About this summary
On Saturday 5 September 2026, Healthed ran a Medical Update for the Brisbane / Gold Coast region. Twelve lectures were captured and published as individual CPD blogs on drkotha.com. This page is a single seminar overview: what each talk covered, clinic-facing takeaways drawn from those blogs, and links to the full write-ups (with audio where published).
Speaker names below match the published blogs and Otter titles. Where Otter did not capture a surname, that uncertainty is left explicit — surnames are not invented.
Talk 1
Obesity management update
Samantha Hockey
The lecture walked through a GP case — Monica, 62, BMI 33.7 with pre-diabetes, hypertension, dyslipidaemia and painful knee osteoarthritis — who plateaued after about 10% weight loss on semaglutide 2.4 mg. The speaker stressed that plateaus after roughly 6–12 months on modern obesity medicines are expected; continued treatment typically holds a flat line rather than rebound. Early weight loss at 3–6 months predicts longer-term response, but individual waterfall plots show large biological variability. Escalation was framed around health goals (knee OA, glycaemia, sleep apnoea, MASLD fibrosis) rather than vanity kilograms. Switching to tirzepatide and the coming semaglutide 7.2 mg “Step Up” dose were discussed as ways to add clinically meaningful loss when goals remain unmet, with counselling about body composition (mostly fat loss, especially visceral) and dysaesthesia risk on the 2.4→7.2 step. NACOS education and advocacy resources were noted for clinic support.
GP takeaways
- Expect plateaus on semaglutide 2.4 mg after ~6–12 months; continued therapy usually maintains weight.
- Use early response (3–6 months) as a practical predictor; variability is large.
- Match further intensity to health goals, not scale aesthetics alone.
- Tirzepatide switch can add meaningful loss (head-to-head figures discussed ~20% vs ~14%).
- Semaglutide 7.2 mg Step Up ≈20.7% mean loss in the talk’s data; drop back if not tolerated; warn about dysaesthesia.
- Treat obesity as a chronic disease for health gain; consider NACOS resources.
Full lecture → obesity-management.drkotha.com
A fireside-chat case centred on a 35-year-old with treated hypertension, strong family history of diabetes and premature cardiac disease, and an eGFR around the mid-60s that still sits in a “green” KDIGO heat-map square. Professor Merwin’s punchline was to ask why a young adult is already in the room with falling eGFR — age-expected kidney reserve matters more than a single reassuring colour. Trajectory (roughly >3 mL/min/year or ~10 mL over three years, as framed in the talk) outweighs one snapshot; albuminuria is never “mild” in isolation on a heat map for young patients. Blood pressure needs real-world mapping (ABPM/home), including nocturnal coverage; SPRINT nuances were discussed carefully. Metabolic unloading (weight, lipids, glucose, BP) aims to preserve residual nephrons; albuminuria can improve without “growing back” GFR. Australian TGA/PBS label gaps versus global CKD guidance for SGLT2/GLP-1 were explicit — document shared decisions when access lags guidelines.
GP takeaways
- Do not reassure solely because the KDIGO square is green in a young adult — compare eGFR to age-expected norms.
- Watch slope: rapid decline changes urgency even if absolute eGFR still looks “OK.”
- Map out-of-clinic and nocturnal BP; control is necessary but not sufficient alone.
- Treat metabolic syndrome aggressively without assuming obesity alone explains low eGFR.
- Advocate nephrology review when decline is rapid; know Australian label vs guideline tensions for SGLT2/GLP-1.
- Headline: early aggressive care to flatten the curve while decades of life remain.
Full lecture → ckd-diabetes-young.drkotha.com
Talk 3
Managing hyperhidrosis in general practice
Dr William Crane
Dr Crane estimated at least ~5% of Australians live with hyperhidrosis — often underdiagnosed because patients assume “that’s just how I am” and only mention spare shirts at the end of a consult. Quality-of-life impact can rival other chronic diseases. The talk separated eccrine volume sweating from apocrine bromhidrosis, and primary focal disease from secondary causes. A key discriminator: if sweating does not stop in sleep, think secondary or vasomotor. Highest-yield secondary drivers flagged included SSRIs/SNRIs and other medicines, plus thyroid / tamoxifen / menopause flushing patterns. Severity should be documented (HDSS) before PBS pathways. First-line aluminium chloride 20% at night on clean dry skin (wash in the morning) for about a month; if failed or intolerant, Axhidrox (glycopyrronium) on the PBS ladder for moderate–severe primary axillary disease — applicator hygiene, daily then 2–4×/week maintenance, roughly 70% reduction discussed. Botox, miraDry, and caution against rushing sympathectomy rounded out the ladder; palms/soles need different tools (e.g. iontophoresis).
GP takeaways
- Ask — hyperhidrosis is common and patients often will not lead with it.
- Does it stop in sleep? If not, hunt secondary causes (especially medicines).
- Document HDSS moderate/severe before PBS pathways.
- Proper aluminium chloride night protocol before Axhidrox; Axhidrox criteria exclude prior PBS Botox pathway as discussed.
- Refer after a proper topical trial; match referral to primary vs secondary cause; do not rush sympathectomy.
Full lecture → hyperhidrosis.drkotha.com
Talk 4
Cognitive assessment tools
Dr Rebecca Moore
Dr Moore’s brief was practical: choose the right screen for the right person and use it properly. Screens help diagnosis in context — they are not standalone diagnostic tests and not population screening tools. Cognition spans more than memory; the talk mapped normal ageing → subjective cognitive decline (SCD) → mild cognitive impairment (MCI) → dementia, with intact ADLs as the line between MCI and dementia. Tool coverage included GPCOG, MMSE plus clock drawing, MoCA (including encoding vs retrieval on five-word memory, Trail-making, serial 7s scored out of three, abstraction scoring, and +1 for ≤12 years schooling), and RUDAS for culturally/linguistically diverse patients. Cases illustrated anxiety masking early Alzheimer’s, and a poor Trail B with good RUDAS that was not dementia. Dementia Training Australia resources and other tools (KICA, FAB, ACE, Snellgrove maze) were signposted.
GP takeaways
- Right tool, used properly — screens are not diagnoses and not mass screening.
- Flag SCD for review; aim to recognise MCI while function is still intact.
- Know MoCA scoring quirks (serial 7s /3, abstraction categories, schooling adjustment).
- Use RUDAS when language/culture make MMSE/MoCA unfair.
- A “normal” screen can still be a red flag if collateral history is concerning — interpret in context.
Full lecture → cognitive-assessment.drkotha.com
Talk 5
New anaphylaxis definitions and management
Professor Peter Smith
Professor Smith outlined the new GALEN/GAPA global definition after Delphi consensus with patient organisations: anaphylaxis is a serious allergic hypersensitivity reaction that can progress rapidly and may cause death — patient groups insisted “death” stay in the wording. Conditional diagnostic criteria and early adrenaline culture were emphasised: if this is anaphylaxis, the first three choices are adrenaline, adrenaline, adrenaline, repeating every 5–15 minutes as needed, with escalation after a second dose. Positioning that can kill, infant device choice, needle-free nasal options (neffy), and Queensland fatality data featured in the briefing. Monday-morning close-the-loop habits — prescribe and dispense before leaving the room, demonstrate with a matching trainer, issue the correct ASCIA plan, refer and document — were presented as non-negotiable GP practice.
GP takeaways
- Know the GALEN/GAPA definition and why fatality language stayed in.
- Early adrenaline remains first-line; repeat 5–15 minutely; escalate after dose two.
- Teach positioning risks; match device to age/ability (including needle-free options where relevant).
- Close the loop before discharge: script, trainer demo, ASCIA plan, referral, documentation.
- Call ambulance if a second dose is needed and escalation is required.
Full lecture → anaphylaxis-definitions.drkotha.com
Talk 6
Youth-onset type 2 diabetes
Dr Terry Lindsay
Using a case of a tired adolescent (“Kai”), Dr Lindsay framed youth-onset T2DM as rising in Australia with a particularly high Indigenous burden — not “mild young adult diabetes.” Screening should follow Indigenous vs non-Indigenous risk rules and prefer OGTT when asymptomatic rather than waiting for classic symptoms. Do not assume type by age or BMI; check pancreatic autoantibodies within about a month and interpret C-peptide after the first week. Care is aggressive: metformin first-line, but start insulin early if symptomatic or HbA1c >8.5% at diagnosis (a lower threshold than many midlife algorithms). Under-18 weight goals use BMI centiles and may mean slowing gain while still growing; young adults need cardiorenal-protective agents (GLP-1/SGLT2) sooner. Whole-family, cultural, and mental-health context — distress and stigma — are part of treatment, as is thinking prevention across generations via antenatal care.
GP takeaways
- Look for it — prevalence is rising; Indigenous burden is especially high.
- Screen by risk, not symptoms; prefer OGTT when asymptomatic.
- Treat aggressively — insulin sooner; avoid therapeutic inertia.
- Do not assume type 1 vs 2 by age/BMI; confirm with autoantibodies/C-peptide timing as taught.
- Treat the person in family, culture, and mental-health context; think intergenerational prevention.
Full lecture → youth-onset-diabetes.drkotha.com
The speaker framed hard-to-heal wounds as often stuck in inflammation, with biofilms needing repeated mechanical disruption. GPs were urged to diagnose before dressing: check perfusion (Doppler ABPI/TBPI; careful interpretation in diabetes/CKD), clinical infection versus colonisation, atypical causes (about 1 in 5), and whether the patient can realistically heal. A >30% surface-area improvement in four weeks predicts a healing trajectory; no change by two weeks means go back to assessment. Antimicrobial stewardship: treat clinical infection, not swabs alone. Keep care simple and affordable — advanced cleansers for chronic wounds, local antimicrobials such as cadexomer iodine or silver when indicated, barrier cream at the edge to prevent maceration, and debridement at each change. Diabetic foot ulcers were split into ischaemic, neuropathic, and neuro-ischaemic patterns with different priorities.
GP takeaways
- Diagnose before you dress.
- Assess perfusion before compression.
- Treat clinical infection, not colonisation.
- If not progressing by ~2–4 weeks, reconsider diagnosis and atypical causes.
- Keep wound care simple, evidence-based, and affordable; protect peri-wound skin.
Full lecture → wound-management.drkotha.com
The panel covered three arcs. First, menopause as a cardiovascular risk amplifier — especially if early — with MHT for vasomotor symptoms after risk assessment (preferring transdermal as risk rises) and a clear statement not to sell MHT as proven heart prevention; five-year calculators under-tell lifetime risk in midlife women. Second, lipids: LDL first, combination early after ACS (statin + ezetimibe, escalate to PCSK9), residual risk via triglycerides and Lp(a), and high-dose EPA where PBS-eligible. Third, SGLT2 inhibitors early in type 2 for glucose, weight, heart-failure phenotypes and kidney protection — PBS revisions allow earlier use in high CV risk; combine with GLP-1 when pathways allow, recognising dual-listing friction. Diet (portfolio pattern), fibrate niches (especially TG >10), and statin intolerance pathways were summarised for Monday clinic.
GP takeaways
- Menopause amplifies CV risk; treat symptoms after assessment; do not market MHT as proven primary prevention.
- Fix BP, LDL and weight even when five-year scores look modest; ask obstetric and COPD history tools miss.
- LDL first; combination early after ACS; secondary-prevention targets discussed around ~1.4.
- Use TG and Lp(a) as residual-risk markers; high-dose EPA where PBS-eligible.
- Start SGLT2 early in type 2 for cardiorenal benefit — don’t wait for complications.
Full lecture → cardiovascular-diabetes.drkotha.com
Speakers framed post-exertional malaise (PEM) — a delayed crash after ordinary activity — as the clinical hallmark, not ordinary tiredness. Audience polling suggested most GPs already see long COVID and many see ME/CFS; stage numbers cited roughly 250,000 Australians with ME/CFS pre-COVID and a combined burden approaching about half a million, with about half of long COVID progressing toward an ME/CFS-like illness by a year. Mechanisms discussed included immune, mitochondrial (dysfunction, not total failure), and autonomic overlap including POTS. First-line framing was pacing inside the energy envelope (about 80–90% capacity), not graded exercise push. Believing the patient and providing longitudinal GP care were presented as clinical interventions when tests are normal.
GP takeaways
- Ask specifically for PEM — delayed post-activity crash.
- Pace inside the energy envelope; graded exercise push can harm.
- Expect heavy overlap between long COVID and ME/CFS phenotypes.
- Watch autonomic red flags (POTS) and metabolic differentials.
- Normal tests ≠ absence of disease; stay with the patient longitudinally.
Full lecture → me-cfs-long-covid.drkotha.com
The chair opened with a claim that something like 20% of COPD patients in a GP book may be biologic-eligible. Dr Gregory focused on the eosinophilic exacerbator already on (or ready for) optimised triple therapy and repeated systemic steroids — not biologics for every COPD patient. Blood eosinophils (often ≥300 as discussed) and exacerbation history define the subgroup. Mepolizumab (Nucala) entered the PBS for severe eosinophilic COPD from 1 September 2026; other agents may remain TGA-only — check current listings. Biologics were framed as controllers that can reframe severe disease toward a milder lived experience while inhalers usually continue. GPs own diagnosis confirmation, COPD-X basics, device technique, smoking cessation, vaccination, and referral packages to physicians who actually prescribe biologics.
GP takeaways
- Target eosinophilic steroid-using exacerbators — not all COPD.
- Search practice software for COPD + eosinophils ≥300 as a QI exercise.
- Optimise triple therapy, technique, vaccination and cessation before or alongside referral.
- Nucala PBS-listed for severe eosinophilic COPD from 1 Sep 2026; verify other agents’ status.
- Refer to clinicians who prescribe biologics to avoid two-hop delay.
Full lecture → copd-biologics.drkotha.com
Two slides were the take-home: AF ablation has moved upstream in 2026 (no longer only after multiple failed drugs and cardioversions), and electrical problems need an “electrician” (electrophysiologist), not only a “plumber” (general/interventional cardiology). Pulsed field ablation (PFA) was described as a non-thermal energy source with major risk reductions versus older thermal approaches, aided by modern 3D mapping compute. Symptoms are often underappreciated until sinus returns; 30–40% of AF is asymptomatic yet carries stroke and heart-failure risk. AF plus reduced ejection fraction was framed as a class I prompt for timely EP referral. The first year after new symptomatic AF is a “golden window” for EP review, often missed when care stays only with general cardiology. Lifestyle risk-factor work runs in parallel from day one.
GP takeaways
- Consider earlier EP referral for symptomatic AF — especially younger, active patients.
- New AF with reduced EF → prompt subspecialist electrical cardiology (class I framing in the talk).
- Use the first-year window after new symptomatic AF for EP review.
- Check pulses; silent AF still needs anticoagulation and pathway thinking.
- Electrician, not only plumber — and keep lifestyle interventions running in parallel.
Full lecture → af-ablation-update.drkotha.com
Dr Ben used the preferred term anabolic-androgenic steroids (AAS) for non-prescribed community use, noting AAS still dominate PIEDs though peptides are rising. Prevalence includes teenagers and people who do not “look like bodybuilders”; disclosure is rarely volunteered, so GPs should ask about supplements in anyone training. The aim was harm reduction — recognise, discuss, and monitor cardiovascular, liver, hormonal, fertility and mental-health harms — not invent prescribing protocols for illicit AAS. On-cycle hormone panels are often unhelpful (levels expected sky-high); monitoring in recovery and agreed follow-ups (e.g. ~6 months) matter more. The PUSH study was cited to show engagement can still change behaviour. Resources named included the Sydney North Health Network steroid harm-minimisation guide (adapted elsewhere).
GP takeaways
- Ask about gym supplements — prevalence is significant and often hidden.
- Practise harm reduction across CV, liver, hormones, fertility and mental health.
- Set monitoring follow-ups; standard bloods matter; on-cycle hormones are usually unhelpful.
- Discuss short- and long-term side effects explicitly; explore mental health beyond “rage” stereotypes.
- Engagement (PUSH) can change behaviour even when “just stop” fails as an opener.
Full lecture → anabolic-steroids.drkotha.com
Cross-cutting themes
Obesity, diabetes & CKD
Obesity medicines for health goals (Hockey); youth-onset T2DM needing earlier insulin and family-context care (Lindsay); young CKD where eGFR trajectory beats a green heat-map square (Merwin / Alder); SGLT2/GLP-1 as cardiorenal tools across the panel and COPD–metabolic overlap.
Airways
COPD biologics for eosinophilic exacerbators once triple therapy and basics are optimised (Gregory); device technique and COPD-X fundamentals remain GP work before referral.
Allergy
Updated GALEN/GAPA anaphylaxis definition, early adrenaline culture, device training and ASCIA close-the-loop habits (Smith).
Cognition
Right screen for the right person — GPCOG, MMSE+clock, MoCA, RUDAS — interpreted with collateral history, not as population screening (Moore).
Wounds
Diagnose and perfuse before dressing; infection vs colonisation; rethink atypical wounds that stall (Wounds Australia chair clinician).
Cardiovascular
Menopause risk, LDL-first combination lipid therapy, residual TG/Lp(a) risk, and upstream AF ablation / EP referral (CV panel; Perth EP).
ME/CFS & long COVID
PEM, pacing (not graded exercise push), autonomic overlap, and longitudinal belief-based GP care (Richard; Charlotte).
PIED / AAS
Ask, monitor, harm-reduce — University of Melbourne PIED research lens for non-prescribed AAS in general practice (Ben).
Clinician educational disclaimer
This page is an educational summary of Healthed Medical Update presentations on 5 September 2026 for Australian general practice CPD reflection. It is not personal medical advice and not a substitute for TGA/PBS product information, Australian guidelines (including ASCIA, COPD-X, KDIGO-informed local pathways), specialist assessment, or the full lecture pages linked above. Speaker surnames are recorded only where the published blogs or Otter titles support them; unclear Otter names are left unclear. Always verify current PBS listings, dosing, and local referral pathways before changing practice. Prepared for clinicians and health-interested readers in an Australian context.
Healthed seminar summary · drkotha.com · September 2026