Summary:
Why on earth are renal physicians so keen on cardiovascular examination? Well, the anatomically distinct heart and kidneys are entwined in a dance of homoeostatic elegance... a dance to the death, where if one goes, it takes the other with it. Hence chronic kidney disease leading to heart failure, or arrhythmias causing kidney injury.
This paper has gorgeous diagrams of the pathophysiology.
Link:
Cardiorenal Syndrome - J Am Coll Cardiol. 2008;52(19):1527-1539
Key Points explored:
What are the factors which cause renal disease to injure the heart?
Similarly what heart factors injure the kidney?
How do the physiological homoeostatic mechanisms go awry?
What can you do to keep these people on track?
Wednesday, 13 February 2013
Sunday, 10 February 2013
Restless legs syndrome: pathophysiology, clinical presentation and management.
Summary:
Restless leg syndrome (RLS) is common; estimated prevalence is 1/10. The symptoms can be debilitating, but are usually mild. "URGE" is an acronym for the 4 key symptoms: urge to move, rest aggravates, getting active relieves, evening and night is worse. Only some people are troubled enough to require treatment, but at that point complexity starts. Both iron supplements and dopamine agonists benefit the majority of patients. Yet numerous underlying conditions may explain RLS. What follows is an exploration of a problem with metabolic, genetic and neurological causes.
Link:
Restless legs syndrome: pathophysiology, clinical presentation and management.
or PDF
Key points explored:
What are the essential diagnostic features of RLS?
What roles do Iron, Dopamine and genetics have in RLS pathogenesis?
What underlying diagnoses should be considered, and how should patients be managed?
How does RLS relate to other movement disorders, like parkinsonism?
Restless leg syndrome (RLS) is common; estimated prevalence is 1/10. The symptoms can be debilitating, but are usually mild. "URGE" is an acronym for the 4 key symptoms: urge to move, rest aggravates, getting active relieves, evening and night is worse. Only some people are troubled enough to require treatment, but at that point complexity starts. Both iron supplements and dopamine agonists benefit the majority of patients. Yet numerous underlying conditions may explain RLS. What follows is an exploration of a problem with metabolic, genetic and neurological causes.
Link:
Restless legs syndrome: pathophysiology, clinical presentation and management.
or PDF
Key points explored:
What are the essential diagnostic features of RLS?
What roles do Iron, Dopamine and genetics have in RLS pathogenesis?
What underlying diagnoses should be considered, and how should patients be managed?
How does RLS relate to other movement disorders, like parkinsonism?
Labels:
basal ganglia,
dopamine,
extrapyramidal,
genetic,
iron,
metabolic,
movement disorder,
neurology,
neurophysiology,
night,
Pathophysiology,
physiology,
restless legs,
RLS,
sleep,
substantia nigra
Resolving inflammation, better than suppressing it?
Summary:
Inflammation is a crucial process in health and disease. Medical training has inflammation as a centrepiece, extolling the importance of molecules and processes which trigger and amplify the inflammatory response. Increasingly the interdependence of the nervous system and immune system have been accepted as scientific fact, allowing more coherent understanding of chronic pain and chronic inflammatory states. Medications have been targeted on increasingly subtle components of the inflammatory cascade, from prostaglandins, to cytokines.
However, why all this talk about starting inflammation? Nobody seems too verbal about what exactly resolves the normal inflammatory process?
Medicines to calm inflammation are typically crude and ineffective, dulling the entire body's response. It is becoming clear that nature has a sophisticated system for terminating inflammatory reactions. A set of key chemical mediators has been termed resolvins: fatty acid molecules derived from Omega 3 polyunsaturated fats. Fascinating research is uncovering how the solution to chronic pain and inflammation may not in fact be suppressing the inflammatory response, but making it resolve earlier.
Link:
Emerging roles of resolvins in the resolution of inflammation and pain
Key Points explored:
What are the properties of Resolvins in animal models of pain?
How do Resolvins mediate analgesia?
What are the links between pain and inflammation?
Enjoy
Inflammation is a crucial process in health and disease. Medical training has inflammation as a centrepiece, extolling the importance of molecules and processes which trigger and amplify the inflammatory response. Increasingly the interdependence of the nervous system and immune system have been accepted as scientific fact, allowing more coherent understanding of chronic pain and chronic inflammatory states. Medications have been targeted on increasingly subtle components of the inflammatory cascade, from prostaglandins, to cytokines.
However, why all this talk about starting inflammation? Nobody seems too verbal about what exactly resolves the normal inflammatory process?
Medicines to calm inflammation are typically crude and ineffective, dulling the entire body's response. It is becoming clear that nature has a sophisticated system for terminating inflammatory reactions. A set of key chemical mediators has been termed resolvins: fatty acid molecules derived from Omega 3 polyunsaturated fats. Fascinating research is uncovering how the solution to chronic pain and inflammation may not in fact be suppressing the inflammatory response, but making it resolve earlier.
Link:
Emerging roles of resolvins in the resolution of inflammation and pain
Key Points explored:
What are the properties of Resolvins in animal models of pain?
How do Resolvins mediate analgesia?
What are the links between pain and inflammation?
Enjoy
When doctors and patients talk: making sense of the consultation
Summary:
In this splendidly evidence based report on how doctors and patients interact in the NHS, there is a wealth of insight for both care givers and seekers. Unlike many resources on the Doctor-patient relationship, which explore exceptional cases, or focus on theory, this report is based on common issues, and grounded in research. A valuable read for anyone who wants to better perceive the consultation, and to become more skilful at navigating it; creating a successful outcome for both parties.
Link:
When doctors and patients talk: making sense of the consultation
Key Points Explored:
What are the commonest experiences that doctors and patients have in the NHS?
What are the driving forces which shape typical consultations?
What is the scope for change from doctors?
How much responsibility do patients have?
Is the professional and cultural normality a necessary focus of change?
In this splendidly evidence based report on how doctors and patients interact in the NHS, there is a wealth of insight for both care givers and seekers. Unlike many resources on the Doctor-patient relationship, which explore exceptional cases, or focus on theory, this report is based on common issues, and grounded in research. A valuable read for anyone who wants to better perceive the consultation, and to become more skilful at navigating it; creating a successful outcome for both parties.
Link:
When doctors and patients talk: making sense of the consultation
Key Points Explored:
What are the commonest experiences that doctors and patients have in the NHS?
What are the driving forces which shape typical consultations?
What is the scope for change from doctors?
How much responsibility do patients have?
Is the professional and cultural normality a necessary focus of change?
Rheumatic disorders as paraneoplastic syndromes
Summary:
So your patient has a new rash and muscle ache, and is diagnosed by a rheumatologist as having dermatomyositis. Or, your patient has symmetrical polyarthritis, and is diagnosed with rheumatoid arthritis. They have a poor response to first line therapy. Two years later they are found to have cancer. Then when the cancer is removed surgically and the patient treated with cytotoxic chemotherapy, their rheumatic disease disappears. This is the mysterious realm of paraneoplastic rheumatic syndromes, which can offer early warnings about growing neoplasms, and can also be a source of diagnostic deliberation.
Link:
Rheumatic disorders as paraneoplastic syndromes
Key points explored:
Why do some tumours produce rheumatic diseases?
What kind of neoplasms can provoke rheumatic paraneoplastic disease?
How can paraneoplastic rheumatic diseases be differentiated from typical cases?
So your patient has a new rash and muscle ache, and is diagnosed by a rheumatologist as having dermatomyositis. Or, your patient has symmetrical polyarthritis, and is diagnosed with rheumatoid arthritis. They have a poor response to first line therapy. Two years later they are found to have cancer. Then when the cancer is removed surgically and the patient treated with cytotoxic chemotherapy, their rheumatic disease disappears. This is the mysterious realm of paraneoplastic rheumatic syndromes, which can offer early warnings about growing neoplasms, and can also be a source of diagnostic deliberation.
Link:
Rheumatic disorders as paraneoplastic syndromes
Key points explored:
Why do some tumours produce rheumatic diseases?
What kind of neoplasms can provoke rheumatic paraneoplastic disease?
How can paraneoplastic rheumatic diseases be differentiated from typical cases?
Labels:
arthritis,
Cancer,
dermatology,
diagnosis,
haematological,
immune,
Inflammation,
laboratory,
lupus,
Malignancy,
neoplasm,
paraneoplastic,
Pathophysiology,
rheumatic,
rheumatoid,
serum,
skin
Saturday, 9 February 2013
The placebo response: How words and rituals change the patient’s brain
Benedetti et al's "The Placebo effect" is a step into the Ben Goldacre-y side of things that even the most reluctantly academically keen medical student reads in their spare time. As the paper notes:
"The placebo effect, or response, has evolved from being thought of as a nuisance in clinical and
pharmacological research to a biological phenomenon worthy of scientiļ¬c investigation in its own right."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055515/pdf/npp201081a.pdf
Juicy things that the paper looks into are:
"The placebo effect, or response, has evolved from being thought of as a nuisance in clinical and
pharmacological research to a biological phenomenon worthy of scientiļ¬c investigation in its own right."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055515/pdf/npp201081a.pdf
Juicy things that the paper looks into are:
- The effect of wording on the placebo effect (and other aspects of the pomp and circumstance surrounding administration)
- The fascinatingly paradoxical world of administering a drug without any effect in the area suggested it would, but instead having an effect which interferes with the suspected messengers in the placebo effect itself.
- The suspected anatomical regions involved.
- The dark art of analgesia.
- The relationship between placebos and the neurology of emotion.
- An ending which gives hints as how better to use the placebo effect in clinical medicine or in trials and to avoid the nocebo effect (the evil twin).
Some of the things discussed in this review are a bit bewildering, because they seem very counter-intuitive, but never-the-less it makes a great read for anyone who wants to know the TRUTH about something as simple as opioid administration.
Good learning,
Marblecake
Marblecake
Saturday, 2 February 2013
The Pathophysiology of Eczema and Psoriasis
This paper has been suggested by one of my esteemed colleagues:
http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2230.2005.01980.x/pdf
Allam and Novak's "the Pathophysiology of Eczema" discusses the processes behing eczematic inflammation. It is particularly good for a review of acute chemotaxis and the underlying chemical messengers and cell activity.
Specifically for eczema, the section on genetics places the disease in the context of malfunctioning immune response. The paper is also pleasingly succinct, with a very nice image AND there is a very medical student-friendly summary at the end as learning points.
And as a nice counterpart, while you are in the mood for dermatology and immunology.
http://ard.bmj.com/content/64/suppl_2/ii30.full.pdf+html
Krueger and Bowcock's "Psoriasis Pathophysiology: Current concepts of pathogenesis" is more dense than Allam and Novak, and a bit turgid to begin with, but assumes very little knowledge of immune cells. It contains a lot of transferable knowledge. There is more genetics than anyone could possibly need, but as with Allam and Novak, the immunology is well described and as all good papers do, it has a great big diagram with arrows in it.
Sit down with a coffee and try to work through these papers when studying atopy or dermatology - it will be very rewarding.
Good learning,
Marblecake
http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2230.2005.01980.x/pdf
Allam and Novak's "the Pathophysiology of Eczema" discusses the processes behing eczematic inflammation. It is particularly good for a review of acute chemotaxis and the underlying chemical messengers and cell activity.
Specifically for eczema, the section on genetics places the disease in the context of malfunctioning immune response. The paper is also pleasingly succinct, with a very nice image AND there is a very medical student-friendly summary at the end as learning points.
And as a nice counterpart, while you are in the mood for dermatology and immunology.
http://ard.bmj.com/content/64/suppl_2/ii30.full.pdf+html
Krueger and Bowcock's "Psoriasis Pathophysiology: Current concepts of pathogenesis" is more dense than Allam and Novak, and a bit turgid to begin with, but assumes very little knowledge of immune cells. It contains a lot of transferable knowledge. There is more genetics than anyone could possibly need, but as with Allam and Novak, the immunology is well described and as all good papers do, it has a great big diagram with arrows in it.
Sit down with a coffee and try to work through these papers when studying atopy or dermatology - it will be very rewarding.
Good learning,
Marblecake
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