Skip to content

Gallbladder Pain, But No Gallbladder…

A few months ago I started having episodes of intense abdominal pain, often accompanied by nausea, that were reminiscent of the gallbladder attacks I had last year. The only problem is, obviously, I had my gallbladder removed. So it shouldn’t be hurting…

It Feels Like a Bad Gallbladder, But Doesn’t Act Like It.

This pain was a little bit different than with my gb. There were no consistent food triggers I could find. Sometimes any food would cause pain, sometimes lack of food would cause pain. This is in contrast to gallbladder attacks being fairly predictably caused by food, especially fats.

Like gallbladder attack pain, this pain almost always started in my upper right abdomen, under my rib cage, but would spread towards the middle and to the left. And I swear it felt almost exactly like the intense, stabbing, bursting/pressure type pain I would get from my lousy gallbladder. It was seriously so weird.

By April I was waking up every night with pain that would keep me up for at least 30 minutes, often a lot longer. During the day my stomach seemed to disagree with everything and I was taking Zofran just about every day to manage the nausea.

I even ended up in the ER for an episode of pain and nausea the evening before my finals started (around the same time of year I went to the ER last year for gb stuff, though I didn’t know it was that at the time). The folks at the ER were also confused, because my pain sounded just like gallbladder pain, but… no gallbladder…

Hmmm, Ulcers Maybe?

867FF43D-D3F6-4849-8020-98D406B7BD07.gifWell I got in to see my GI shortly after finishing my finals. I experienced some serious dejavu–one year later, same time of year, same office, same GI, same symptoms. She even said basically the same thing as she had one year before: she suspected ulcers. So she wanted me to try acid suppression medication to see if it helped and we would also schedule an ultrasound of my biliary system.

The thing is last year I tried the acid suppression medication and it didn’t help. In fact it made me feel lousy. And then we found out she was wrong and it was my gallbladder. So I was not surprised, but not thrilled when she said the same thing again.

This time though, the trial ulcer meds really helped. The first day I was on them I slept through the night, without being awoken by pain, for the first time in weeks and weeks.

So we’re doing a month worth of treatment with Prilosec in the morning and Zantac at night and then we’ll see where we’re at. If my symptoms return I’ll probably need to have an upper endoscopy to actually see what’s in there and test to see if I’m infected with H. Pylori–one of the most common causes of peptic ulcers.

No NSAIDs For Me. Good Thing Tylenol’s So Effective…

In the meantime I’ve been instructed to stay away from all NSAIDs. My frequent use of NSAIDs for migraines is one of the things that has caused her to suspect ulcers (twice). Certainly they could be a problem. But staying off them is no easy thing. Even though my migraines are doing better with a preventative regimen of Prozac and Verapamil, and especially since I started Concerta for my ADHD, my head still hurts a lot. And Tylenol is not super helpful. But so far I’ve been able to manage. Thank goodness it’s summer.

What is Primary Immunodeficiency?

April was Primary Immunodeficiency Awareness Month, but I was so overwhelmed with crazy end-of-semester stuff and crazy body stuff that I totally goofed—I didn’t write a single PI awareness post on my blog about PIBut better late than never right? So let’s talk about it. What is a primary immunodeficiency and what is it not?

What PI is:

  • A hereditary/genetic defect in the immune system.
  • A defect occurring in one or more components of the immune system.
  • A blanket term to describe more than 350 rare, chronic disorders in which part of the immune system is missing or functioning improperly.
  • Lifelong.
  • Treatable, but not curable.


Basically a primary immunodeficiency is a problem with your immune system that you’re born with (although they can develop later in life and often aren’t diagnosed for many years either way).


What PI is not:

  • Contagious.
  • An autoimmune disorder.
  • Just a “bad” immune system.
  • Visible.
  • A defect in the immune system caused by something else—like AIDS or chemotherapy (it’s not “acquired”).

So when someone tells you they have PI don’t get all weird about it. They’re not contagious. Most likely, they’re not dying. Just be cool.


What having PI means:

  • Increased susceptibility to contagious illnesses.
  • Increased susceptibility to infection.
  • Infections that are recurring, chronic, difficult to clear up, severe, or caused by unusual organisms.
  • You don’t build immunity from a previous infection (whether viral or bacterial).
  • You’re a medical zebra—PI is rare, so it’s a “zebra” condition instead of a more common “horse” condition.

Let me explain—no there’s too much. Let me sum up. Having a primary immunodeficiency means you get sick a lot, because your immune system doesn’t work like it should. Since it’s a genetic/hereditary disorder, having PI usually means it either runs in your family, or you’re really lucky and your genes mutated…

To better understand PI it’s important to understand how the immune system is supposed to work

How it Works – The Immune System

There’s two basic parts to the immune system: the innate immune system and the adaptive immune system.


The Innate immune system starts, like all of the cells that make up the immune system, in the bone marrow with a stem cell.  The several types of cells that make up the innate immune response (neutrophils, monocytes, natural killer (NK) cells, complement proteins) are ready to go straight to work once formed. They require no additional training to do their jobs.

In most cases of PI the innate immune response is a-okay. The problem occurs in the adaptive immune response.


The Adaptive immune system also starts in the bone marrow. There they become either  B-cells or T-cells, the two major parts of the adaptive immune sytem. Then they are split up. T-cells go to the Thymus to finish developing and get trained for their jobs as Killer T-cells, Helper T-cells, or Regulatory T-cells—which all basically deal with the body’s adaptive response to foreign substances (ie viruses) and make sure they don’t attack the body’s own tissues (as in autoimmune conditions).

B-cells stay behind and get edumacated in the bone marrow. They mature into Plasma cells, which in turn can mature further into Memory B-cells. Plasma cells are responsible for producing antibodies, which are highly specialized proteins that fit “invaders” like a key in a lock. Memory B-cells remember the invaders that you’ve encountered before so a rapid response can be mounted if you encounter it again.

In a lot of primary immunodeficiencies the main problem is with the B-cells. They don’t mature like they’re supposed to. They don’t pay attention in bone marrow class or just skip it all together. So they don’t make antibodies like they should and they definitely don’t remember past infections. It’s like your adaptive immune army is made up of a bunch of cats—they just do whatever the heck they want, which is usually nothing. So bacteria and viruses waltz in again and again, and even if they’ve gotten in before your cells are perpetually unprepared.

Basically your B-cells look like this:



So you can see why they might not be super effective…