Vasculitis in diabetics

#KYJ - Vasculitis

Nurse M asks "can you do a blog on vasculitis and why it's a diabetic complication?"

So here we go...

Vessel disease and in particular, vasculitis has recently been found to be associated with fibromyalgia and related Neuralgia (nerve pain).

Literally, vasculitis means inflammation of the blood vessels.  It is just one of a myriad of Autoimmune disorders.

Think of it as rheumatoid arthritis inside blood vessels.   Some medical co-morbidities are often prerequisite. Perhaps the most well known is  Diabetes.

Diabetes is commonly associated with both microvascular (small vessel) and macrovascular  (large vessel) complications. Vessel hardening (sclerosis), endothelial injury from viscous blood, and fatty plaques (atheroma) all contribute to the vessel inflammation that is vasculitis.

Hypertension, frequently present in diabetics, accelerates the onset of vasculitis. Over the past 10-15 years, we have developed a good understanding of the underlying chemical changes in diabetic blood vessels. 

What we know, is that vasculitis is immune, mechanical (BP) and metabolic; and that these factors interact to stimulate the release of cytokines (cell communication proteins) and growth factors in branches of small blood vessels.  Eyes, kidneys, and hands/feet.

In diabetics a common factor is byproducts of glycated proteins in diabetic blood.  You better know of these proteins as HbA1C. The higher their HbA1C is, the more vasculitis and subsequent effects.

Two important substances over secreted in diabetics, is seen in the glomerulus, and the retina vessels. 

In the kidney, "transforming growth factor-beta" has been observed to be prosclerotic (causing hardening) in  renal arterioles.  This fuels and exacerbates the Renin-Angiotensin response which pushes up BP.

In the retina, vascular endothelial growth factor and its receptor, vascular endothelial growth factor R-2 are increased.  Gobbledygook I know, but these cytokines cause new blood vessel growth (angiogenesis). 

Ultimately, the cell changes caused by these cytokines stimulates inflammation- Vasculitis.

Now here is the clincher, inflammation inside blood vessels, traps the smallest cholesterol carrier proteins called LowDensity Lipoproteins (LDLs).  This is in essence, the formation of cholesterol deposits in arteries (atheromas), narrowing and hardening the vessels (atherosclerosis).

DM and cardiovascular disease are inextricably linked.

So the next time the diabetic you are looking after complains of fatigue and flu like aches, it may very well be vasculitis, and is contributing to kidney failure, blindness, small peripheral vascular disease (ulcers and slow healing), and a massive increase in risk of MI and CVA.

Keep those HbA1C levels in check, monitor vision, renal function and manage hypertension aggressively.

#ECT4Health 

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Wee.

Obstructive Sleep Apnoea

Sleep Disorders Week

So I thought I'd do a quick #KYJ on Sleep Apnoea.

This is part 1 of 2.

There are two main types of Sleep Apnoea.  Central Sleep Apnoea (CSA), and 

Obstructive Sleep Apnoea (OSA).  As the name implies, OSA is a condition where soft tissues of the throat relax when sleeping, occluding or obstructing the airway. During periods of apnoea, oxygen levels in the blood fall (often dramatically -SpO2<75%).  While blood CO2 rises slightly, the effect of hypoxaemia is the most profound, and causes most of the acute sequelae. 

Let's just recap normal breathing stimulus.

Normally your brain stimulates you to take your next breath, based on a complex biofeedback mechanism.

When pH of the blood (and CSF) falls - acidosis; this is the primary trigger of breathing. Unlike you were probably taught, high CO2 isn't a direct stimulator of breathing, but it is secondary stimulant due to the fact that high plasma CO2 causes pH to fall (Carbonic or Respiratory Acidosis). So it is true to say high CO2 stimulates breathing, but indirectly through acidosis.

The second and more primitive stimulus to breathe is low plasma oxygen.  You were born with this mechanism, which you probably learned about when you were taught why a new born baby draws that first breath.   It is called "Hypoxic drive", but early in your infancy you switched to the high CO2/low pH trigger.  Called Hypercarbic drive, this mature lung, primary mechanism isn't in play during OSA, because CO2 doesn't dramatically rise.  You are asleep (or trying to), and at rest, you just don't make as much CO2.

So.  The Snorer is left with multiple obstructions, and apnoeas.  This leads to drop in plasma oxygen (hypoxaemia).  When oxygen falls low enough, the secondary hypoxic drive mechanism kicks in waking the snorer. They adjust position and inhale, restoring plasma oxygen levels.   The sleeper then drifts back to sleep with out realising that they woke up, and the whole cycle starts again.

Snoring is almost always present (even diagnostic).

Daytime tiredness morning headaches hunger and weight gain are common.

Poor concentration irritability and its extreme breathlessness on exertion, and ankle swelling which is the hallmark of right heart failure.

In its mildest form, people stop breathing every 5-12mins (5-14 episodes of apnoea/hour)

Moderate OSA is diagnosed at 15-30 Apnoea/hr

And severe OSA >30/hr.

That's an Apnoea every 1-2 mins.

Waking that often, causes the sufferer to feel like they are never well rested.  They may think they sleep all night, but realistically never completed important restorative sleep cycles, and this takes it toll on tissue healing, cell regeneration and hormone levels.

The body, in a constant state of stress, releases massive amounts of cortisol (our natural hydrocortisone) and Adrenaline driving up BP, and heart rate. While cortisol exerts its effects as glucose intolerance, insulin and leptin increase/resistance, obesity, atherosclerosis and T2 Diabetes, the adrenergic stress response contributes to the development of heart failure.

Just let that sink in for a minute.  Your snoring is causing your heart failure obesity and diabetes.

The age-old question of does a obesity cause OSA, or does OSA cause obesity is yet to be completely answered, but there is a biochemical body of evidence to suggest that poor sleep equals neurohormonal changes that lead to altered carbohydrate metabolism, and all the diseases linked to it.

You don't need to snore and snoring is the single most important feature of obstructive sleep apnoea. recognise it early nip it in the bud.   If you are sleeping next to that special someone who snores. Know this- it is not about your sleeplessness, it is about theirs.

Diagnosis :

Sleep studies are done to measure EEG , ECG and oxygen saturation, then when the moon is full a respiratory physician gazes at the cauldron of data and diagnoses OSA.

Treatment 

1. Surgery to remove or cauterise part of the soft palette.
2. Continuous positive airway pressure (CPAP) ,which blows air into the throat to splint the pharynx open. 
3. Jaw manipulation devices that thrust the lower jaw forward in an under-bite, while sleeping.  You remember from airway management courses that jaw thrust pulls tongue off the pharyngeal wall.
4. Tennis ball in a bum-bag.  Stops old mate rolling on his back and occluding his airway.

Big topic that we can't tackle comprehensively in one post.

Tomorrow (in our Sleep Week) we will look at Central Sleep Apnoea (CSA).

Hope you catch some zzzz! 

#ECT4Health 

ECT4Health