Diabetic Neuropathy (nerve Disease)

Let me start with I’m a diabetic. I developed neuropathy, which basically you lose all sensation in the feet, but it’s over a period of time. It was very painful. I would have sensations in my feet like I was standing on fire, walking on glass. Last October it got so bad that I couldn’t sleep at night. Then I met Dr. Bullard, because he’s just a great physician. I wouldn’t think twice, I’d recommend him to anybody. Very compassionate, very thorough, I can’t say enough about Dr. Bullard. He’s just a great physician and I don’t know.

If there’s anything he couldn’t do he could probably move mountains if he wanted to! Glen, probably one of the biggest questions people are asking you is what’d we do, what’s happened. Of course, you had a tremendous improvement in your pain and the tingling and the numbness. Easiest explanation is, to tell everybody, that this big nerve here, which is on the inside part of your left foot, was getting strangled. There was a noose around it. What we did is we went in and loosened the noose, and that allows that nerve to begin to function and work like it’s supposed.

To. Now, the sensation is coming back, it’s something that’s going to take time but I can feel more. My quality of life has greatly improved since I had the procedure done by Dr. Bullard. There’s no other physician that I would recommend. Glen, in the next couple weeks, what we’re going to do is make sure that the swelling is improving, hopefully begin to transition you out of your compression socks, because I know it’s kind of hot right now, and then look at making sure that your shoe gear and things like that are where they’re supposed.

Diabetic Leg Cramps Causes and Treatments Dr. Mia Cuddihy UHC TV

This viewer is a diabetic and gets leg cramps at night. They’re asking whether this could be related to their diabetes or possibly a medication side effect. Certainly, this is a complicated question, and leg cramps at night could be from a number of causes. Probably the most concerning cause would be neuropathy or damage of the nerves that occurs with diabetes. It’s always important to bring this to your physician’s attention. If you do have signs of neuropathy, there are specific treatments, and controlling your diabetes is going to be one of the most important things to prevent progression. Medications could also be a cause.

Of your cramping. Sometimes diuretics cause a loss of potassium, which is a common cause of cramping. So it’s important to follow closely with your physician, understand your medications, and what types of tests are needed to monitor. Your pharmacist is an excellent resource for medication questions. They would have, hopefully, your whole list and could tell you if there are specific medication side effects that you need to be concerned about. So, in summary, it’s an important question. Legs cramps could be a mild concern that isn’t caused by anything,.

Neuropathy Solution Program by Randall Labrum Review

Neuropathy Solution Program by Randall Labrum Review Neuropathy Solution Program by Randall Labrum Review is a safe and simple treatment program for permanently and effectively getting rid of neuropathy, stopping chronic peripheral neuropathy and diabetic nerve pain without having surgeries. The easy to implement techniques taught in the course use an instant relief from the agonizing pain, prickling and numbness and focus on the root causes of the neuropathy pain. They work on the microscopic level to cure nerve endings as well as macroscopic needs like lifestyle changes which can resolve many diseases like heart disease, diabetes and arthritis.

The stepbystep, doneforyou program inside Randall Labrum’s Neuropathy Solution Program guide works regardless of your age, ethnicity, gender, background, no matter your peripheral neuropathy results from chemotherapy, diabetes, hypertensions, without any costly drugs or pills or supplements. Examples Of Techniques And Concepts Taught In The Course Little known technique for relieving pain in most neuropathy sufferers Ways to start eradicating not only numbness, but also various kinds of pain popularly associated with peripheral neuropathy, such as prickling, tingling, stabbing, burning,. General understanding about peripheral neuropathy, why you have that problem.

And how to execute the selftreatment procedures. Why the sensory nerves become unhealthy and why they send abnormal signals to the sufferers’ brain. The thing associated with diabetes condition which often leads to the growth of peripheral neuropathy and what sufferers should do to prevent it. The link between circulatory health and the onset of peripheral neuropathy, how to make use of this connection to reverse the effects of neuropathy. The reason why a lot of middleaged people suffer from peripheral neuropathy, even when they do not suffer from diabetes or chemo at all.

Why those sufferers could expect a rapid, full recovery if they properly follow the steps introduced in Neuropathy Solution program. The reason why aging usually increase the degeneration of the sensory nerves and what you should do to prevent this process, reducing the risk of peripheral neuropathy. The littleknown link between the common ailment of lower back pain and the condition of peripheral neuropathy and what people could do to lessen the pain in lower back and impacts caused by two conditions. The simple routine that supplies you with dramatic results than your imagination.

Diabetic nephropathy Mechanisms

One of the most serious chronic complications of diabetes mellitus is a condition known as diabetic nephropathy. Which, if you break down the term into nephro and pathy literally means kidney disease that occurs secondary to diabetes. And it’s actually pretty common as it eventually affects about 20 to 40 of all individuals with diabetes, including both type I and type II. In this tutorial, let’s talk about the mechanism underlying the cause of diabetic nephropathy and how individuals with diabetes develop the condition. So diabetic nephropathy is a chronic complication.

Of diabetes mellitus. Meaning, it usually has a slow progression over decades after the initial diagnosis of diabetes. And to give you an overview of what happens, an insulin deficiency due to the diabetes results in hyperglycemia, which then causes hypertension and kidney dysfunction. This kidney function is actually then further worsened by the hypertension. And ultimately, all of this results in kidney failure, which can have very severe and potentially even life threatening complications, such as anemia, electrolyte imbalances, such as metabolic acidosis, and heart arrhythmias. Now, before we dive into the mechanism.

Of diabetic nephropathy, let’s briefly review the structure of the glomerulus in the kidney, by bringing in a diagram here. So, the glomerulus is the portion of the kidney where blood is initially filtered. So blood enters the glomerulus over here, through this afferent arterial, and then leaves the glomerulus through the efferent arterial. And you can remember this, that it leaves through the efferent arterial for E for exit, or efferent. And while the blood is within the glomerulus, there’s this advanced filtration system, which we’ll talk about more in a minute.

And the filtered fluid that exits the blood is known as a filtrate and it collects in Bowman’s space before it enters into the tubules of the nephron where further reabsorption and secretion occurs before it exits the kidney into the ureters as urine. Now, one last structure to point out in this diagram is this vessel coming off the efferent tubule, here. Now, this vasculature actually wraps around the tubules of the nephron, and contributes to the reabsorption and secretion of solutes. Now, to add to this diagram, let’s imagine we took a cross section of this glomerulus,.

And looked at it on its end. And it would look a little bit something like this. Now, we can use this diagram here to better depict some of the important structures within the glomerulus. So here you can see the capillary vessels, and each of them I’ve drawn in here a little red blood cell to help remind you that it’s a blood cell. And as you can see, these vessels are surrounded by a few additional structures that we couldn’t really appreciate in that first diagram. So these are the structures that contribute.

To the three layered filtration system of the glomerulus. The first layer is that of the vascular endothelium. So the endothelial cover, the inside of the blood vessel, so the capillary wall, there. And then the second layer is the glomerular basement membrane, or GBM for short, which is a specialized basement membrane that surrounds the vascular endothelium. And then the last filtration layer is the visceral epithelium, which is also known as the podocytes. Now, in between all these capillaries here is the mesangium, which is comprised of cells known conveniently as.

Mesangial cells. And they produce a collagen network that structurally supports all of these capillaries and it’s across this space that filtration occurs within the glomerulus of the kidney. So how exactly does diabetes, a problem with insulin deficiency, result in kidney damage Well, the answer includes multiple compounding factors. Now, the first component is an increased pressure state within the nephron. And this is due to two mechanisms. And the first is hypertension, which is a common comorbidity associated with diabetes mellitus. So hypertension or high blood pressure results in an increased pressure throughout.

The entire arterial vascular system. And this includes the afferent arterial of the glomerulus. So, to think about how this increases the pressure within the glomerulus, let’s think about a simple garden hose. So, in the middle of the garden hose, there’s a hole. And as water flows through the hose, a small amount of water will leak out through this hole. But if we open up the spigot all the way this is going to increase the pressure of the water traveling through the hose, and intuitively, this change is going to result.

In more water leaking from the hole here in the center and that’s because there’s increased pressure forcing it out of the hole. Now this is similar to what occurs in the glomerulus. The hypertension increases the pressure, just like turning on that spigot, which in return increases the filtration rate of the glomerulus, which can be thought of as that leakiness from the hole in the garden hose. Now, the other mechanism contributing to this high pressure state, is something known as vasoconstriction of the efferent arterial. Which is just a fancy way of saying.

That this blood vessel constricts or gets smaller in diameter. So, to understand why this occurs, we need to briefly review the reninangiotensinaldosterone system, or RAAS, for short. So renin is a hormone that’s secreted by the kidneys in response to decreased renal profusion, or low blood flow to the kidney. This is a sign of low fluid volume throughout the body. So in the response to a low fluid volume, renin has a cascade of effects in order to maintain blood pressure as well as volume status. And one of these effects is constriction.

Of the efferent arterial, which then maintains this pressure within the glomerulus in the presence of a decreased renal profusion. So once again, let’s go back to this garden hose to understand this a little bit better. Now, instead of turning up the spigot, as we did before, what do you think would happen if you were to kink the hose on the other side of the hole Once again, intuitively, this is going to increase the pressure behind the kink and subsequently will increase the rate at which water leaks out the hole.

So once again, this is similar to what occurs in the glomerulus in response to activation of this reninangiotensinaldosterone system. There’s a constriction of the efferent arterial to build up pressure within the glomerulus to maintain the necessary filtration and therefore, it will increase the filtration rate even further. But why exactly is this happening If I just said that individuals with diabetes often have increased renal profusion due to the hypertension, then why is a low pressure system such as the reninangiotensinaldosterone system activated And this is a good question,.

And the answer is not exactly intuitive. For some reason, the underlying physiology of diabetes, specifically the hyperglycemia, results in a direct intrarenal or within the kidney activation of this reninangiotensinaldosterone system. And subsequently, efferent vasial constriction independent of the volume status of the individual and therefore increases the glomerular filtration rate. So how does this increased pressure relate to diabetic nephropathy Well, as the pressure within the glomerulus increases, this results in a process known as mesangial expansion. The increased pressure results in trauma and damage to the mesangium of the glomerulus.

And in response to this damage, the mesangial cells respond by secreting cytokines that produce inflammation, as well as oxygen free radicals that result in endothelial dysfunction, and all of this kind of combines into hypertrophy and matrix accumulation within the mesangium, which is known as mesangial expansion. And as you can see over here on the right, as the mesangium expands, the spaces, or what are known as the fenestrations between the podocyte foot processes expand. Now, this has two effects. First, it decreases the surface area available within the glomerulus for filtration,.

And second, the dilation of the fenestrations causes the filtration system to be leaky, and larger molecules such as proteins are filtered out of the blood in the kidney. Then, the last factor contributing to diabetic nephropathy is a combination of the previously mentioned factors. And this is ischemia. As I mentioned earlier, the blood vessels supplying the tubules of the nephron come off of the efferent arterial, and vasoconstriction of this arterial from the intrarenal activation of the reninangiotensinaldosterone system decreases this blood flow. And in addition, the cytokines and free radials.

Produced from the barotrauma to the mesangium further damage the nephron vasculature. And over time these processes result in ischemia, or cell death, and atrophy of the vasculature that supports the glomerulus, as well as the tubules. So this will decrease the kidney’s ability to filter blood, and is ultimately what will lead to kidney failure in diabetic nephropathy. So as you can see, there are many different mechanisms that are going to contribute to the progression of kidney failure in individuals with diabetes mellitus. However, it’s important to note that they are all directly associated.

Eva Feldman, MD Tutorial Profile

Gtgt Dr. Eva Feldman So when I completed college I had the dilemma whether I wanted to go straight into medical school or whether I also wanted to do research because when I was in college, I got very excited about the brain and had, again a professor who told me that he felt that in the next century all the major advances in medicine and in research we’re going to be in the nervous system particularly in the brain. So when I finished college, I decided oh maybe I’ll get a PhD and a M.D.

And so I started my graduate studies first and I began in a neuroscience program at the University of Michigan. Fell in love with the brain completely and when I started medical school there was no doubt from the very first day in medical school, I said I was going to be a neurologist and I loved every day of it. One of my passions as a neurologist is also to be a neuroscientist. So I’m very privileged to have a fairly large laboratory that I work in with about 30 young people who do research with me.

And we’ve become very interested over the last 5 years in using stem cells in regenerative medicine particularly in neurodegenerative diseases in neurology. Lou Gehrig’s disease is one passion that we have. We’re also interested in Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease. So from our basic findings in the laboratory of how stem cells can promote nerve regeneration and protect nerve cells from dying, we’ve actually begun a clinical trial using stem cells in patients with Lou Gehrig’s disease. So it’s very exciting because what I do in my basic science laboratory I can then transition.

Over to my clinical practice and ALS or Lou Gehrig’s disease is one of the disorders that I am familiar with and I take care of hundreds of patients with that disorder. And so I’m able to serve as a bridge from the basic science to the clinic. I can go to the clinic and tell my patients what I’ve learned in my basic science laboratory. I can go back and tell my basic scientists what my patients have taught us and they teach us so much. And so stem cells is one of the major avenues I see translating in the near future.

T2DM Diabetic Retinopathy, Chronic Kidney Disease

Hello, I’m Norman Swan. Welcome to this program in our series on guidelines and type 2 diabetes. Every year there are about 3.8 million deaths globally attributable to diabetes. In Australia, type 2 diabetes is the fastestgrowing chronic disease, with the total number of Australians with diabetes and prediabetes estimated at a whopping 3.2 million, and it’s the sixthleading cause of death. This program looks at two NHMRC evidencebased guidelines that are new and address complications and comorbidity in type 2 diabetes. They are the evidencebased guidelines for diagnosis and management.

Of kidney disease in type 2 diabetes, and the guidelines for the management of diabetic retinopathy. For those of you watching on your computers, you can type your questions directly in to the studio. Just click on the LiveTalk tab at the top of the web page you’re looking at. That also means, of course, that we can ask questions of you. Here’s one to get you going away on that one, and we’ll give you results of that in a moment. As usual, there are a number of useful resources available.

On the Rural Health Education Foundation’s website Now let me introduce our panel to you. Stephen Twigg is an endocrinologist at the University of Sydney and President of the Australian Diabetes Society. Welcome, Stephen. Good evening. Alan Cass is the senior director of the George Institute for International Health, and director of the Poche Indigenous Health Centre at the University of Sydney. Welcome, Alan. Good evening, Norman. Paul Mitchell is Professor of Ophthalmology at the University of Sydney, and runs the Blue Mountains Eye Study. Welcome, Paul. Thanks, Norman. Good to be here.

And David Guest is a rural general practitioner in Goonellabah in NSW. Welcome. Thanks, Norman. David, challenging, dealing with comorbidities in general practice, I assume. It’s a growing area. It’s a bigger and bigger problem. It’s something that’s taking more and more of GPs’ time. If you get systems in place, you can probably cope with the challenge. Talk to me about the trends that are going on, Stephen. As you’ve mentioned already, diabetes is on the rise. We believe that approximately 100,000 people per year in Australia are developing diabetes.

It’s very similar to the worldwide trend. There are a number of factors that are probably critical in the process in terms of the development of diabetes. The prevalence changes in different groups in Australia Yes, there are certainly higherrisk groups, particularly an ageing population. There are certain ethnic groups that are at higher risk than others. There are also issues to do with lifestyle change. As we can see on this slide this data is from the turn of the millennium approaching a million people, or 7.4 of adults aged over 25 had diabetes.

In Australia at that time, well over 90 of it being type 2 diabetes. The other conditions, impaired fasting glucose and impaired glucose tolerance, or as you referred to them, the prediabetes conditions, also extremely common. So approaching one in four Australian adults have some form of glucose abnormality. NORMAN Extraordinary. It’s a remarkable figure. NORMAN It’s also agedependent Yes, very much so. If we dissect this out further, the same study, the AusDiab study, demonstrated a strong agedependence for diabetes, indicating that the ability of the pancreas to produce insulin tends to deteriorate with time.

Approaching one in four Australian adults in their 70s will have diabetes in comparison to a much lower percentage of people earlier in their life. We’re trending upwards faster than we thought Very much so. World Health Organisation data, recent trends have suggested, rather than seven million people per year developing diabetes, it’s more like ten million people. We’re going to hear about that in the more recent estimates, in the next year 2010 data from the International Diabetes Federation and WHO. NORMAN This graph shows we’re tracking faster than we thought.

And the Australian data, very similar. In the AusDiab study, whilst ‘e’ on the far right is an estimate based on previous decades, in the last decade, the late ’90s, then into the 2000s, the figures are well above what the estimates were on the trend line. A study from the Australian Institute of Health and Welfare 2006 indicated it’s more like 1.5 million people who have diabetes, then increasingly, 100,000 a year. So really, even off that scale, if we look at more recent estimates of diabetes in the Australian community.

We’re talking here about absolute risk, global risk, just as much as we’re talking about glucose Definitely. Glucose, if you like, is the marker. People with diabetes have two to fourfold the rate of cardiovascular disease as the general community. As you’ve pointed out, it does emphasise global cardiovascular risk and the importance of tight blood pressure and cholesterol control. David, on the day of broadcast, yesterday’s Medical Journal of Australia described the fact that general practitioners are not measuring absolute risk to the rate they should be. What are the barriers to measuring absolute risk.

It’s a GPeducation problem to start with. There are tools available now that make it much easier. I have a preference for a computerised electronic health record. Getting data out of the computer makes these sort of assessments much easier. A website which I think is the one recommended by various colleges to assess absolute cardiovascular disease risk is available on the web and available on the desktop. That’s a very useful tool for GPs. You’ve got an example of this risk tool that’s in the guideline That’s right, Norman. If we look at the next slide, this is an example.

This is for people with diabetes. The charts are divided into those with and without diabetes. People with diabetes are a highrisk group. They can be stratified on the basis of their cardiovascular risk in terms of looking at their systolic blood pressure, their cholesterol, HDL total cholesterol, HDL ratio, gender status and smoking status. It’s possible then to identify whether a person would be deemed at a high cardiovascular risk, in which case the intensity of the management of their surrogate markers their blood pressure, their cholesterol, their glucose.

And also antiplatelet therapy can be modified appropriately. NORMAN You’re arguably more likely to save their life by managing those other factors than their sugar It’s not one or the other, but it’s both. All of them are important. For example, diabetic retinopathy glucose is the major factor that will contribute to that complication. In terms of cardiovascular disease in people with diabetes, the risk is probably approaching 15 to 20 of the variation in risk will be glucose, depending upon the degree of glycaemic control. And cholesterol and bloodpressure control, very important in that setting.

How important, Paul, are these other risk factors than glucose We know that glucose control can help diabetic retinopathy, but those other risk factors There’s growing evidence, isn’t there That’s right. The effect of good diabetes glucose control on preventing the development and progression of diabetic retinopathy has been shown both in type 1 and in type 2 in the UKPDS. That latter study, UKPDS, actually demonstrated almost an equivalent effect in type 2 diabetes of bloodpressure management. Indeed, recent studies, the ACCORD studies and the RASS study, just recently published,.

Have shown that in fact really tight bloodpressure control, perhaps with modern bloodpressure agents, ARBs, can actually reduce the incidence of diabetic retinopathy and may result in regression of existing retinopathy lesions. And in kidney disease, Alan Cass Again, the key factors to control are blood pressure. Also, how well you control glycaemia is a key factor in terms of progression of kidney disease. NORMAN What’s the management challenge, Stephen Diabetes, as we know, is extremely challenging. There’s the combination of lifestyle management and pharmacotherapy. There’s the importance of vigilance with respect to diabetes management,.

Because, as we know, targets can be difficult to maintain over time. When we look at the optimisation of care, in terms of patient care, we have tight blood pressure, blood glucose and cholesterol targets monitoring for complications. This slide indicates that in general, we will achieve a lot if we have a generic, crowdbased approach. If we go on to the one which shows the management challenge to optimise care, once we can assess cardiovascular risk for the individual and we can target more appropriately lipids and blood pressure and glycaemia.

For the particular person the career stage of their diabetes then we can expect to achieve even better outcomes when we customise or individualise the care. Whilst the world is obsessed with obesity, it’s not the whole story Definitely not. We have these other major risk factors, we have to target those. We try and bring our waists in and reduce body weight if not stop it going higher, but there’s a lot we can do to prevent endorgan damage from diabetes. Alan, you’ve got a lot of experience working with Indigenous communities.

Indigenous rates of type 2 diabetes and complication rates are enormous. Is it a different disease or just worse I think the evidence is that it’s not a different disease, that the issues of poverty, poor access to care, a whole series of factors come together that make the same common problems of diabetes and related chronic illnesses worse rather than an entirely different approach being needed. What are the targets we should be aiming for The RACGP has generic targets, as shown here glycaemia, total cholesterol and blood pressure.

In general, these will work well for patients and for health professionals. So, the A1C target, less than or equal to 7. Total cholesterol, less than 4. These days, we focus on LDL cholesterol, less than 2.5, if not down to 2. Then blood pressure, less than or equal to 13080. However, if we do customise or individualise it for the person who has significant proteinuria, we want a tighter bloodpressure target than that. People with known ischemic heart disease, we want a tighter LDL cholesterol level less than 1.8.

And depending upon the stage of the person’s diabetes, early on we know that tight glycaemic control can reap rewards decades down the track. There’s even quite a push for HbA1c levels 6 to 6.5 early on after the diagnosis. That’s controversial. If you look at the most recent type 2 diabetes guidelines for glycaemic control, which you might address in subsequent weeks I know we’re not addressing those today the generic targets, A1C, less than 7.0, and we know we can achieve that for a lot, if not all, of our patients.

We can achieve it for a lot. There’s increasing data, again from ACCORD and ADVANCE and VADT, a number of studies over the last 18 months, 2 years, that early on in the diagnosis and also from the UKPDS followup early on, we need to aim for very tight glycaemic control, get in early. We know that in general, type 2 diabetes is a delaying diagnosis of four to five years between when it develops and when it’s diagnosed. We’re missing years there when we can help achieve tight control.

Of these surrogate markers for our patients. Paul, you’ve been following this group of people in the Blue Mountains for many years, many of whom have diabetes. Getting them early makes a difference Absolutely. In fact, one of the messages that has come out in the last year is this issue of metabolic memory. So, good control of diabetes in the first period of diabetes is really important. It’s been shown in the UKPDS in type 2 diabetes that good diabetic control over the period of the study persisted, despite the fact that the haemoglobin A1C levels.

In intensive versus routine control. We’ve got a graph to that effect to show. That metabolic memory effect was shown initially in the DCCT and is now being shown in UKPDS for retinopathy and for other complications. That probably tells us where the challenge is. We know that on average, we’re picking people up with diabetes several years after the diabetes is established. For primary care and the health system generally, what can we do to opportunistically pick up people For example, coming each year, most Australians do attend a general practitioner’s at least once.

There is strong evidence in the Australian context that if we opportunistically screen 50 to 69yearolds for diabetes, we can pick it up earlier and intervene and prevent heart attacks, strokes and premature mortality. Are you doing that, David Putting you on the spot. Yes, probably indirectly. A lot of patients have lots of blood tests. You’ll flip through and see that the sugars are in the 6s or occasionally higher, and it behoves us to concentrate on that and get a fasting glucose, get a twohour glucosetolerance test done and see where we’re up to.

Just take us through quickly the algorithm to remind us of the basic management of the glycaemic side of things before we move on to the complications. The algorithm involves intensive lifestyle management. That is both the diet and regular physical activity. We do find in most people as time goes on they do require pharmacological agents in addition to focusing on lifestyle. In terms of the HbA1c targets that will help determine what type of additional medications are needed and when, following the initial lifestyle intervention, metformin is our firstline agent.

It certainly is effective at lowering bloodglucose levels, has a relatively low sideeffect profile, well tolerated, and on top of that, in the UKPDS we’ve referred to, had good outcomes in terms of cardiovascular and microvascular outcomes. Subsequent to that though, as time goes on, HbA1cs often deteriorate and people need more than metformin alone. Sulphonylureas in Australia for decades have been our second port of call. Then, multiple thirdline options. Each of the thirdline options will sit on that line because they are newer agents which might be less well studied.

Than sulphonylureas, or they have challenges associated with them, for example, injections, as in the case of insulin. NORMAN We’ve got the results of your first poll question. We asked where you were located Here are the findings. 16 evenly split between metropolitan, regional and remote. And that big one, the blue one, is rural. Welcome to you all. It’s good to see such an even split and an appropriate split in terms of your location. I’m going to ask the second question now, which is So, we’ll get your answers to that while I ask David Guest,.

What is the general practice annual cycle of care when you’ve got somebody with diabetes With patients with established diabetes, it’s a protocol with which to manage them. It involves clinical measures that we probably should do every time we see the patient, but certainly sixmonthly, you need to check the blood pressure, the weight and hopefully the feet, but that’s sometimes something we don’t get around to. Annual tests needed, HbA1c certainly annually, more frequently depending on the level of control. We want to know what the lipids are doing,.

And HDL in particular in relation to some new riskfactor calculators. With diabetic nephropathy, we want to keep an eye on the albumin in the urine. There’s also the necessity for secondyearly eye examination, either yourself or more commonly where I come from, with optometrists and ophthalmologists. Keep on eye on the social factors smoking, alcohol, exercise, diet areas. If you get yourself into a regular pattern with that, either on your own or with the help of your team, you can keep your diabetic patient under control. Take us through the issues.

In terms of chronic kidney disease. Chronic kidney disease is common in diabetes. Chronic kidney disease is manifest evidence of kidney damage. The way that this is picked up is either through a simple blood test, then estimation of the glomerular filtration rate, where the GFR is less than 60ml per minute, evidence of significant kidney damage. The other way is through picking up protein leakage into the urine microalbuminuria through to more overt nephropathy. When we think about how we measure these things in terms of the serum creatinine on one hand,.

How much protein in the urine on the other hand and the estimation of GFR, it’s sometimes complex. Some of the keys to be cognisant of is that often leakage of albumin into the urine, microalbuminuria, is one of the earliest markers. This usually occurs when someone has normal renal function. NORMAN How best to measure that There are different ways in which that’s measured. Ways that are felt to be equally valid would be a spot, particularly morning urine for albumincreatinine ratio or a timed urine collection, again, looking for albumin.

We were originally trained in terms of 24hour urines, but in terms of common use in primary care, both of those methods are commonly used. NORMAN That should be part of the annual cycle of care Yes. Today’s patients expect fasting blood tests, so during the urine test at the same time has become part of the protocol, part of the routine. So that’s. You’ve knocked off a lot of your kidneys before your creatinine rises. Absolutely right. That’s the way to pick it up early, focusing on the albumin.

A key thing with the creatinine, a common measure we do it on many patients is that you might have lost half of your kidney function before you get an abnormally elevated creatinine measure. That’s where the simple calculation of the estimated GFR, which is done routinely by labs throughout Australia now, will provide a more ready measure of the amount of renal dysfunctional damage. Why are we interested in that Both of those are important. Both the level of albumin in the urine and the level of kidney dysfunction.

Are known predictors of events for people with diabetes. In other words, chronic kidney disease predicts heart attacks and strokes. Correct. Why are we interested It’s very common. From AusDiab, perhaps a quarter of people with diabetes have evidence of chronic kidney disease. And of all people with chronic kidney disease, what’s the diabetes in relation to the cause for endstage kidney disease Diabetes is now the leading cause of endstage kidney disease in Australia and in similar countries throughout the world, and interestingly also in developing countries. That relentless drive of diabetes contributing to endstage kidney disease.

Is quite clear in the Australian context. The ADVANCE study related cardiovascular disease risk with albuminuria and renal disease. Absolutely correct. The ADVANCE study was a large, randomisedcontrol trial with over 11,000 type 2 diabetics looking at bloodpressure control and glycaemic control. There is quite clear evidence there that both of these markers are predictors of heart attacks and strokes and progression of kidney disease to renal death or dialysis. Both independently and together, they add one to the other, so people at highest risk are people with reduced kidney function and.

Significant albumin leakage in urine. NORMAN Do they go hand in hand They do go hand in hand. The figure that one in four people with diabetes probably has some early kidney disease is about the figure for retinopathy. It used to be thought that retinopathy occurred before kidney disease. That’s before we measured kidney disease properly. They do go hand in hand. We know that once kidney disease really starts to accelerate, retinopathy really gets a hold on particularly macular oedema. People, as their creatinine starts to rise, that’s when we see retinopathy, if it hadn’t already needed treatment,.

Really become aggressive. Because they’re parallel processes according to severity Probably a parallel process, but certainly people who have got significant proteinuria have a major increased risk for macular oedema. What are the other risk factors for diabetic retinopathy The principal risk factor is glycaemic control, but in type 2 diabetes, it looks like blood pressure control is probably almost or as important. Lastly, blood lipid control might also be important. Data from field studies suggests that an aggressive approach to blood lipids might also be helpful, although that’s not so solid.

We certainly know that elevated lipids are associated with macular oedema specifically. The nice thing about that is, it’s blood pressure and glycaemic control that are also related to progression of kidney disease. So similar approaches to management of these factors that complicate diabetes can reap the rewards in terms of keeping people’s vision and keeping their kidney function. How reversible is diabetic retinopathy It’s quite reversible in the early stages. The recent data on this came from the. Got a blank on the study It’ll come to you later. One of the most recent study of ARBs.

Showed that if you had retinopathy at the first two stages, microaneurysms only or a few microaneurysms and retinal haemorrhages, those stages were reversible with really tight bloodpressure control. But once the retinopathy became slightly more advanced than that, then it was not reversible. These are the direct study findings. We’ll come back to do more on diabetic retinopathy in a moment. I’ve got the answer to the poll question, which is The red is sixmonthly, and it’s 27. 18 said it depends on the patient. 54.5 said annually. What’s the right answer, Professor Twigg.

STEPHEN I would say annually, but it depends on the patient. You’re happy with both You’ve got a thinking physician there. I’d prefer a thinking physician any day. Annually is the cycle of care. NORMAN So most people have got it right. As is recommended in the NHMRC guidelines, which Stephen cowrote. Just testing, just testing. We’ve talked about screening, just to go back to kidney disease. We’ve talked about the test that you do. What about albuminexcretion rates What validity does that have People use both albumincreatinine ratios and albuminexcretion rates.

In screening for damage to the kidney causing albumin leakage into the urine. Both are tests that are valid and have good sensitivity and specificity in terms of their role in screening and measuring response to therapy for diabetics. What are confounders when you’re doing urine tests It’s critical that there are a number of key confounders. Urine infection, menstruation in women, people who might have exercised significantly in the preceding 24 hours. Many Australians who eat highprotein diets, these people will have artificially elevated readings, for example, and some medications, for example nonsteroidals.

And others that are commonly taken. When you’re talking about blood pressure control, are we talking about angiotensin receptor blockers and ACE inhibitors or others work as well The answer is both. Yes, there is accumulating evidence from a number of trials that for people who have, in terms of prevention of early chronic kidney disease in diabetes and people with early stages that ACE inhibitors and ARBs might have a particular protective role. As well as that, it’s the overall level of blood pressure control. Indeed, there now seems to be added evidence.

That even for people who are normotensive with diabetes that there is the same benefit as people with any level of blood pressure in lowering their blood pressure in terms of kidney disease, for example. As you implied earlier, Paul, similar findings now for diabetic retinopathy Certainly the UKPDS didn’t differentiate between different blood pressure agents, and there’s never really been fantastic data suggesting that one class of blood pressure lowering medication would be better. Recent studies of ACE inhibitors and ARBs seem to show the best effects, but there hasn’t been a headtohead comparison.

Stephen I agree. You look at all the national and international guidelines and firstline for hypertension for people with diabetes is an ACE inhibitor or ARBs. As Paul and Alan mentioned though, the critical issue is tight blood pressure control. Lipid control is not as strong but still worth doing Lipid control is important, because people with diabetes have high cardiovascular risk. There is not strong evidence that lipid control prevents progression of kidney disease. But they are at high risk of heart attack and stroke, therefore require good lipid control in that context.

David, were you going to say something Just agreeing that at the macrovascular level, that’s what you’re looking for. The place of aspirin in patients Does aspirin help with kidney or eye disease Here we go. Put on your seatbelts. We’re in for a rough trip now. Perhaps I can address the issue of lipids. No, let’s have the aspirin question. Professor Twigg For secondary prevention, there’s no question antiplatelet therapy is critically important, and that gets back to the cardiovascular link. You’ve got to have an event before you start the aspirin.

for it to be of benefit Yes. For primary prevention, this is where cardiovascular risk tables can be extremely helpful. If a person is deemed to be at high risk, you’d be prone to use antiplatelet therapy. I would under those conditions. NORMAN But there’s no evidence for it. That’s for cardiovascular protection. There is, but you have to extrapolate. There was the Hypertension Optimal Treatment study, which had 1,700 with type 2 diabetes in it, but they’re only 10 of that population. Aspirin worked very well there.

There was also the Physicians’ Health Study for primary prevention. From a cardiovascular point of view, there’s a basis for using aspirin under those conditions. It is complex in people with diabetes. There’s some evidence that maybe aspirin resistance occurs resistance to the action of aspirin. And what is the correct dosage From the point of view of kidneys and eyes, we’ll move on to my esteemed colleagues. But from the cardiovascular point of view, tables can be helpful for antiplatelet therapy. I’ll come back to Paul ’cause I so rudely interrupted him.

To go on the aspirin point, one of the original diabetic retinopathy studies, the ETDRS, looked at whether aspirin was beneficial for people with diabetic retinopathy. It really showed no benefit over no aspirin. Of course, in people who needed aspirin for cardiovascular reasons, there was no contraindication to giving aspirin because there was no increase in haemorrhages, even in people with severe retinopathy. There was no increase in vitreous haemorrhage. So it’s safe, but there are no protective effects on its own. Can I add to that Stephen talked about the HOT trial.

There was a recent analysis, presented this year at the World Congress of Nephrology, showing that people in that trial who had chronic kidney disease people we’re talking about here with chronic kidney disease in the context of diabetes had the greatest absolute benefit from aspirin therapy of the entire group. Because they’re at much higher cardiovascular risk. Even though they had some increase in some risks, the added benefit in terms of the prevention of, in that case, heart attack and vascular events outweighed that. So people with CKD had particular benefit from aspirin therapy.

And smoking cessation affects the kidneys and eyes Smoking has been looked at a lot in terms of retinopathy, but no good data suggests that cessation of smoking benefits retinopathy. NORMAN So smoke doesn’t get in your eyes I’m sure it does, and it’s great to stop if you’ve got diabetes. It gets in your eyes from macular degeneration rather than anything else. What about kidneys There is evidence people who smoke are at greater risk of progression of chronic kidney disease. What about protein restriction with grade 3 renal disease.

I wouldn’t advocate that now. That was something. So generations of people with impaired kidneys have been eating that horrible stuff all that time Correct. The evidence of benefit is that it might at best delay the onset of dialysis by one or two months. And you feel every month of that. The clinical care guidelines are very helpful here in terms of the points that Paul has raised about aspirin not being a risk in terms of intercurrent retinopathy. They are nicely covered in the guidelines, and as Alan points out, the smoking issue too.

Even the executive summary, I’d encourage people to go online and have a look at it. Excellent marketing, Professor Twigg. We’re most impressed. What about salt reduction in kidney disease Does that have any benefit Salt reduction is becoming increasingly an issue of focus in Australia. In general we eat a highsalt diet. A lot of that is about not salt that we add but that salt is in..takeaway foods and foods that we buy at the supermarket. It’s quite clear that the highsalt diet has implications for hypertension. Therefore, I think it will be an area of increasing focus.

How can we reduce that in terms of interaction with the food industry, for example, so we can lower blood pressure That will be very relevant for management of diabetes. A question from New South Wales ‘What is the incidence of chronic kidney disease with gestational diabetes’ Maybe I can answer the gestational diabetes part, then pass on to the colleagues for chronic kidney disease. Gestational diabetes by definition is diabetes that develops in pregnancy, then usually resolves shortly afterwards. You wouldn’t expect kidney disease with it Yes. It does affect about 5 of the pregnant population.

After saying that, pregnancyinduced hypertension and preeclampsia and eclampsia, they do cosegregate with gestational diabetes, probably through body weight and equivalent risks. In terms of renal disease per se, in some of the renal diseaserelated conditions, there is some link. I’ll stop there and pass on to others. The actual risk of significant renal disease at the time of gestational diabetes or preeclampsia, for example, is low. People who might already have overt diabetic nephropathy at the time of becoming pregnant and high blood pressure and things are at more risk.

In that condition of worsening of renal function and of having greater difficulty in managing those comorbid conditions. There are a lot of people interested in following people after having the pregnancy, having a baby, in terms of their then ongoing risk of developing type 2 diabetes and related chronic kidney disease, where it does appear that there is, in longterm, some increased risk. Another question is, ‘How does steroid abuse influence the incidence of chronic kidney disease in existing type 2 diabetes’ I assume we’re talking anabolic steroid abuse here.

That’s not something I have any particular knowledge about. You haven’t got many muscledup. What about steroids as in corticosteroids There’s obviously concerns about obesity and its interaction with diabetes as to whether that’s a risk factor for development and progression of chronic kidney disease in diabetes. But again, it’s not something that features steroid use, in terms of development of chronic kidney disease. Let’s have a look at our first case study. Back a while, back about 10, 11 years, I was working in the coal fields then. I went to the doctor because the diabetes had sort of caught up with us,.

The high blood pressure and that. The doctor had taken blood tests and that and said, oh, yeah, there’s something wrong with your kidneys. So I had to go to Townsville. They took a biopsy on the kidney. They thought it was a diseased kidney. They took a biopsy, and the result of that was, neither kidney was diseased. We had to go and see a dietitian in Mackay when he came back. They said, don’t eat this and don’t eat that. Eat this and eat that. So he did it, but nobody ever said, you’ve got to follow it up.

It wasn’t until about five years ago that he started feeling down. He said he was feeling a bit tired a lot. I said, you need a good sleep. Stop eating so much. He got the flu. He was away working in a mine. He used to fly in and out. And then he got sick. He flew back in, and I couldn’t believe he was a person when I opened the gate. I thought, what’s wrong with you He said, I’m really sick. Jeez, it nearly killed me. It was just something unbelievable.

That’s when he asked his doctor if he could get his kidneys checked, and lucky he did do that. Next I know, I’m at the renal area of the doctor’s. It just went from there. I knew something was wrong when he didn’t come out. I kept seeing people going out, and I thought, something’s wrong. Then I thought, oh, no. When I walked in and saw the faces, I knew then. It just hits you like a brick. It all happened so quick. It obviously was over a long period of time.

Probably the good life caught up. Personally, it gets back to the way you’re brought up, I guess. The foods that you eat when you’re in your younger days, grog, everyone does it. A lot of people overindulge. It just depends. It gets back to your diet and the way you look after your body. I didn’t show him, I’d just go out and cry. I couldn’t handle it. Not only my father died, his father died of it. I’ve got aunties on my mother’s side that have died of it.

Down in South Australia. So you think, he’s got it, so I must have it. It knocked the whole lot of us. Really knocked the family. The grandkids just couldn’t believe Poppy could get sick, not their poppy. Not a good story there, David. No, no. Like he said, it happened so quick, but it really is something over a decade or more, isn’t it I think it’s probably a good idea when we have patients with diabetes early on that we have our registers set up so we can keep track of them.

It would be even better if we could negotiate some plan on how we’re going to manage it according to the cycle of care so they don’t get away from us. And using a team. And using a team to ease the burden, particularly on rural GPs who don’t have much time. He looked as if he was trucking along with a haemoglobin of about 9. I think that’s right. They talk about the devastating impact of diabetes and kidney disease on the family. The key issue is multiple missed opportunities for engagement.

In the management of the diabetes. He talked about all the factors we know are crucial his blood pressure, diet, all of the approaches to management that could have made a difference and prevented his severe kidney failure. This problem is writ large again and again across the country. I’m going to ask you another question. How would you rate your understanding of correlation between serum lipid levels, good blood glucose control and blood pressure control and eye complications It’s probably a bit better since we’ve been speaking about it for a while.

Let’s see how you rate it now. While you’re answering those questions, we’ve got another case study to watch. Let’s look at Darren’s story. My name’s Darren Dorey. In September, I’ll be 43. I live in Warrnambool, in the southwest corner of Victoria. It’s approximately 300km or three hours from Melbourne, a little seaside town that is a nice, little friendly community. I was diagnosed with type 2 diabetes when I was 27. I was told to change diet, and I was put on some tablets. But as time went by and I didn’t feel any different,.

I got more and more slack with it. Probably for the next ten years, I lost focus on control of the diabetes. At the time I was told, you have to have your eyes checked. OK, well, that’s pretty serious. I drive a truck for a living, so I’ve got to keep on top of the eyes. After a couple of years of going, yep, your eyes are fine, you stop worrying about it. Around about 2001 I was starting to struggle a little bit with seeing some road signs. I went in to the optometrist’s to get some glasses.

She had a look in my eyes and said, you’ve got a massive bleed in the eye. She said, you need laser surgery and you need it now. I walked out of the ophthalmologist’s rooms after having something like 300, 400 shots of laser in the eye. I ended up having a vitrectomy. Probably 18 months later, I developed a cataract, which I had out in about 2006, in the left eye. That brought back vision beautifully. It was like, wow, a whole new world. This is all good. In 2007 I’d actually gone back to truck driving.

I guess going back into trucks was, for the diabetes, one of the worst things I did. I did a lot of travel where you’d take off for a few days’ trip and forget to take your medications with you. I noticed it was getting harder to read the paperwork, and the headlights of cars started to become more glarey the lights would flare. I thought, I’d better go back to the ophthalmologist. He looked at my eyes and said, ‘Are you still in sales’ I said, ‘No, I’m a truck driver.’.

He just said, ‘Not anymore you’re not. Hand in your licence tomorrow.’ I then had to go home to my wife and four kids and say, ‘I don’t have a job, and it looks like I might be going blind.’ The same day, our landlord called over to mention that he’d put the house on the market and we’d have to move. Yeah, life just crumbled. Paul Mitchell, entirely preventable I think that blindness from diabetic retinopathy should be preventable. There really should not be any cases of people who go blind from this disease anymore.

There are still people going blind from it, and there will still be some people. But if you look at every one of those cases, you can really detect what went wrong. Clearly, in the early stages of his diabetes, he was poorly managed. He put his head in the sand. Maybe his doctors didn’t impress on him the absolute importance of having regular checks, but it should have been prevented. After he had that first lot of therapy, it looks like he again lost contact. He should have had pretty intense followup after that first therapy.

But he didn’t go, and he went back to driving again. If you look at Darren’s story, there are many circumstances where really, the wrong path was taken, and his blindness, or severe vision loss, could have been prevented. How do you screen your patients for retinopathy, David Do you send them to the optometrist I send them off to the optometrist or ophthalmologist, probably a 5050 split, or a bit more to the ophthalmologist where we are. Question from Michael Stuckey in Queensland ‘Why not annual retinopathy screening’ Paul.

It’s been looked at. Around the world, most diabetes associations recommend annually, but in fact, the development of retinopathy occurs relatively slowly. It’s been shown that twoyearly is actually sufficient. If someone has difficulttocontrol diabetes, if they’ve already got other complications, of course they need to be seen more frequently, even if they have no retinopathy. How good are the screening tests This is ophthalmoscopy Yeah, this is ophthalmoscopy. The eye doctor, or optometrist, wouldn’t use a handheld ophthalmoscope. He would use a slit lamp with a much wider area, being able to screen the retina much more effectively.

Than the handheld ophthalmoscope. We also have the potential availability for clinics of nonmydriatic photography. This is what they’re using in some Aboriginal communities That’s right. That’s very effective. You see a blownup picture, you can immediately see if there are any retinopathy lesions. The standard though, at the moment, would be pupil dilation Yeah. The standard is pupil dilatation, then examination of the retina by someone who can do it properly an ophthalmologist, an optometrist or a welltrained GP or physician. What are the criteria for referral to an ophthalmologist.

Certainly nonophthalmologists can manage people with diabetes in terms of retinal screening until the point at which any significant retinopathy is present anything more than the occasional haemorrhage or microaneurysm. From that point people should see an ophthalmologist. Marisa Pilla from North Queensland asks, ‘Is there any ACE inhibitor that’s superior to the others in helping to prevent retinopathy or the worsening of the condition’ We don’t know. There are two recent studies looking at two different ARBs and they both showed beneficial effects, but there’s been no headtohead comparison.

She also asks about antioxidants. The AREDS study suggested that a certain cocktail might help macular degeneration. Does it help in diabetic retinopathy There’s no evidence that it helps diabetic retinopathy. Talk us through laser photocoagulation here. There are some new therapies coming on when you’ve got microaneurysms and bleeds. Once ophthalmologists take over followup and management of people with diabetes, what they’re really critically interested in doing is evaluating the patient at an interval so that they would detect visionthreatening retinopathy and could apply laser treatment at the optimal time.

The indications for laser treatment are the presence of either new vessels, and this is an advanced stage of the background type of retinopathy. New vessels are fragile, they bleed, they don’t really help, they don’t bring new blood to the area. The second is macular oedema. This is the more frequent and more important complication to detect. That is harder to detect with ophthalmoscopy. That’s why you really need an ophthalmologist or optometrist to examine the patient. And the treatment of macular oedema The treatment of macular oedema is currently laser treatment.

Using the guidelines that have been around for 25 years. It’s reasonably effective but not brilliantly effective. Certainly many people will still lose vision. We now have some other adjunctive therapies that can help. The main one is antiVEGF therapy. This is vascular endothelial growth factor. This is like Avastin or Lucentis. That’s right. These agents are an adjunct to therapy. They don’t do away with the need for laser, but they can help to dry out the macula until laser treatment can be a bit more effective. Laser treatment is probably more effective if it’s applied.

When the macular oedema is resolved. And the role of fluorescein angiography Becoming less and less. Fluorescein is not a particularly pleasant test to have done. We actually do it very rarely. We might do it at the onset, before we start laser treatment for macular oedema, once, but we rarely repeat it these days. We don’t do it at all for screening or for the followup of people with diabetic retinopathy. Unlike retinal detachment, vitrectomy has a different reason. You’re trying to get rid of the haemorrhage from the vitreous.

There are two circumstances. The first is to get rid of the haemorrhage and scar tissue, because new vessels that bled will then develop scarring, and that scarring will cause traction on the retina. Because retinal detachment is increased in diabetes Correct, and it’s a tractional type of retinal detachment. The other type of need for vitrectomy surgery is for traction on the macula itself, which can cause macular oedema to persist and be chronic. But we are doing less and less vitrectomies now because physicians are managing people with diabetes much better.

We’re seeing less people presented at Act V, Scene IV, and we’re needing to do a lot less vitrectomy surgery. Just to explain, the vitrectomy involves microdissection to remove scar tissue. Correct. It involves usually two ports on the side of the eye with instrumentation which can dissect and peel off membranes and coagulate blood vessels. People have said that doing cataract surgery can also damage the retina. What risks are there in cataract surgery and diabetes This is an important issue, and it’s still important. We know that people with diabetes develop cataract much earlier.

Than people without diabetes. There’s a direct effect of glucose on the lens in the eye. The type of cataract they get is a cortical cataract the spokes when you dilate the pupil you can see them quite easily with an ophthalmoscope or an opacity on the back of the lens. The problem is that when people with diabetes develop cataract, they may also be developing retinopathy. If there is any early macular oedema or moderate retinopathy, then you can develop macular oedema after cataract surgery, perhaps as a response to the inflammation of the surgery itself.

One of the issues that all ophthalmologists know is that we must stabilise the retinopathy before cataract surgery as much as we possibly can. What about access to good ophthalmological care when you’re living in a small country town This is always difficult. Ophthalmologists like to live in the nicer suburbs, and don’t necessarily go to the country so often. But in all country areas in Australia, there is some degree of access. It always needs to be better, but there is reasonable access. And if there isn’t, you need to let us know.

So the College of Ophthalmologists can look at this. Local ophthalmologists in some of the larger rural areas will be prepared to travel to smaller areas if they think there’s a reasonable need. This nonmydriatic screening can be transmitted for people to look at. Correct. Right now there’s another application to the Medicare group to consider funding nonmydriatic photography. This would produce a fantastic way of screening people. It means they wouldn’t have to travel a long way to see an optometrist or eye doctor. GPs themselves could read the photographs quite well.

With relatively minor training. That has not yet been approved, but we’re hoping it will be. Let’s have a look at Darren’s story again, and what his life is like now. My left eye has been left with 25 vision. The right eye, about 10. The hardest thing with the eyes is that they see totally differently. I describe it as being like the old fun mirrors at Luna Park, where everything is distorted, or fog up your windscreen, jump in your car of a cold morning, going for a drive without a clean windscreen.

Then put a few little lines and black dots into your line of vision then go crosseyed so you’ve got double vision on top of that. I was never actually told about the correlation between diabetes and depression. If my sugar levels were high, my moods would swing. But once I lost the sight, the depression came in like a tidal wave. It became allencompassing to the fact where I attempted suicide. I lost all selfesteem, I lost all selfworth. It cost me my marriage. I haven’t seen my children for two years.

October ’07, my life fell into a hole a very, very deep black hole. It took me another six months to crawl my way out of it and restart my life. One of the biggest things that helped me get my life back on track, or helped me out of the hole that I was in, I made an appointment to see my GP and couldn’t get in, so they said, we’ve got another doctor here with an appointment open. Do you mind seeing someone else I said, I just need a script, so that would be great.

I sat down with this new female doctor. Very young, she was. She had a look at my file and said, you haven’t had this test done for a while. You haven’t had this test. What’s going on here What’s going on there We’d better take control of this. It was almost a lightbulb moment for me, like, someone is listening, someone is taking note. The GP I was seeing, we had a good rapport, but it just became the usual, yep, I’ve run out of tablets. Can you help me here.

It was in and out, script in hand, thanks very much, see you later. She also linked me in with the local psychiatric services through the local hospital, and I was given a case manager, who, once again, showed a lot of compassion and care and was listening to me. Also Vision Australia really came on board and helped me with a lot of adaptive stuff. They sent out a person to help me learn how to walk again. It sounds silly, but you learn to feel the ground rather than see the ground.

I couldn’t see the normal, everyday things anymore, simple things like how to put something in the microwave, push the button to go. I couldn’t see that button. I couldn’t feel that button ’cause they’re flatpanel. Vision Australia said, we’ve got these dots, put them on the go and stop buttons. I can’t read how many minutes I’ve got up, so I count how many times it beeps. It’s just one of the little things you take for granted that suddenly become an issue. It was the supports behind me that helped me.

I’m now employed by South West Healthcare, Psychiatric Services Department. Vision have come down from Melbourne and put in a program which helps with email, it enlarges the font automatically. I can’t read normalsize font. Also, enlarged keys or enlarged stickers on the keyboard. Without them, I’ve got no hope. The main thing for someone who’s new to diabetes, or even a doctor that’s treating a new diabetic, is to emphasise what it is and how it works. Doctors need to emphasise, you won’t feel it coming. As I said earlier, I expected to have signs.

If there’s any damage, I expected to have the signs of it coming. You don’t feel it coming. It creeps up very, very slowly until suddenly it’s out of control. A lot of the things I did was, if it’s serious, they’ll tell me about it. Of course they think you’ve understood it, so they let it go. Suddenly it becomes a huge issue down the track. I honestly feel, if it had been more of a team effort between my GP and myself, maybe I wouldn’t have lost the sight.

Tragic, David. DAVID Yes. You feel bad as a GP when you see a story like that. There’s a place for having a register of your diabetic patients and reviewing that regularly and getting your team to help you in the management of these patients and make sure they’re not lost to followup and you can keep on them. I joke with our diabetes educator who visits our surgery that we play good cop, bad cop. She tells them all the things they have to do, then I come in and say,.

Sharon says this, so you’d better do the right thing for next time. Let me get the results of the poll question 6 of you said you had no understanding. Hopefully we’ve improved that tonight. 62 said you’ve got moderate, and 31, comprehensive. So over 90 of you have got a reasonable understanding, at least on a selfassessment basis. We won’t be administering any multichoice questionnaires tonight. Paul, not a good story there, but you’re saying it’s becoming rarer. It’s becoming rarer. One of the points we could say about Darren.

Is that he’s been through the gamut of therapy. Usually their vision is stable from that point. Usually there’s no further progression, because the disease becomes relatively quiescent after it’s done all that damage. He probably will hold his vision from now on. We should be looking at his case and say, this should have been prevented. We really need to work hard to prevent all these cases, and I think we can. We mustn’t forget the psychosocial issues. Depression goes along with it. It makes diabetes worse. Absolutely. It’s an important part of the package.

We know people with diabetes have a two to threefold higher prevalence rate of depression. It’s a vicious cycle. What are your takeaway messages for the audience, David Know who your diabetic patients are, and keep them under careful, close review. Don’t try and do it all yourself. Your diabetes educators, dietitians, podiatrists, they’re all there to help, and make sure the necessary gets done. And get the targets right. Get the numbers right. Paul At least twoyearly, I review by competent examiner. Make sure that you really work hard.

At the control of diabetes blood pressure and blood lipids. Alan Chronic kidney disease is common. It can be readily detected and followed with simple blood and urine tests. And again, blood pressure and glycaemic control are crucial to preventing progression. For me, those two case histories show that too many people fall through the cracks. Both as individuals in our own clinical practice and the health system generally, we need to do something better to prevent those disastrous outcomes. Stephen Vigilance is key. Diabetes does tend to be a progressive condition,.

And the complications. We need to get to know our patients well. Work with them as one of the key members of the team. Recognise that we can prevent at many different levels. Hopefully we can prevent many people from developing diabetes, many others from diabetes complications developing once they’ve been diagnosed with diabetes. Even those who develop more severe laterstage complications, there’s a lot that we can do. Never give up, prevent at multiple different levels and get to know your patient. Thank you all very much. Very interesting and very important.

I hope you got a lot from the program too. The series of four programs we’re making on type 2 diabetes guidelines will be available in December free on DVD. To order, visit the Foundation’s website. Copies of the guidelines can be downloaded from Diabetes Australia diabetes.au. If you’re obtaining even more information about issues raised in tonight’s program, there are a number of resources available on the Rural Health Education Foundation’s website Don’t forget to complete and send in your evaluation forms and register for CPD points by completing the attendance sheet.

48 Nerve Damage Morphine Addiction Gone Faster EFT

The most amazing thing I’ve ever had happen in my life and really we all have amazing things but the this is a situation that I have been dealing with, and dealing with it very terrible pain that occurred from a happening in my life where, what was it Sherrie 1998 They damaged that major nerve. 1998 I end up going in for a angiogram, after being treated by physician for in ear infection and I went in a hospital in Orlando. If you guys are ever in Orlando and you need to go to hospital, that’s a topflight.

Place. We were very blessed that they come up with what they call a crises radiologist, but they discovered that I had a a blood clot in my right vertebral artery and they had to go back up my groin and bust the blood clot, then they went back up it again in put in a stent, due to the condition of the right vertebral artery. The left one was gone and it’s just something that happens to people. but anyway I was just sitting there and, just feeling this awful knot in my groin and.

Since this happened. they have, invaded my brain like 12 or 13 times, so if I say something crazy, or I’m doing something crazy you understand, It is a situation from having your brain invaded and it has made a big difference by Robert very capably set me down and we went through the tapping method. and. hey folks I’m not I’m not lying to you, Robert quit and he says How’s the pain and it’s gone! And this is after four or five years. I was treated oneyear, a couple years ago, for.

I was on morphine and spent a month in the hospital trying to get off of it. And now my groin, the pain has gone the burning has gone and I haven’t smoked a cigarette since last Tuesday afternoon about 2 o’clock! I’ve never been happier in my life and I feel like, thanks to our friend here, he was very capable, I was very much at ease with him and I feel very fortunate, very blessed to have crossed paths with with Robert. Thank you. I’ve watched Paul and his suffering and we almost lost him a couple years ago.

Because the morphine that they were giving him had shut down his system his colon and he was severely obstructed and then they put him on this patch that is, I guess, very addictive and the VA Veterans Administration doctors are just he got special permission to to use the patch, because they said once this nerve is damaged it cannot be repaired, it will not heal itself. And yet he’s pain free now! He’s suffered from a terrific amount of burning and it’s just been a miracle, an absolute miracle.

Diabetic nephropathy Clinical presentation treatment

Voiceover Diabetic nephropathy is one of the most common and serious chronic complications associated with diabetes mellitus. In this tutorial, let’s discuss how the mechanisms underlying diabetic nephropathy correlate with the clinical presentation as well as the treatment of the disease. Now fortunately the mechanisms underlying diabetic nephropathy, directly correlate with the clinical presentation. And the first clinical finding of the disease is somewhat paradoxically an increased kidney filtration rate or glomerular filtration rate. So, diabetic nephropathy, if you break down the term into nephro and pathy literally means kidney disease caused by diabetes.

Now typically kidney disease is marked by a decreased filtration rate, so why is it that the first clinical stage of diabetic nephropathy is that of an increased glomerular filtration rate Well recall that the earliest mechanism contributing to diabetic nephropathy is an increased pressure state, over here in blue. And this is due to hypertension and efferent vasoconstriction. So let’s use a common garden hose to help illustrate how this increased pressure state will ultimately result in an increased glomerular filtration rate. So, imagine you have this garden hose and it has a small hole in the middle of it.

So first you’re gonna open up the spigot and increase the pressure and flow through the hose. Intuitively, this is going to increase the rate at which water is leaking from the hole in the hose. Next, you partially kink off the end of the hose distal to the hole, and once again this is gonna further increase the rate at which water leaks from the hose. This is essentially what’s occurring in the glomerulus with the hypertension representing the opening up of the spigot and increasing the pressure before the glomerulus,.

In front of the glomerulus, and the efferent vasoconstriction representing the kinking off of the hose, which causes this back pressure. Both of which are going to increase the filtration rate. This stage of diabetic nephropathy is most commonly asymptomatic, so it goes typically unnoticed. However, it’s going to set the stage for the next clinical step of diabetic nephropathy and that is detectable proteinuria. And what proteinuria is is protein in the urine. So this increased pressure state causes trauma on the mesangium, in the middle of the glomerulus here.

And it results in mesangial expansion, which is this second mechanism of diabetic nephropathy. Now as the mesangium expands, this also increases the size of these fenestrations or spaces between the podocyte foot processes, so let’s go back and look real closely at these fenestrations and watch how they increase in size. Now, these podocyte fenestrations are a component of the glomerular filtration mechanism. So, let’s think of these podocyte foot processes as a coffee filter. A proper coffee filter is porous enough to allow for the water to flow through,.

But will retain the coffee grounds within the filter. This is because the molecules of water are much smaller than the size of the coffee ground, so over time the coffee pot is gonna fill just with the coffee but no coffee grounds. Now imagine if the coffee filter was replaced with a cooking strainer, which has considerably larger pores. If you were to try and use a cooking strainer as a coffee filter, when you pour the hot water through, it’s not gonna work because the pores of this cooking strainer are much larger.

Both the coffee as well as the grounds are gonna start to spill through and you’re gonna end up with coffee grounds in your coffee. So in the glomerulus, the fenestrations between these podocyte foot processes are kind of like coffee filters and normally in the filtration of blood no proteins or large molecules are allowed though. However, with mesangial expansion these fenestrations become much larger and when filtration occurs they become leaky, and they allow for molecules, such as proteins, to be spilled out into the urine. So this is what causes the detectable proteinuria.

In diabetic nephropathy. One of these proteins is albumin. Urine tests are available to detect the presence of albumin in the urine, so frequently individuals with diabetes will have routine screening to test for this albumin or for protein in their urine, which is a sign that they may be developing diabetic nephropathy or kidney disease due to diabetes. Then the next clinical stage of diabetic nephropathy is that of a decreased glomerular filtration rate. So you can see that we’ve gone from an increased glomerular filtration rate, then to a decreased glomerular filtration rate.

So what exactly causes this Well, recall that part of the reason for this mesangial expansion is the release of cytokines which cause inflammation and oxygen free radicals. Now, these cytokines and oxygen free radicals damage the mesangium, resulting in the mesangial expansion. However, they don’t just damage the mesangium. They damage the cells throughout the tubules as well as the vasculature that supports the nephron. Now in addition to the cytokines and oxygen free radicals, this vasculature is further damaged by this efferent vasoconstriction here. Which is one of the causes of that increased pressure state.

And this combination of damage from decreased blood flow and cytokines and oxygen free radicals results in ischemia and atrophy of this vasculature. As this vasculature kind of dies off, it no longer can support the tubules of the nephron, so the nephron itself begins to die off as well, and so there’s a decreased ability to filter the blood. Now initially this occurs in just a small percentage of the nephrons in the kidney, and the kidney’s able to compensate, but eventually over time if this diabetic nephropathy is not treated, a large enough number.

Of nephrons throughout the kidney are gonna die off, and it’s gonna be detected as a decreased filtration rate. The kidney’s no longer able to keep up with the dying off of nephrons. If this is present, this decreased filtration rate is present for more than three months in a row, then it’s known as chronic kidney disease. As it continues to progress, eventually it will become a permanent decrease, which is then known as endstage renal disease. Now that we have a better understanding of the mechanisms that cause diabetic nephropathy.

And how they correlate with the clinical presentation, let’s just briefly touch on how diabetic nephropathy is treated. This is, once again, gonna be directly correlated to the underlying mechanisms. So, the most important thing in diabetic nephropathy is to treat the underlying diabetes. This is because the hyperglycemia associated with diabetes is the cause of this increased pressure state, so if you can treat the diabetes, you can prevent the increased pressure state, which will then prevent the cascade of effects leading to diabetic nephropathy. However, if this increased pressure state.

Does start to occur, the next step is to treat the pressure. And what I mean by that is treat the hypertension. So if you can decrease the blood pressure, that goes into the afferent arteriole here, you’ll decrease this increased pressure state. In addition, one of the most common medications to treat blood pressure are known as ACE inhibitors. Now ACE inhibitors stands for angiotensin converting enzyme inhibitor and angiotensin is one of the hormones in that reninangiotensinaldosterone system that results in the efferent vasoconstriction. So by treating the blood pressure with an ACE inhibitor,.

You’re also going to decrease this vasoconstriction to further decrease this pressure state within the glomerulus. These two treatments should be occurring regardless of whether or not an individual with diabetes is in any of these clinical stages of diabetic nephropathy. So these are not only treatments, but they’re also good for preventing the progression of diabetic nephropathy before someone even enters this first clinical stage. However, if someone does develop diabetic nephropathy and it unfortunately progresses far enough to have this decreased glomerular filtration rate and they end up in endstage renal disease,.

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