Inflammatory Bowel Disease (Memel, 8/19/26)

A recording of this presentation is available HERE.

Thanks to Dr. Memel for a super packed fact-filled presentation on Inflammatory Bowel Disease (mostly focused this time on ulcerative colitis  with an important preamble on nutrition). Thankfully, she is coming back to do Part 1 in December, because we were all on the edge of seats and we didn't get through the whole slide deck and we want to learn more about Crohn's Disease!

My take homes:

• Ultra-processed foods (containing additives like dyes, emulsifiers, and excess salt) are bad for our gut. In particular, emulsifiers are to be avoided!
• The Mediterranean Diet is the best for patients with IBD and everything else)
• FIBER is actually good for patients IBD (contrary to old thinking), just need to modify the texture as needed for tolerance
• Fecal calprotectin is an excellent screening test for IBD and can be used to trend over time to monitor treatment response
• 5ASA is mainstay of UC treatment (lifelong), budesonide can be added on for flares (less systemic effects than prednisone)

IBD is an idiopathic autoimmune disease with objective inflammatory evidence>> chronic inflammation is key, and it tends to progress in severity

IBD incidence is rapidly increasing worldwide (in both developing and developed countries). Older adults getting more and more IBD>> keep on ddx

Genetic susceptibility (163 genetic loci identified, very genetically inherited) is an important factor. Crohn's has higher genetic risk than UC. Higher risk of passing to first degree relatives.

Environmental triggers causing patients to express the phenotype. Immune system is "over reacting>> changes in gut microbiome>> expression of IBD. Ultra-processed foods, sugar (highest risk factor for developing IBD). Chemicals that allow foods to be shelf stable are the most problematic part of ultra-processed foods. Excess salt causes inflammation in GI tract. Artificial sweeteners disrupt the microbiome. Once bacteria get past the mucosa>> inflammatory cascade!

Emulsifiers (that allow oil and water to mix) are used widely in the food industry (ice cream, peanut butter) are TERRIBLE for the GI tract. Disrupt a mucous layer causing an inflammatory environment. Try to avoid emulsifiers as much as possible, read labels and look to eat things with LESS chemicals in the food label.

What you can do?

• Breastfeeding is protective and beneficial to the  microbiome.
• Pets in the home under 2 benefits children's microbiome (hygiene hypothesis)
• Mediterranean diet (2023 practice update) is the best diet for people with IBD, first degree relatives less likely to develop IBD
• People who eat more fruits/veggies/whole grains have less inflammation in their gut
• Fiber is GOOD for the gut (unless they have a stricture/penetrating disease). All the data suggests them more fiber, less likely they are to flair. Not all fiber is the same. Can cook fruits/veggies and make them softer. Texture can help them be better tolerated (smoothies, cooked veggies)
• Red meat is bad for the colon-- Crohn's and UC, specifically processed red meats (salami, prosciutto)
• Dr. Memel says she always starts with breakfast: oatmeal, fruit smoothies (frozen fruit is cheaper, blended is tolerable), chia seeds can be integrated into everything (and cheap at TJs)

Dieticians for IBD:

Crohn's vs. UC

Labs to evaluate a patient with IBD:

• CRP helpful to track inflammation
• albumin used to assess severity of inflammation in IBD (albumin can inform the dose of infliximab)
• enteric pathogen panel important because infection can provoke IBD flare

Fecal calprotectin: protein released by neutrophils. Most helpful in someone with chronic diarrhea and trying to determine if this is inflammatory or not. If normal fecal calprotectin, much likely NOT IBD. Borderline levels can be tricky, trending in 4-6 weeks can be helpful. Very high needs colonoscopy. Used in IBD to trend over time and track in place of colonoscopy.

Mayo endoscopy score, GI uses as standard objective assessment 

UC Treatment has two parts:

1-induction (put out the fire)

2-maintenance (prevent fire from coming back)

Stride 2 guidelines recommend three goals for treatment of patients with IBD:

1-Clinical remission (living life again)

2-Endoscopic remission (no disease evident on colonoscopy)

3-Complete histologic healing (no inflammation on biopsy)

Treatment protocols are driven by risk to progression to colectomy. Low risk involves mild disease with limited anatomic extent. High risk include younger (<40), extensive colitis, severe disease (Mayo 3), elevated CRP, low albumin (admit to hospital for IV steroids)

IF Mild UC>>5-ASA or budesonide

5ASA formulation and rx depends on where UC is anatomically

3 phenotypes: 

• Proctitis (5ASA suppositories are often good enough), if really struggling can do steroid suppositories as well, can do daily 5 ASA>> taper to qod> taper to q 3 days (for life, otherwise will flare)
• Left sided colitis (5 ASA enemas can reach further): oral + enema at the beginning, if they don't respond, can add budesonide (selective steroid), budesonide foam can be squirted up the rectum (not as far as an enema but easier to use). For maintenance, oral 5 ASA because patients hate doing enemas the rest of their life
• Pancolitis (need oral 5 ASA as well): can do oral budesonide + 5 ASA. Very rare risk of AIN (renal function should be checked once a year)

Budesonide used by GI a lot! Added on as a flare treatment Much LESS side effects than oral prednisone (safer, lower risks of systemic side effects). Not as strong as prednisone

Patients should be on lifelong therapy for UC (to prevent flares!!!)

IF Mod-Severe disease>> Tx is Biologics (see chart below)

There are MANY many biologics. Many more than just infliximab (the original anti-TNF). Patients google biologics and get very scared but the options are many and they are much safer than they used to be. See the triangle of safety down below. Dr Memel tells patients now, "The risk of developing colon cancer from recurrent flares is greater than the risk of being on today's biologics".

Decisions about which agent the gastroenterologist will choose are complex, including insurance/comorbidities/physical needs/travel needs, etc. . .

There is still emerging data on how long patients need to be on biologics. . .Dr. Memel tells people that biologics are "life long therapy" due to the risk of relapse/flare. 

Treatment of acute UC flares

-always order stool cultures, including CDiff (infection is risk for flare)

-always order CRP (GI trends daily)

-trend bowel movements (by nursing)

-DVT ppx is important even if bloody bowel movements due to 3-5x increased risk of VTE (flares are inflammatory)

-40-60mg IV methylprednisone in AM (to reduce insomnia)

-check PPD/quant gold  and Hep B serologies on admission (because they take a long time to come back)

-Try to avoid opioids and NSAIDs due to risk of toxic megacolon

Kratom and 7OH (Dembar & Rubin, 8/12/26)

A recording of this presentation is available HERE.

Thanks so much to our Addiction Medicine Fellows, Drs. Allie Dembar and Rebecca Rubin for a super super important presentation on Kratom and 7OH, two opioid like substances with high dependence risk and rising rates, despite a 2026 California ban on sale of such products.

Please watch their presentation if you don't know what 7OH is and/or if you work in primary care, emergency rooms, with children, etc. . .

Here are my notes:

Kratom is a plant from Southeast Asia, formal name, mitragyna speciosa. The active ingredient, mitragynine, has a mild stimulant effect when the leaves are chewed (think coca leaves from S. America) as well as a mild opioid effect at higher concentrations. 

7OH is a synthetic version of mitragynine, which is much more potent (and only present in <2% of the plant substance). It appeared in the US market ~2024. Some studies suggest higher potency than morphine

Both have been available for sale across the US, mostly in gas stations and smoke shops and until recently were not regulated. In 2026, Governor Newsom announced a ban in California of their sale (though they can still be found in local smoke shops per reliable reports). 

The increase in Kratom/7OH availability has led to an increase in kratom toxicities. By 1200%!

Men>> Women

Age group most affected is 20-39 year olds, followed closely by 40-59 year olds

There have been 233 Kratom-associated deaths between 2015 and 2025, 79% included multiple substances, and opioids are often co-reported

There are advocacy groups pushing for liberation of Kratom/7OH across the country, most of whom are being led by  chronic pain patients who feel abandoned by the medical system and looking for an answer to treatment for their chronic pain (in light of opioid prescription reduction over the last decade+). Kratom and 7OH are largely unregulated. This map below is produced by a pro-Kratom advocacy group. Notice the variance across traditionally aligned red and blue states and even the discrepancy up and down the Pacific coast.

The political landscape is evolving quickly

On July 1, 2026, the DEA "moved temporarily schedule 7OH and related substances to protect public safety". This federal action was aimed at synthetic 7OH (not directly at the plant based Kratom). A Schedule 1 label means that the drug has a high potential for abuse with no accepted medical use. 

Note that 7OH intoxication and withdrawal closely mirror that of opioid intoxication and withdrawal. 7OH is a potent mu opioid receptor full agonist. Small amounts can lead to euphoria>> larger amounts to respiratory depression. 

Withdrawal is functionally similar to opioid withdrawal. Half life is 1-5 hours (patients usually start withdrawing within 2 hours of stopping-- use habits require frequent use during the day, up to 6 times per day). You can increase the half life with chronic use up to abou 24 hours.

Treatment of Kratom withdrawal is buprenorphine, buprenorphine, buprenorophine. . .

Unlike with fentanyl, you will not precipitate withdrawal and you do not need to micro-dose, but can go straight to micro-dose-- 16mg SL plus don't forget your adjunct (ondansetron, loperamide, gabapentinoids, hydroxyzine, and if inpatient, can consider benzos for anxiety/agitation). 

Of note, you can order a sendout lab checking for mitragynine in urine (but this will typically not show up as an opioid in our standard utox).

Functional Disorders, Somatic Symptoms and Chronic Pain (Jones, 8/5/2026)

 A recording of this presentation is available HERE

Thanks to Dr. Kendall Jones for a fantastic opener for R3/Senior Grand Rounds presentation this week. She borrowed from a lecture she attended last spring at the Family Medicine Colloquium by Kaiser Family Medicine teachers. . .but really brought it home to our patient population. 

If you are a primary care clinician caring for patients with functional disorders (think IBS, migraine, fibromyalgia. . .and all those unn-nameable conditions), you should watch this!

Functional Disorders

Medical school trains us well to investigate mechanical/structural abnormalities (e.g. SBO, carotid stenosis, hip fracture), assess for biochemical abnormalities (e.g. low hb, elevated a1c, hyperthyroidism), but does not prepare us for functional disorders-- which, by definition, have no specific tests. Functional disorders are diagnosed with symptom assessments, validated tools, in combination with negativing imaging/labs or other work-up. 

And yet, in primary care, we see a LARGE number of patients with functional disorders. Here are a few:

These patients are challenging. They bring up a lot in clinicians, and they don't always get the care they need. Sometimes they are left to steer their own ship (which doesn't reliably make them better), they get HUGE work ups (all of which turn out negative or equivocal), and they get labels that do not really apply, labels that are hard to remove. 

Dr. Jones reminded us that we use clinical judgement all the time to make diagnoses-- think a viral URI or a migraine. For these patients, we use illness scripts and confidence in our experience. This same notion applies to patients with functional disorders.

Central Sensitization

Central sensitization is a state of persistent CNS hyper excitability in which the brain and spinal cord amplify incoming signals beyond their objective magnitude. The "volume of the nervous system" is literally turned up. This is not psychological. It is driven by neuroinflammation, HPA axis dysregulation, synaptic plasticity in the dorsal horn, reduced descending inhibition, and more. This phenomenon is propagated via ACEs, chronic stress, trauma, perception, expectation, and neuroplasticity. 

I LOVE this fire alarm analogy!

Reminder: our job is NOT to keep searching for a fire.

We need to be able to recognize patterns of central sensitization:

• multi-system symptoms with no unifying biomedical lesion (though don't forget connective tissue and EDS)
• severity out of proportion to objective findings-- the gap is the signal amplification
• symptoms fluctuate with stress, sleep
• prior extensive negative work up but patient remains symptomatic
• presence of ACEs or chronic stress (which patient may not have insight into)
• hypervigilance: symptom tracking, googling, frequent visits, lots of messages
• sensory hypersensitivity: light, sound, temperature, touch, odors (more than just pain)

Language matters

When tests come back negative, avoid "everything is fine", "your tests are normal", "nothing is wrong", "maybe you're stressed". These statements do not explain what IS happening for the patient and leave them searching for another explanation. 

Communication is key!

Remember patients can have central sensitization AND something else!!!

Validated Tools for assessing for Central Sensitization include:

• Somatic Symptom Scale - 8. Gierk B et al. JAMA Intern Med. 2014.

• Eight items rated 0-4 over the past 7 days (GI, back pain, limb/joint pain, HA, CP/SOB, dizziness, fatigue, sleep)

• 8-11 = medium, 12-15 = high, 16-32 = very high.

• Each category increase is associated with 53% more healthcare visits

• CSI: Central Sensitization Inventory. Mayer TG et al. Pain Pract. 2012; Neblett R et al. J Pain. 2013

• Part A: 25 items, scored 0-100 

• Part B: Prior CSS diagnoses (unscored, clinical context)

• Cutoff ≥ 40: 81% sensitivity, 75% specificity for CS syndromes

• <30 = subclinical, 30-39 = mild, 40-49 = moderate, 50-59 = severe

Treatment of Central sensitization:

Education: normalize, reframe: "Your symptoms make sense to me. Let's try to understand what is going on." Discuss the context/ask the question: "What do you think is making your nervous system so sensitive?" Help change their relationship with their symptoms-- to decrease their fear. Remember, having somatic symptoms is part of living inside a body.

Nervous system retraining: mindfulness based pain reduction, breathing exercises, cold exposure (resets the mamalian dive reflex), singing, humming, yoga, meditation, massage (feet and neck)

Central sensitization and Chronic pain

• nociplastic pain happens over months to year; it can be at least partially reversed with desensitization of the oversensitized alarm
• patients have to be patient (months to years) to notice improvement
• patients and physicians benefit from moving away from "symptoms" into acceptance, understanding an rehabilitation>> goal is improving quality of life and increasing function
• movement is key: motion is lotion

Primary care needs united partnership with specialists.

We don't need to get it all done in one visit, even 2 minutes can help shift mindsets

We are not just asking patients to relax, we are helping them re-calibrate their nervous system.

Central sensitization does not invalidate the patient's experience, it only offers an explanation with evidence-based interventions.

Clinicians must NOT miss red flags

References:

Mohabbat AB & Wilkinson J (2023). Central sensitization: when it is not all in your head. Am Fam Physician. 101 (1):92-96

G. Lorimer Moseley & D Butler (2017). Explain pain supercharged: the clinician’s manual. 

tamethebeast.org (refer patients with chronic pain to this website)

Van Oosterwick J et al. (2013). Pain physiology education improves health status in fibromyalgia. Clin J Pain. 29(10):873-82.

Difficult (aka Dysregulated) Patient Encounters (Pimental, 7/29/26)

 A recording of this presentation is available HERE

***

Thanks to Dr. Britni Pimental, who gave us a fantastic presentation on Difficult Patient Encounters. She started by changing our word choice from "difficult" to "dysregulated".  When we label patients as difficult (angry, demanding, emotionally intense), we should be really calling them dysregulated-- shifting this label can help us shift in how we see patients. 

There were SO many pearls in this presentation, I definitely recommend listening to it yourself. But for the notes version:

It's not surprising that patients being seen in the clinic or hospital are dysregulated-- their nervous system is literally being stressed-- they are scared, in pain, feeling a loss of control, triggering old trauma and sensing systemic pressures.

When people get overwhelmed, their executive function goes down. They cannot listen. They cannot process high level medical information.

Clinician response to dysregulation can lead to to an unfortunate feedback loop:

Trigger>>>> Arousal>>>> Behavior>>>>Clinician Response>>>Trigger 

We are not neutral. We are human beings too.

Countertransference is the phenomenon in which our own emotional reaction to the patient is shaped by our own previous experiences. This can lead to helplessness, frustration, avoidance, over compensation, and assertion of control. 

We must strike a balance between empathy and limits/boundaries. Empathy does not require agreement. Most people do better with limits and effective boundary setting helps people who are dysregulated. Rather than being exclusive, empathy and boundaries are complementary.

3 steps to empathic boundary setting:

1. Validate the emotion
2. Set clear limits (without excessive justification-- see above, people's ability to tolerate info is low)
3. Offer alternatives (a small # of choices) to give control back

Restore regulation

Our tone, posture, body language and pacing will impact our patients' behaviors.  Clinician regulation is the most powerful de-escalation tool. Patients are highly attuned to non-verbal cues from clinicians (pacing, tone, body language)

The goal of de-escalation is NOT to win the argument or to convince the patient of a particular viewpoint. The goal is to maintain a functional relationship, create a safe and collaborative environment. 

Self-regulation for clinicians

-lower tone

-slow speech

-adapt a non-threatening posture

-sit down (if safe)

NURSE

Name

Understand

Respect

Support

Explore (options)

Offer choices as much as possible. Patients want to feel they have some say in their care.

Allow for pauses>> to avoid rushed decision-making. People need wiggle room. 

Ask open ended questions

Practice reflective listening

Avoid escalation

-avoid interrupting

-avoid power struggles

-avoid defensive responses

-avoid arguing the facts

A simple self-check re. countertransference:

What am I feeling right now?

What is this patient activating in me?

How is this helping/hurting their car?

Re-engage with your own executive function

-pause

-slow breathing

-relax your shoulders

-consciously slow your speech

-decrease your own physical arousal

RESPOND INTENTIONALLY RATHER THAN REACTIVELY 

The clinician-patient alliance builds trust, creates psychological safety and decreases emotional arousal. Regulation+ relationship + respect= safer encounter