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By Dr Luke Crantock
The podcast currently has 175 episodes available.
Rhinitis, Sinusitis, and Rhinosinusitis are common conditions frequently seen in primary care. Studies indicate that 1.4 out of every 100 general practice encounters involve acute or chronic sinusitis, and over 2 million Australians are estimated to suffer from chronic rhinosinusitis. In some studies, this condition has shown a greater impact on social functioning than chronic heart failure, angina, or back pain.
Anatomy and Pathophysiology: The paranasal sinuses—frontal, maxillary, ethmoid, and sphenoid—are lined with ciliated epithelium and goblet cells, forming a mucociliary blanket that traps and moves harmful particles to the nasopharynx. The maxillary sinus, the largest air-filled sinus in the body, has a draining ostium only 2.4 mm in diameter, making it particularly prone to blockage during infection or inflammation. Treatment for sinusitis focuses on restoring mucociliary clearance and drainage while addressing underlying inflammation.
Acute Rhinosinusitis: The spectrum of acute rhinosinusitis (ARS) includes the common cold, post-viral ARS, and acute bacterial rhinosinusitis. Though less than 2% of viral upper respiratory infections progress to bacterial infections, antibiotics are prescribed in over 85% of sinusitis cases. Symptoms of ARS include nasal obstruction, discharge, changes in smell, facial pain or pressure, and cough. Facial pain may worsen when bending forward and can radiate to the teeth. Diagnosis requires the sudden onset of two or more symptoms, with at least one being nasal blockage, congestion, obstruction, or discharge, accompanied by facial pain or pressure and/or a reduction in smell. Nasal examination should assess for discharge (clear or purulent), polyposis, swelling, and erythema.
Chronic Rhinosinusitis (CRS): CRS presents in two forms, distinguished by the presence or absence of nasal polyps. It is defined by the persistence of symptoms for more than 12 weeks, including nasal congestion, discharge, facial pain or pressure, and reduced smell. Viral and bacterial infections are the most common causes, with Streptococcus, Pneumococcus, Haemophilus, and Moraxella being the usual bacterial suspects. Other factors such as allergies, structural abnormalities, ciliary dysfunction, immunodeficiencies, and fungal infections should also be considered.
Allergic Rhinitis: Allergic rhinitis, commonly known as hay fever, affects around 18% of Australians. Despite its name, allergic rhinitis is not caused by hay and does not result in fever. It typically presents with sneezing, itching, rhinorrhoea, nasal congestion, and lacrimation, triggered by allergen exposure. These allergens can often be identified through patient history, but RAST serology may be required when clear precipitants are not evident.
To deepen our understanding of these conditions, we welcome Dr. Andrew Martin, a practicing ENT surgeon in Melbourne's Southeastern suburbs and Northern Tasmania. Dr. Martin completed his MBBS at The University of Queensland in 2008 after earning a Bachelor of Pharmacy Sciences with Honours from Monash University in 2003. He completed his fellowship with the Royal College of Surgeons in Otolaryngology and Head and Neck Surgery in New Zealand in 2021, followed by an Advanced Fellowship in Head and Neck Surgery at The Royal Melbourne Hospital in 2022.
Dr. Martin’s specialties include nasal obstruction, obstructive sleep apnoea, ear and balance disorders, chronic sinus disease, mid-facial pain, paediatric ENT, and disorders affecting swallowing, voice, and throat. Outside of his medical practice, he is a devoted family man with two young daughters and enjoys hunting and fishing. It was a privilege to have this conversation with him as we explored rhinitis and rhinosinusitis in more detail. Please join me in welcoming Dr. Andrew Martin to the podcast.
References:
Dr Andrew Martin
National Institutes of Health - Rhinitis and Sinusitis
Journal of Allergy and Clinical Immunology - Rhinitis and Sinusitis
In an earlier episode titled Breathing we had the privilege to explore heathy breathing patterns and the Bohr effect which governs oxygen delivery to tissues with physiotherapist and breathing expert Allan Abbott, if you haven’t had an opportunity to listen to that podcast, I recommend it as an introduction to the subject we are covering today.
In an earlier episode titled 'Breathing' we had the privilege to explore heathy breathing patterns and the Bohr effect which governs oxygen delivery to tissues with physiotherapist and breathing expert Allan Abbott, if you haven’t had an opportunity to listen to that podcast, I recommend it as an introduction to the subject we are covering today.
Allan has been exploring breathing techniques to enhance exercise performance and improved health for many years and has created a dynamic company called Health Innovations that can be found at healthinnovations.net.au in order to bring this important knowledge into public forum. Although most of us pay little attention to breathing technique in our busy world, many cultures and alternative health practises such as YOGA and Ayurveda have focused on this for centuries and the recent excellent book Breath by James Nestor explores the importance of breathing technique in detail including the influence on facial structure and disease brought about by mouth breathing and poor execution of this seemingly automatic task.
Allan takes us further in this podcast episode in which we explore functional breathing, breathing during exercise and how we can utilise breathing techniques to replicate high altitude training at sea level to improve performance and stamina in ways you may not have considered possible. Allan was generous enough to give up a good deal of his spare time taking me on a deep dive through these breath training techniques one on one. We focused first on nasal breathing light, slow and deep utilising the diaphragm rather than purely chest muscles and aiming for a 4 second nasal inhalation followed by a slow nasal exhalation over 6 seconds. This develops the habit of six breaths per minute.
We then worked on the breath oxygen level test - the so-called BOLT with the objective of building CO2 tolerance to reduce the ‘gassing out’ feeling that can occur when one trains at a moderate exercise intensity. Subsequently Allan took me to ‘altitude’ with some strong breath holds during exercise simulating the reduced partial pressure of oxygen experienced as we venture 2000 metres above sea level and more, slowly resetting central CO2 chemoreceptors, increasing our haematocrit, erythropoietin and 2-3 DPG levels as well as enhancing myoglobin production, mitochondrial density, and cardiac output.
Allan is meticulous about this training and on establishing correct technique noting this would not be appropriate for those with advanced lung disease. I really enjoyed learning from him and have implemented these exercises into my daily routine. I hope this conversation will pique your interest as it did mine as we share the art of functional breathing.
Please welcome Allan to the conversation.
References:
Allan Abbott at: healthinnovations.net.au
(+61) 0419379371
Buteyko.com
Acute Effects of Repeated Cycling Sprints in Hypoxia Induced by Voluntary Hypoventilation. Woorens/ European Journal of Applied Physiology. September 2017
Repeated Sprint Training in Hypoxia Rugby. Woorens . European Journal of Sport Science. 2018.
Intermittent Hypoxia Training. Sohagatay et al. Journal of Human Kinetics Vol32/2012 197-210
Hypercapnic Hypoxic Training. Bakovic et al. Journal of Applied Physiology 2003, Vol 95 No 4 1460-1466
Breathing Pattern Disorders and Functional Movement. Bradley et Al. International Journal of Physiotherapy Feb 2014,9(1),28-39
James Nestor- Breath - The New Science of a Lost Art. Riverhead Books, 2020
Amyloidosis is a group of diseases in which abnormal proteins known as amyloid fibrils build up in various tissues including the kidney, heart, liver, skin, and nervous system resulting in a variety of clinical sequelae including organ dysfunction and death. There are over 23 unrelated proteins known to form amyloid fibrils, many of which are aggregates of misfolded proteins that are neither biodegradable nor can be recycled by our bodies.
Abnormal Immunoglobulin light chains known as AL (amyloid light chain), transport protein transthyretin (ATTR) which normally transports retinol and thyroxine, and amyloid A (AA) are some of the better recognised examples of amyloid proteins.
It is important to note however that hereditary, dialysis associated, localised and ocular forms also exist, and Beta protein precursor is implicated in Alzheimer syndrome as are other amyloid fibrils in different dementia diagnoses.
The quoted incidence of amyloid disease is 12 per million and it is estimated that over 20 000 cases of amyloid are undiagnosed and untreated in Australia alone. It is noteworthy that 13-17% of patients with heart failure and degenerative aortic stenosis have amyloidosis and that up to 50 % of patients with amyloid see five doctors before a diagnosis is made. Up until recently only a four-year life expectancy was anticipated, fortunately pharmacological breakthroughs are expanding this horizon.
Although the term amyloid was originally coined by German botanist Mathias Schleiden to describe the normal amylaceous of plants, it was Rudolf Virchow in 1854 who adopted the term to describe abnormal extracellular material seen in the liver during autopsy.
As we will explore in this podcast we now think of amyloid disease in terms of primary systemic amyloid (AL) where a clone of abnormal plasma cells secretes excess immunoglobulin light chains that misfold and aggregate as non-biodegradable non-recyclable amyloid fibrils. Such a clone is also observed in about 5 % of myeloma diagnoses and about 12% of MGUS (monoclonal gammopathy of uncertain significance).
Additionally, age associated amyloid transport transthyretin protein ATTR is an acute phase reactant produced predominantly in the liver in response to multiple cytokines which may become amyloid in form with senescence depositing in the heart and kidneys where diastolic dysfunction and renal impairment develop.
In this podcast I was curious to explore how we can improve our surveillance for this condition and to raise our awareness. I was also keen to understand how to confirm the diagnosis and to explore treatment options.
To explore this interesting area further please welcome to the podcast Dr Simon Gibbs from Precision Haematology who is a clinical haematologist and amyloidosis specialist, and a Senior adjunct lecturer at Monash University.
After attaining his medical degrees from the University of Melbourne he moved to Cambridge in the United Kingdom to gain further experience in autologous and allogeneic bone marrow transplantation as treatment for myeloma and leukaemia and completed a four-year fellowship at the National Amyloidosis Centre at University College London, focusing on novel therapies for AL amyloidosis.
Upon returning to Australia, he was appointed the Myeloma Lead at Eastern Health and established the Victorian and Tasmanian Amyloidosis Service (VTAS).
He is the Chair of the Australian Amyloidosis Network (www.amyloidosis.net.au), and a member of the Haematology Society of Australian and New Zealand (HSANZ). He serves on both the Educational Subcommittee for the International Society of Amyloidosis, and the Medical and Scientific Advisory Committee (MSAG) for Myeloma Australia and is the author of over 40 publications in international medical literature.
References :
Dr Simon Gibbs: https://precisionhaematology.com.au/doctor/dr-simon-gibbs/
Australian Amyloidosis Network: https://aan.org.au/
The use of faecal microbiota transplantation (FMT) to treat severe C. Difficile enterocolitis was visited in episode 14 of Everyday Medicine with Dr Darcy Holt as our guest. If you haven’t had an opportunity to listen to that conversation, please do and hopefully it will pique your interest.
In this episode we invite a guest involved in active research at Melbourne’s St Vincent’s Hospital to discuss FMT in IBD broadly then more specifically as it applies to her current research project evaluating its efficacy in Crohn’s disease.
FMT is defined as the infusion of faeces from healthy donors into the gastrointestinal tract of recipients to treat disease associated with gut dysbiosis. Noting that the precise aetiology of IBD is unknown, a multifactorial pathogenesis is proposed influenced by genetic susceptibility, host mucosal immune responses and the environment including diet, the gut microbiome and smoking history. Particularly with both ulcerative colitis and Crohn’s disease a deficiency in Faecal bacterium prausnitzii recognised for its potential anti- inflammatory properties has raised interest in the FMT space.
To date FMT has been investigated in patients with inflammatory bowel disease (IBD) both in non- randomised and subsequently randomised controlled trials showing promising results although with significant differences in FMT protocols and procedures. The adoption of FMT for the treatment of IBD is compromised by recruitment of donors, preparation of faecal material, determination of the optimal route of administration and lack of established regulatory framework. Establishing an optimal framework is essential for the future management of IBD should the merits of this therapy stand up to scrutiny.
The first international Rome consensus conference on gut microbiota and faecal microbiota transplantation in inflammatory bowel disease, published in Gut.bmj this year has attempted to set this framework and is a very helpful publication.
In this episode we introduce Dr Sasha Fehily who is actively engaged in the MIRO study looking at FMT in Crohn’s IBD. The MIRO Study is a randomised, double-blind placebo-controlled trial where all recruited patients receive active standard IBD treatment and those on placebo who don't respond are administered active FMT therapy. This is an excellent study with greatly anticipated results, and I was curious to learn more about the research directly from Sasha. Please welcome her to the podcast.
References :
Dr Sasha Fehily - St Vincent’s Hospital Melbourne
[email protected]
Guideline: The first international Rome consensus conference on gut microbiota and faecal microbiota transplantation in inflammatory bowel disease. Lopetuso et al. https://gut.bmj.com/content/72/9/1642
Primitive single-celled organisms had patches of photoreceptor proteins to detect light. The first eyes, developed over 550 million years ago, are now the second most complex organ after the brain, with over two million working parts and more than a million nerve fibres connecting each eye to the brain via the optic nerves.
An estimated 20% of Australians have an allergic disease, with Melbourne as a hotspot where one in three people experience hay fever and thunderstorm asthma. Allergies can affect the skin, sinuses, airways, gastrointestinal tract, or other organs.
Allergies are immune reactions to foreign antigens, causing tissue inflammation and organ dysfunction. Symptoms depend on prior immune response, antigen exposure, and genetic factors. Atopic individuals have a genetic predisposition to conditions like allergic rhinitis, atopic dermatitis, allergic asthma, and IgE-mediated food allergies. Reactions can be immediate (within 60 minutes) or delayed (hours, days, or weeks).
In 1963, Gell and Coombs classified hypersensitivity reactions into four types based on the immune response.
Type 1: Immediate hypersensitivity: IgE antibodies on mast cells bind to antigens, causing cell degranulation. This leads to vasodilation, smooth muscle contraction, mucous secretion, and inflammation. Anaphylaxis is a severe form needing adrenaline intervention. Food allergies affect 4-7% of children, often involving milk, eggs, peanuts, tree nuts, shellfish, wheat, and soy.
Type 2: Antibody-mediated hypersensitivity: IgG or IgM antibodies, with complement or phagocytic cells, cause reactions seen in blood transfusions, rheumatic fever, and autoimmune diseases.
Type 3: Immune complex-mediated hypersensitivity: Antigen-antibody complexes cause inflammation, as seen in chronic glomerulonephritis, SLE, and rheumatoid arthritis.
Type 4: Delayed hypersensitivity: T cells and persistent antigens trigger cytokine secretion and monocyte activation. This occurs in conditions like tuberculosis and leprosy, with reactions peaking 48-72 hours after exposure.
In this podcast, we explore the prevalence of allergies, their signs and symptoms, and common diagnostic tests. We also discuss non-allergic sensitivities like reactions to nitrates, sulphites, and food additives.
Dr Colin Little, a Melbourne-based immunologist and allergist with over 40 years of experience, provides insights on treating common and rare allergic conditions.
References:
Dr Colin Little: 1/324 Stephensons Rd Mt Waverley 3149
"Hypersensitivity - an overview," Science Direct
"Immediate Hypersensitivity Reactions," AAJ Vaillant, 2022, www.ncbi.nlm.nih.gov
"Hypersensitivity Reactions," April 2009, Rutgers New Jersey Medical School
Barrett’s oesophagus is a common condition, named after the Australian born thoracic surgeon Norman Barrett who practised in England and laid the foundation descriptions of this condition but incorrectly concluded the abnormal columnar tissue lining was embryonic in origin due to the presence of a congenitally shortened oesophagus leading to a tubular portion of stomach being trapped in the chest. We now recognise that between 5-10 % of patients with chronic reflux disease develop columnar metaplasia as a response to repeated oesophageal acid exposure.
Long segment disease extends for more than 3 cm, short segment less than 3 cm and metaplasia at the OG junction (less than 1 cm in length) is not considered to be pathological.
Its presence informs us that our patient has GORD and alerts to the possibility of dysplastic change and malignant transformation. Although the latter is relatively unlikely in any individual the risk is real. Estimates quote 0.33 to 0.5 % risk per year, that is 1: 200 per year which is 30-125 times the average population risk. Malignant risk increases with longer lengths of Barrett’s, Caucasian males and smokers but is probably not influenced by alcohol history.
In the absence of invasive malignancy, nodular areas are removed by a mucosal stripping technique described as endoscopic mucosal resection (EMR) and remaining lengths of Barrett’s mucosa may be removed using radio frequency ablation (RFA). This ablative technique involves the use of radiofrequency energy delivered with balloon-based catheters that heats the oesophageal mucosa and destroys non dysplastic and dysplastic tissue.
Randomised control trials have demonstrated superiority over sham ablation in limiting dysplasia and metaplasia at one year. The technique is associated with a lower stricture rate and decreased post procedure morbidity than other techniques sometimes utilised in this situation such as photodynamic therapy or cryotherapy.
I was keen to have a conversation with Professor Finlay Macrae on this important subject exploring the topic of Barrett’s in more length as well as the techniques of EMR and RFA. Professor Macrae is a gastroenterology mentor, head of colorectal medicine and genetics at the Royal Melbourne Hospital and has public and private practices focusing on the management of Barrett’s oesophagus, inflammatory bowel disease and familial bowel cancer. He trained both in Melbourne and at St Marks Hospital in London. In 2016 he was awarded the Order of Australia for his work in genetics and genomics.
Professor Macrae has been delivering advanced therapeutic solutions for patients with complex Barrett’s disease for over 30 years and was therefore, an obvious choice of expert guest to discuss this topic today, it was a great privilege to have this conversation with him.
References:
Professorfinlaymacrae.com
Spechler S.et al. Barrett’s Esophagus. N ENG J Med 2014; 371:836-45
Whiteman et al. Journal of Gastroenterology and Hepatology 30 (2015) 804-820
Cancer Council Australia Barrett’s Oesophagus Guidelines Working Party. Clinical Practice Guidelines for the Diagnosis and Management of Barrett’s Oesophagus and Early Oesophageal Adenocarcinoma. Feb 12.2015
The advent of complex therapies including biologics and small molecules has provided a new paradigm for the treatment of many immune mediated inflammatory conditions notably in rheumatology, gastroenterology (Inflammatory Bowel Disease) and also in dermatology. New dimensions of treatment can now be applied from this amazing therapeutic armamentarium at our disposal. In this podcast we will turn our attention to how this relates to management strategies in dermatology.
Neurosurgeon Rondhir Jithoo has led an extraordinary life, growing up in South Africa with a medical father and deeply thinking anthropologist mother. He obtained his medical degree from the Nelson Mandela School of Medicine at the University of Natal and trained in neurosurgery at South Africa’s Wentworth Hospital where he received the Registrars Prize from the South African Society of Neurosurgeons and obtained his neurosurgery fellowship in 2000.
After relocating to Australia, he was awarded the Australasian Fellowship in Neurosurgery in 2004 and worked at Royal Melbourne Hospital where he developed an interest in spinal trauma, anterior spinal surgery and cranial surgery. This interest in cranial surgery took him to Frances’ famous neurosurgical epicentre in Montpellier to further his study and skills in the art of awake craniotomy.
At Montpellier Rondhir was able to develop skills reflecting the modern connectionist approach to neurosurgery which has revolutionised treatment of brain tumours. The traditional concept proposed by Paul Broca, and still taught, is that the brain is organised into different areas controlling specific functions. This localisation theory has now been disproven, and work with contributions from Montpellier has shown that the brain is organised in dynamic interactive networks capable of constantly readapting.
This connectionist approach explains why some patients can lead a perfectly normal life despite having a large tumour affecting an area of the brain previously considered crucial for brain function. The brain is able to compensate for lesions and its incredible plasticity allows it to reorganise itself to continue functioning normally. In awake craniotomy, providing lesions have not caused disability, tumours may be safely removed in real time using cortical mapping. By keeping the patient awake to verbal commands the impact of surgical resection can be carefully assessed and damage minimised.
After returning to Australia with this skill Rondhir served with the Australian armed forces in Iraq, assessing and providing acute neurosurgical assistance for battlefield traumas and is now intrinsically involved in contributing his skill and expertise to establishing and independent neurosurgical service in Darwin where he travels at repeat intervals throughout the year.
He is a head and clinic consultant of Neurosurgery at Alfred Health in Melbourne and is a member of the Victorian Audit of Surgical Mortality Committee as well as a postgraduate examiner for the Royal Australasian College of Surgeons.
I found Ron to be deeply philosophical and spiritual in his approach to the art of medicine and I’m sure you will enjoy this conversation with him.
References :
Mr Rondhir Jithoo: www.healthshare.com.au
www.alfredhealth.org.au
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