are the features that differentiate it from Alzheimer's, where memory loss is the dominant early symptom. Language variants also occur, but there are no licensed treatments.

Oliver Hart

All four subtypes are diagnosed through the same general framework per NICE NG97: clinical history plus informant account, cognitive testing with ACE 3 preferred, blood tests to exclude reversible causes of cognitive decline, and a brain MRI.

Alys Davies

DATscan is the specific investigation that distinguishes Lewy body dementia from Alzheimer's — it shows reduced striatal dopamine transporter uptake in Lewy body and is normal in Alzheimer's.

Oliver Hart

Pharmacological treatment is subtype-specific, and this is where NICE TA217 applies. For mild to moderate Alzheimer's, acetylcholinesterase inhibitors are first-line, donepezil, rivastigmine, or galantamine. They work by inhibiting acetylcholinesterase, preventing ACh breakdown and increasing cholinergic transmission. Side effects are nausea, diarrhoea, and bradycardia. Rivastigmine is the only AChEI licensed specifically for Parkinson's disease dementia.

Alys Davies

For moderate to severe Alzheimer's, memantine is added. It is an NMDA receptor antagonist that blocks pathological glutamate excitotoxicity. AChEIs and memantine have no role in vascular dementia; the treatment is vascular risk factor modification. A non-pharmacological obligation that is frequently examined is the DVLA notification duty.

Oliver Hart

Remember. Antipsychotics are contraindicated in both Lewy body dementia and Parkinson's disease dementia due to neuroleptic sensitivity in up to 50% of patients. This applies to typical and most atypical antipsychotics at any dose and is one of the most heavily tested safety points in exams in this module.

Oliver Hart

The next topic is BPSD, Behavioural and Psychological Symptoms of Dementia. This topic sits alongside dementia because it is a consequence of the underlying disease process, but it has its own assessment and management framework which might be tested in exams. BPSD covers agitation, aggression, wandering, sleep disturbance, psychosis including hallucinations and delusions, depression, and anxiety.

Alys Davies

Up to 90% of people with dementia experience BPSD at some point, so this is not a rare or specialist scenario, it is something that appears routinely in clinical practice.

Oliver Hart

The management hierarchy and the order of the steps is the core of what you need to know. Step one, identify and address any underlying medical or environmental causes. This includes pain, constipation, infection, an unfamiliar environment, or a change in routine. Any of these can drive agitation in a person with dementia who cannot communicate the cause verbally. This step is not optional, it is the first response.

Alys Davies

Step two, person-centred non-pharmacological approaches. Things like structured activity, music therapy, and reminiscence therapy. These are the preferred interventions once reversible causes are excluded. Step three is pharmacological, and only if steps one and two have not been sufficient. Risperidone is the only licensed option for severe agitation in Alzheimer's disease specifically, at the lowest effective dose for the shortest duration, with a documented best interests decision or consent.

Oliver Hart

One important nuance from dementia pharmacology: AChEIs and memantine also have evidence for reducing BPSD symptoms in Alzheimer's. So optimising dementia treatment is part of BPSD management. And the contradiction that connects BPSD back to the dementia subtypes: in Lewy body dementia, antipsychotics are contradicted. If agitation is present in a patient with Lewy body, the pharmacological options are melatonin or clonazepam, for REM sleep behaviour disorder specifically, and only under specialist guidance.

Oliver Hart

Next we move on to depression. Depression is the most common underdiagnosed functional impairment in this age group, and partly because it presents differently from younger adults and overlaps with other geriatric syndromes in ways that create diagnostic confusion. Rather than expressed low mood, older adults with depression more often present with somatic complaints, withdrawal, and psychomotor slowing. That atypical presentation means it gets missed, and the GDS-15 is the validated screening tool to use, a score of 5 or above indicates probable depression.

Alys Davies

There are two diagnostic distinctions to remember here. The first is between depression and dementia, because depression can mimic cognitive decline, this is sometimes called pseudodementia. The key is that the cognitive symptoms improve when the depression is treated. Clinically, this matters because treating the right condition first can avoid unnecessary dementia workups.

Oliver Hart

The second distinction is between depression and delirium, because both can present with acute confusion. Delirium is distinguished by its acute onset over hours to days, fluctuating course, and identifiable precipitant. Depression develops more gradually.

Alys Davies

Treatment follows NICE NG222. With first-line: SSRIs, sertraline or citalopram are preferred in older adults because of their more favourable side effect profile. CBT is equally recommended for mild to moderate depression. Avoid TCAs — tricyclic antidepressants carry significant anticholinergic burden, fall risk, and cardiotoxicity in older adults. Monitor for serotonin syndrome when combining serotonergic agents, particularly in patients also on tramadol or linezolid.

Oliver Hart

Next, osteoporosis and hip fracture. While osteoporosis appeared briefly in the falls topic as part of fracture risk, it has its own clinical management pathway that is examined in detail, particularly the hip fracture pathway, which has specific time targets and a specific model of care.

Alys Davies

Hip fracture is the reason osteoporosis matters acutely: it carries a 30-day mortality of around 8% and a 1-year mortality of around 30%, making it one of the most clinically significant consequences of bone disease in older adults.

Oliver Hart

The model of care that improves outcomes is the orthogeriatric model, with a geriatrician and orthopaedic surgeon co-managing from the point of admission. This reduces complications, reduces time to surgery, and improves survival. That model is referenced in NICE CG124.

Alys Davies

Remember, one really important aspect is the time target of surgical repair, which is within 36 hours of admission.

Oliver Hart

The full hip fracture pathway is worth knowing as a sequence: admission and assessment, anaesthetic review, surgery within 36 hours, CGA, early mobilisation the following day, bone protection assessment using FRAX and DXA, discharge planning with rehabilitation, and then Fracture Liaison Service follow-up for secondary prevention.

Alys Davies

The last step, FLS, is specifically about preventing the next fracture, not just treating the current one. A patient who has had a fragility fracture and is not on bone protection.

Oliver Hart

While prescribing for bone protection, look at alendronate, calcium, and vitamin D, unless dietary intake is confirmed sufficient. If oral is not tolerated, use zoledronic acid 4. If neither is suitable, use denosumab, but be aware that denosumab-to-bisphosphonate transition must be planned before starting, because stopping denosumab without transitioning causes rebound vertebral fractures.

Alys Davies

Remember. Secondary fracture prevention may be included in exams. A patient who has already sustained a fragility fracture should be on bone protection unless there is a documented reason otherwise. The Fracture Liaison Service is the recommended pathway for identifying and treating these patients in the community.

Alys Davies

Our penultimate topic is urinary incontinence. The exam approach here is type-specific, matching the mechanism to the correct intervention is how these questions are answered. There are four types, each with a distinct underlying mechanism and a defined first-line treatment, and confusing them in the exam means selecting the wrong management. So let's go through each one.

Oliver Hart

Stress incontinence is caused by urethral sphincter weakness, leakage occurs with physical effort, coughing, or sneezing. First-line treatment is pelvic floor exercises. If those are insufficient, second-line is duloxetine or surgical repair.

Alys Davies

Urgency incontinence, also called overactive bladder, is caused by detrusor muscle overactivity. The patient experiences a sudden, urgent need to void followed by leakage before they can reach the toilet. First-line is bladder training. Second-line is antimuscarinics or mirabegron.

Alys Davies

Mixed incontinence has features of both stress and urgency. The management targets whichever component is predominant. Overflow incontinence is caused by incomplete bladder emptying, the bladder fills beyond capacity and leaks. Causes include benign prostatic hyperplasia, detrusor underactivity, and neurological disease such as spinal cord compression or diabetic neuropathy. Management depends on the cause: alpha-blockers like tamsulosin for BPH, or catheterisation for acute retention.

Oliver Hart

Remember, antimuscarinics, like oxybutynin, carry significant anticholinergic burden in patients with cognitive impairment, or those already on multiple anticholinergics. Instead, look at mirabegron, it’s a beta-3 agonist and has no anticholinergic effect, making it a much safer choice in this population.

Alys Davies

Our last topic is polypharmacy and pharmacokinetics. Older adults are often on multiple medications, and the way the body handles drugs changes with age, which means polypharmacy is more dangerous in this population than in younger adults. Polypharmacy is defined as five or more concurrent medications. Problematic polypharmacy is when the combination or doses are inappropriate.

Oliver Hart

The structured approach to medication review is STOPP and START. STOPP identifies medications that should be stopped. START identifies medications that should be started but are being missed. These criteria run through multiple Geriatric Medicine topics and knowing the key items from each list means you can apply them across different scenarios.

Alys Davies

Key STOPP items are anticholinergics in cognitive impairment, long-acting sulphonylureas like glibenclamide, benzodiazepines and Z-drugs in fall-risk patients, and PPIs without a clear indication.

Oliver Hart

Key START items are statins in established cardiovascular disease, bisphosphonates with long-term corticosteroids, and ACE inhibitors in heart failure with reduced ejection fraction.

Alys Davies

The Anticholinergic burden is the reason why the STOPP anticholinergic alert matters so much. It is the cumulative effect of multiple drugs, each with some anticholinergic activity. No single drug may be obviously problematic, but the combination tips the balance. Medication review, which is a core component of the CGA and falls assessment, is the process for identifying and reducing this burden.

Oliver Hart

That leads into pharmacokinetics, which is the mechanism that explains why drug doses and drug choices in older adults differ from standard adult prescribing. Four key changes. Reduced body water means higher concentrations of hydrophilic drugs, with digoxin and lithium accumulating faster. Increased body fat means accumulation and prolonged half-life of lipophilic drugs, typically where benzodiazepines and amiodarone stay in the system longer. Reduced albumin means more free drug available for protein-bound agents like warfarin and phenytoin, wich means more effect and more toxicity at the same dose.

Alys Davies

The fourth chain is reduced GFR despite a normal-looking creatine. In a frail older adult, muscle mass is reduced, so creatine production is low. The serum creatine can look normal while eGFR is significantly impaired. This matters because renally cleared drugs with a narrow therapeutic index will accumulate. Always calculate eGFR before prescribing in this population. The key drugs: digoxin, lithium, metformin, DOACs, and aminoglycosides.

Oliver Hart

Remember, normal creatine in a frail patient does not rule out significant renal impairment. Calculate eGFR, not just creatine. This often appears in examinations.

Alys Davies

Let’s move on to our rapid-recall.

Oliver Hart

This section is all about what you know, and quickly!

Alys Davies

We’ll ask you a question, give you a couple of seconds to answer, then give you the correct answer. Just try to shout out your answer in time!

Oliver Hart

Question 1. What does the K stand for in the frailty mnemonic WEAKS?

Alys Davies

The correct answer is kinesis, slow gait speed. This measurement should be adjusted for the sex and height of the patient.

Oliver Hart

Question 2. A patient scores CFS 7 on the Clinical Frailty Scale. What does that mean?

Alys Davies

A CFS 7 score means that a patient is severely frail, dependent for all personal care.

Oliver Hart

Question 3. What is the definition of postural hypotension?

Alys Davies

The answer is a sustained drop in systolic BP of 20 mmHg or more, or diastolic 10 mmHg or more, within 3 minutes of standing.

Oliver Hart

Question 4. What does C stand for in the delirium mnemonic PINCH ME?

Alys Davies

C stands for constipation.

Oliver Hart

Question 5. On the 4AT, what score indicates probable delirium?

Alys Davies

The answer is 4 or above.

Oliver Hart

Question 6. What does F stand for in the dementia mnemonic FLAP?

Alys Davies

F stands for fluctuating cognition.

Oliver Hart

Question 7. Which acetylcholinesterase inhibitor is specifically licensed for Parkinson's disease dementia?

Alys Davies

The answer is rivastigmine.

Oliver Hart

Question 8. What is the time target for surgical repair of a hip fracture?

Alys Davies

The target is within 36 hours of admission.

Oliver Hart

Question 9. Urgency incontinence. What is the first-line treatment?

Alys Davies

Bladder training.

Oliver Hart

And finally, question 10. In a frail older adult, why can a normal serum creatine be misleading?

Alys Davies

The answer is the reduction of muscle mass, which means that creatine production is low. The creatine can look normal while eGFR is significantly impaired. Always calculate eGFR before prescribing.

Oliver Hart

And that is your rapid recall done.

Alys Davies

Thank you for joining us for this episode. If you would like any more information on any of these topics, you can find it all on the module.

Oliver Hart

Thanks for joining.

Alys Davies

Bye!