I sympathize with her. This woman lost her life to breast cancer and she saw it coming and she was pissed. I would be too. Like everyone else here (I imagine), my life has been shaped by the cancers of those close to me, and I dread it as much as anyone. But her “hopping mad” comment implies an understanding which I think is faulty to the core, and I feel compelled to set the thing right, because getting mad is not going to solve the problem. Nor will throwing more money at cancer research (though I doubt that would hurt).

Back when I taught residents and med students, I used to give a talk about cancer that had one purpose only: to impress upon my audience the hugeness of the problem. I’d like to see if I can do the same thing here, in relatively few words, with what I assume is a medically unsophisticated audience (for the most part). Here goes. Follow my logic . . .

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1. Cancer is uncontrolled growth: your own cells gone renegade, growing too fast and going places in the body they have no business going, ultimately compromising the function of nearby organs.

2. With respect to cancer, two types of genes regulate cell growth: tumor suppressor genes and oncogenes. Tumor suppressor genes help to down-regulate growth while oncogenes tend to promote uncontrolled growth. If a tumor suppressor gene is destroyed by mutation, the cell harboring that gene has one less check on its growth potential. Yes, the distinction between oncogenes and tumor suppressor genes is a bit artificial. Used to be very clear to me back in the 80s, but as time goes on, I find the dividing line to be less and less clear.

3. Cancers generally form as the end result of a multistep (multi-mutation) process. How a particular cancer behaves (whether this person’s cancer will respond to radiation or chemotherapy, for example) depends on that tumor’s mutation history. If we assign letters of the alphabet to particular oncogenes or tumor suppressor gene mutations, then a ZJVAST cancer might behave very differently than a ZJVASL cancer. Capisce?

4. And so we come to problem #1: there is no single disease “cancer.” Any organ you might name can play host to a range of cancers, some rotten, some evil incarnate. If I learned tomorrow that I had papillary carcinoma of the thyroid, I wouldn’t be happy about it, but I wouldn’t let the news devastate me. If I learned instead that the cancer were an anaplastic carcinoma of the thyroid, I would write my will. Quickly.

Breast cancer is not lung cancer is not brain cancer is not intestinal cancer. Each organ system has its various subtypes of cancers. Each subtype of cancer can be further broken down into whether a particular gene or genes is involved in the pathway leading to cancer.

To give one concrete example: squamous cell carcinoma of the oral cavity has a very different behavior if it is a smoking-related cancer rather than a papillomavirus-related cancer(the latter being the more treatable, and more survivable, of the two).

5. The same type of cancer — oh, let’s pick on another baddy, squamous cell carcinoma of the esophagus — may be very different from one patient to the next. The two cancers will likely have different mutation histories, but it’s worse than that: the two patients have different genomes, too. Host factors, that’s the term we use. And one should never underestimate the importance of host factors.

Thus problem #2: not only is there no single disease “cancer,” the same named cancer is very different from one patient to the next.

And it gets worse.

6. Problem #3: cancer cells are genetically unstable, usually as a result of the mutations which led to their development in the first place. In a population of cancer cells, not all of the cells are identical. They’re not little clones of one another. They are quite literally a population of diverse individuals. You will readily appreciate problem #4: this population evolves (changes) over time, due to this same instability.

What’s bad about a changing population? Try making the whole damn thing go extinct. It’s tough*.

So unlike Ms. Ziskin, I’m not hopping mad about the problem. Despairing is probably a better word to describe how I feel. I’m amazed we do as well as we do in treating cancer patients — and I give a lot of credit to those “host factors” that I mentioned above but gave little attention to (the immune system is only one small part of the story, FYI).

As of 2011, the vast bulk of cancer therapeutic research is aimed at developing and testing particular treatments for particular cancers. That’s the research that will have the fastest impact on today’s cancer patients. I would like to argue, though, that the better approach — or at least, an approach we neglect at our peril — would be to put more effort into basic research. Not just cancer research, or biological research. All basic research. Because who knows when some materials scientist or nanotechnologist might chance upon the Next Big Thing that lets us throw our current treatments out the window, because it’s just that good?

D.

*But hey, we humans are clever that way! We make populations go extinct all the time.

I don’t have much excuse aside from the usual one — it’s difficult to juggle work, family, and sanity with projects like this one. Rest assured I’m here, not often, but I am still here.  I have a great job here in Bakersfield and my commute is now a very reasonable 20-25 minutes.

Oy, maybe it’s like weight loss. I just need to do it.

D.

For starters: any questions? Post ‘em below and let’s see how fast I can answer them!

D.

Congestion and pain also accompany one another in a condition known as contact point neuralgia, sometimes also called Sluder neuralgia. Facial pain occurs when structures within the nose press against one another.  Structures that ordinarily do not touch may be brought into contact when the tissues swell from allergies, a cold, or a sinus infection.

Here is how I approach a patient in whom I suspect contact point neuralgia. I ask the patient to come see me when he is in pain. (In some cases, I have to squeeze someone into the schedule, but it’s worth it.) I then examine the patient’s nose with a fiberoptic scope. I do this BEFORE spraying a decongestant or topical anesthetic into the nose. Since I’m examining an unanesthetized nose, needless to say I have to be careful. I’m looking for one or more areas in which two structures touch — most commonly, the septum and one of the turbinates*.

Next, I place a cotton ball moistened with a decongestant spray (like Afrin) and an anesthetic (lidocaine) against the contact area. If the patient notes rapid relief of his pain, AND if reexamination of the nose with the fiberoptic scope reveals that the “contact points” are no longer in contact, this is fairly convincing evidence that the patient’s pain is contact point pain.

Another good maneuver is to place a saline-moistened cotton against the contact area. This should be done before the lidocaine/afrin application, as a control to see if the patient receives benefit from just any intervention. Saline won’t decongest or numb the nose, so it shouldn’t have an effect on the patient’s pain. If saline helps, then the afrin/lidocaine results will be suspect.

Treatment of contact neuralgia can be medical or surgical. Medications which reduce swelling in the nose can bring these areas out of contact. If this doesn’t work, usually there are good surgical options for accomplishing the same thing on a more permanent basis. These operations are known as turbinatoplasty (to change the shape of the turbinates) and septoplasty (to change the shape of the septum) . . . great topics for another day.

D.

*The septum is the cartilaginous/bony partition between the two nasal cavities. The turbinates are shelves of bone, covered with mucosa, which jut out from the lateral walls of the nose. The turbinates warm, humidify and filter the air that we breathe.

In my opinion, this doc is far too liberal with his application of silver nitrate. Towards the end of the video, you’ll note that the grayness (evidence of silver nitrate burn) is nearly circumferential. Sometimes this is unavoidable, but I try my best NOT to do this, because it can lead to troublesome scarring.

Many bleeding sites are capillaries which do not rise above the surface of the mucosa. In contrast, these little volcanoes are often more troublesome. In my experience, they laugh at silver nitrate. I prefer bipolar electrical cautery for such vessels. This is more painful than silver nitrate, but it also results in a far smaller area of injured tissue. Silver nitrate-treated noses sometimes stay irritated longer than bipolar-treated noses. More to the point, bipolar cautery is more successful for treating these larger vessels.

The first time I treat a patient with epistaxis, the usual question is, “Will this stop me from bleeding again?”  I ask the patient to imagine a pyramid. Most patients will get better after one or two treatments — think of the size of the base of the pyramid. A few patients will have to return for several treatments (we’re a little higher up in the pyramid, and the volume is smaller), while some will need still more aggressive interventions. A very few (the apex of the pyramid) will need surgical or angiographic intervention.

Yes, probably not the clearest metaphor, but folks seem to understand. It helps me to convey that the goal is to begin with low-risk, mild interventions (like silver nitrate or bipolar cautery) and reserve more aggressive methods for folks whose problems are sufficiently severe or stubborn to warrant such.

I will admit an ulterior motive to my pyramid discussion: I know that some of these folks will be back again and again no matter what I do. It’s the nature of the problem. I want them to know from the start that there’s a chance they could be in the apex of the pyramid. Otherwise, come the third or fourth office visit, they might think I’m some yutz who doesn’t know his nostril from a hole in the ground

D.

A: Yes, this is something to worry about. One out of ten nosebleeds occur far back in the nasal cavity — “posterior nosebleeds” or “posterior epistaxis.” These nosebleeds typically occur in older people and are often more severe than the more common anterior nosebleeds. Posterior bleeds are usually found in people with high blood pressure and atherosclerosis (hardening of the arteries). Older people are often on blood thinners such as aspirin, Coumadin, or Plavix, which can contribute to the sometimes catastrophic blood loss.

Without medical treatment, posterior nosebleeds are far more difficult to treat at home than anterior nosebleeds. You can’t just pinch your nose — you have to depend on your natural clotting mechanisms to do the job.  Blood loss can, at times, be severe and even life-threatening. Your father-in-law’s bout of dizziness and lightheadedness suggests that his blood loss may have been severe.

Less commonly, posterior nosebleeds can be symptoms of other life-threatening problems, such as tumors or arteriovenous malformations. Without a specialist’s examination, these illnesses could go undetected.

ENTs have a range of options for dealing with posterior epistaxis. A variety of packs can put pressure on the bleeding site, enabling the body to clot off the relevant blood vessel. The bleeding site can also be located and treated endoscopically. Less commonly, surgery is needed to tie off larger vessels leading into the bleeding site; in some circumstances, a specialist known as an interventional radiologist is needed to stop the bleeding via a procedure known as angiographic embolization.

For the reasons described above, I urge you to do whatever it takes to get your father to see a doctor, preferably an ENT.

D.

A: Polyps are weird creatures, really. They are almost always related to chronic inflammation — sometimes from allergies, sometimes from chronic sinusitis. Since corticosteroids like prednisone are potent anti-inflammatory agents, it makes some sense to  treat with steroids. By themselves, nasal steroid sprays rarely shrink polyps, which is why some doctors resort to oral steroids.
Is surgery better or worse than taking oral steroids? With both treatments, there is a high probability of recurrence IF the underlying problem (allergy or chronic sinusitis) is not addressed. I’m usually a very conservative guy, but this is one instance where I think surgical treatment may be safer than medical treatment, at least in some instances. If a patient’s polyps stay away for a long time after a course of steroids, fine. But if he requires steroids several times a year, we have to consider the risks of oral steroids.

Although a short course of oral steroids is relatively safe, the key word is “relatively.” A short course of steroids is safe relative to being on steroids for a long time. There is an incredibly long list of potential complications due to steroid use, and we’ll get to that in a moment.

Please note: these are not the “bulk you up” steroids that you hear about in the press. In medicine, we differentiate between “anabolic steroids,” which are the drugs that athletes abuse to add muscle bulk, and “catabolic steroids” — more commonly called corticosteroids — which are anti-inflammatory drugs. Both drug classes carry considerable risks.
Don’t get me wrong, corticosteroids can be life-saving for many medical problems. But your polyps, no matter how uncomfortable they may make you feel, are not going to kill you. Given that fact, you should weigh the risks of therapy carefully.
Steroids often cause side effects such as water weight gain, increased appetite, insomnia, mania, or depression. They can also cause serious problems with virtually every organ system in the body. Brain: temporary psychosis. Eyes: cataracts and glaucoma. Stomach: ulcers. Diabetes in individuals who are “borderline diabetic,” and out-of-control diabetes in diabetics. Bone: osteoporosis, and also a really nasty problem called “aseptic necrosis of the femoral head” (the ball joint of the hip dies and must be surgically replaced with an artificial joint).  And this is a partial list.
The more serious side effects occur primarily with long term use, but have been known to occur with short term use also. I know of one case of bilateral aseptic necrosis of the femoral heads following a two-week course of prednisone, which was prescribed for nasal polyposis.
The main risks of surgery are: risks from anesthesia, bleeding, and the chance that the polyps will recur. Depending upon how aggressive your doctor wishes to treat the polyps (i.e., does he want to clean out your sinuses as well) there are also risks to your eyes and brain, since these are in the neighborhood, after all. Fortunately, such serious complications are rare. Talk to your doctor in detail about the risks of surgery if you decide to take this option.
Mind you, this is a controversial topic, and many excellent ear, nose, and throat docs treat polyps with steroids and reserve surgery only for people who do not respond to steroids. The usual argument is, “If I can buy the patient 6 to 12 months of relief from their polyps, it is worth the risks of steroids.” So my answer to your question is, ultimately, wishy-washy. Talk to your doctor about the two options. Both treatments are considered acceptable, so you will have to do what seems right to you.
One last comment. If you have polyps on only one side, this is a whole different ball game. In this case, we worry about whether the patient has a cancer that merely looks like a polyp. We also worry about whether the patient has something called “inverting papilloma.” This polyp-like tumor can spread aggressively. Although it is not a cancer, a small percentage of these tumors can become cancerous. The only way to know if a polyp is an inverting papilloma or cancer is to biopsy it! In each case, the tumor must be aggressively removed to prevent recurrence.
Best treatment for a blocked Eustachian tube: figure out why it’s blocked and fix that problem. Basically the same way we (try to) get rid of polyps: deal with the underlying problem. Bacterial rhinitis, chronic sinusitis, and allergy are all possible explanations. If all else fails, your ENT can, under local anesthesia, cut a small hole in your ear drum — really not a bad operation.

D.

A: If your ear feels blocked and you are noticing a hearing loss, here are the possible explanations (please note, you may have more than one of these problems):

• Wax impaction (or other foreign body… such as wax from an ear candle)
• Infection of the ear canal skin (“swimmer’s ear”… but usually, you would also have a lot of pain with swimmer’s ear)
• Inflammation of the ear drum
• Middle ear infection and/or middle ear fluid
• Eustachian tube dysfunction
• Occasionally, a large perforation of the ear drum could give both a hearing loss and (paradoxically) a blocked sensation
• Finally, a low frequency hearing loss can cause a plugged feeling

Unfortunately, the only way to diagnose your problem is for someone with intelligent eyes to LOOK, so you may have to wait until your July appointment for an answer. Can you see a regular doctor sooner? At the very least, I would try to keep water out of the troubled ear until someone gets a chance to examine it. Put a cotton-and-vaseline ear plug (rub the vaseline into the cotton ball) into your ear when you bathe.
(Note: I strongly discourage the use of ear candles. They are unsafe and ineffective. In this case, used in an individual with a perforated eardrum, candles could result in severe pain, infection, and irreversible hearing loss.)

However, every few months or so, dizziness will just come on suddenly. It is not a ‘spinning around’ dizziness but more like I am standing still and the floor is going up and down (sort of a ‘vertical’ type of motion although I am perfectly still). Walking up or down stairs poses somewhat of a problem during this time. Most recently I felt this way at night. When I woke up the next morning, even before opening my eyes, I knew I was going to feel the dizziness which I did. I simply opened my eyes (my head still lying flat on the pillow) and I was dizzy. It will go away after about 10 minutes but then reappear during the day a few times. This will last for about 3 or 4 days and then will disappear completely for the next few months. I spoke to my G.P. about this who has only said, “There is nothing I can do. There is no blood test for this.” I had mentioned this to him a few times!

From what I can recall, I feel somewhat fatigued when these spells occur. And, perhaps I am eating more carbohydrates than usual, but I don’t really think that such would affect this. My eating habits do not change too radically from one day to the next….

I would love to know if there is a certain food group that I should be avoiding (i.e. carbos, more protein, etc.) or what in fact is really going on! This does concern me. I haven’t been happy with my doctor’s response to this.

A: Regarding your question, first of all, I would like to take this opportunity to respond to your GP’s comment, “There is nothing I can do. There is no blood test for this.”

PHBBBBBT!

He can refer you to an ENT, if nothing else! Jeez, that is the lamest comment I have heard in a long while.

The character of your dizziness is reminiscent of a symptom called “oscillopsia.” (Aw-sill-ops-ee-uh.) Typically, people with oscillopsia notice that their visual field pops up and down as they walk or climb stairs. But does this up-and-down sensation happen even when you are lying still? If so, then it is not oscillopsia.

I do not know of any dietary links to dizziness, except perhaps hypoglycemia (low blood sugar). Most of the time, people who say they are hypoglycemic are experience lightheadedness, not the bouncing sensation that you describe.

If your thyroid hormone levels have been checked and are within the normal range, then there is probably no link between your hypothyroidism and your dizziness.

That’s about all that’s worth saving from a ten-year-old letter. Now that it’s 2009, I would add the following . . .

I don’t often feel the need for vestibular testing, but this person would have benefited from such tests. And so I stand by my insistence on an ENT referral. I find her symptoms as puzzling now as I did then. Most of the things that cause her symptoms would not tend to be episodic. I’m thinking of aminoglycoside toxicity or superior canal dehiscence syndrome. But what about the episodic syndromes: could Meniere’s disease do this? (I doubt it.) Benign paroxysmal positional vertigo? (Maybe, but it’s a stretch.) Vestibular migraine? (Hmm . . . now we’re talking.)

Point is, it’s hard to do much more than generate a differential diagnosis when a letter-writer provides you the barest snapshot of her symptoms. That’s why most of the time I’m preaching “get thee to an ENT,” because there really is no substitute for a good history and physical examination.

I still think her PCP is a ditz.

D.