Doctor, Doctor, Give Me The News. Vol I

Diabeetus Cha Cha Cha

Welcome to the first edition of an ongoing series built to break down common medical conditions and emergencies so all of us can have a better understanding of just why doctors do what they do. One of the most enjoyable parts of my day to day is explaining physiology and pathology to my patients. I’ve made it a habit to go over every test sitting side-by-side with the patient. I tell them what every element means; very briefly if normal and with a little more in depth explanation if abnormal. I break down the fancy schmancy radiology jargon and explanations, telling them what the reading means in plain language and what it means for them. Most people appreciate it, I think.

Diabetes.

So prevalent. So destructive. Many times preventable.

Once in a while patients present to the clinic with complaints related directly to a new onset diabetes. The ones that do are often type I, or in the olden days, juvenile diabetes. This is a very different process than type II. In brief, type I is probably an autoimmune over reaction to some kind of stressor, perhaps a viral infection. Often other autoimmune diseases or processes may be found. For all tents and porpoises this is not a preventable disease. Of note, often times the first signs and symptoms of new onset diabetes is unexplained weight loss, going pee all the time (with no good explanation) and fatigue. Type I patients can develop DKA (diabetic ketoacidosis) which is a dangerous state, lethal if not caught or managed properly. It is important to note that roughly 40% of patients are asymptomatic, especially in the early parts of the disease, where damage can be mitigated, if not outright reversed.

Are you surprised to learn that there is a larger genetic component with type II? I was, when I learned this fact. But like most aspects when it comes to diseases like this, it is basically a variance in vulnerability, not a sealing of fate.

Okay. Anatomy and physiology time.

The pancreas looks like, uh, well, like something that should be submitted to this Instagram page. I’ll leave it at that. It sits right behind the stomach. It’s buried back there, right under the diaphragm. As an aside I had a patient quite a while ago who was admitted for a recurrence of pancreatic pseudocysts. Not good — super painful and in this case, super dangerous. See, one of the functions is to produce juices that are squirted into the intestines to continue the break down of what once was food. It is caustic. This sack of caustic fluid was pushing up against the diaphragm, and as a reminder, the diaphragm is a thin layer of muscle that separates the abdominal cavity from the pleural cavity — where our lungs live. Having that flesh eating juice spill into the pleural cavity is not ideal and potentially incompatible with life. We transferred him out.

Other shenanigans the pancreas is involved with include insulin production. Insulin is a key. The locks, so to speak are on just about every cell in the human body. This analogy holds up very well and we’ll continue with this premise. In actuality the “lock” is a microscopic receptor protruding from a cell’s surface and the “key” is a folded up protein that is chemically attracted to the receptor. When we eat, signals are sent to the pancreas with instructions for insulin to be squirted into the blood. A small caveat is that carbohydrate concentration with the food will further direct the level of insulin squirting.

Type II diabetes is, at least at first, not a problem with the insulin factory, it is a problem with the locks. We have plenty of keys, it’s just that the locks aren’t interested in working properly. This is called insulin resistance and is a component of metabolic syndrome which are all just lay overs on the way to full blown diabetes. When this happens, the level of sugar in the blood remains high.

And here we move into the second analogy and it’s where the action is. High levels of sugar in the blood functions as an acid — now for those who are versed in the chemical sciences, it is not as simple as a low pH and hydrogen ions destroying the tissues but the end effect is close enough, and that is why this analogy works. What structures would you venture to guess are the first to be destroyed with this acid? That’s right — the smallest and most vulnerable stuff. In this case, because the acid is in the blood, very small blood vessels are obliterated first. Where does this usually show up first? That’s right — in the feet, kidneys and eyes. Once the tiny little blood vessels which feed the tiny little nerves are destroyed, the nerves die too. The rest of the flesh that depends on blood supply and innervation will also, with time, rot away.

In my fourth year of medical school I did a lot of away rotations, some in rural areas of Oregon and in hospitals in Portland that would accept transfers from rural areas. One guy came in, a well experienced alcoholic with diabetes that he had made no effort to control for at least a decade or two, perhaps longer. The morning of his admission he had dried up a little from a few week bender and went to take his socks off, to shower (which he had not done once during the bender) and one of his toes went with the sock. He showed us the sock, and the toe was still in there. He had not showered that morning either.

That is an extreme case but it speaks to the process. His toe died because, ultimately, the acid slow-burned through the all the structures, and it just rotted off.

This is happening all over the body. We focus on the feet, kidneys and eyeballs because it is where the symptoms first appear. Over time other structures will begin to be affected in so much that they will cause problems. Diabetic gastroparesis — a fancy word for — gut stop moving cuz’ I gots the sugar disease. Literally, the nerve signals that tell the intestines to milk the recently food and soon to be poop stuff are gone, because the nerves are gone.

Recent data shows 8.5% of the US population has type II diabetes. I did a double take of sorts, when I looked up some demographic information for this piece. It is because waaaaaaaaay more of my hospitalized patients have type II diabetes. Maybe a third. Granted I work in a hospital that primarily serves a certain population that has higher rates of DMTII but still — the number may vary, but diabetes is just an appetizer for the real problems. Toe, foot and then below-the-knee amputations. Hemodialysis for end-stage-renal-disease patients. Blindness. Inability to eat because of pain associated with a very, very slow moving GI tract. Heart attacks and strokes galore. All of this will happen if DMTII is not controlled. These are the highest correlated risk factors for getting the sugar disease:

Obesity

Positive Family History

Specific Racial and Ethnic Groups

Female

Conditions Associated with Insulin Resistance

Some truly can control with diet and exercise alone. Some, despite sincere best efforts are left with hyperglycemia, or, high blood sugar and depend on medications to prevent their toe rotting off into their sock.

Something that I picked up from an endocrinologist during medical school and that I still tell patients who struggle to control their blood sugar is that there is one situation where blood sugar can bypass the lock and key mechanism. When skeletal muscles are working like they do while walking, for instance, they will suck blood sugar from the blood into the muscle cells so they can burn the sugar for energy. So, after a meal it is significantly beneficial to go for a walk. My grandparents made it a habit to go for a walk after dinner and they weren’t thinking about insulin resistance and circumventing insulin receptors. It came naturally.