⚕️September IM and Hospitalist Recap!⚕️

Hepatitis C: Are We There Yet? (UCSF Grand Rounds)

Such a fascinating history - we've come a long way, and yet there is so much to be done!

My favorite lessons below.

https://www.youtube.com/watch?v=XrJdMxTmQOw

In the 1970’s hepatitis C was just known as “non-A, non-B” hepatitis.

In 1989, the Hepatitis C virus was identified via molecular cloning.

This meant it could be screened for in the blood supply - this essentially eliminated post-transfusion hepatitis in the U.S by the early 1990’s.

In the late 1980’s, interferon monotherapy was standard of care and it was grueling for patients.

By 2011, standard management was a year long course of pegylated interferon and ribavirin - this course has debilitating side effects and only 50% chance of cure. Many patients were never even treated.

In 2013, sobosbuvir, a direct-acting antiviral (DAA) was approved. These oral medications were well tolerated and achieved cure rates in 95% of cases.

DAA medications prevent cirrhosis, cancer, and improve all-case mortality.

Treatments are now pan-genotypic, all oral regimens like Mayvret (8 weeks), or Epclusa (12 weeks).

While we have a cure, we are far from elimination. Rates of new infections are actually increasing due to the opioid epidemic. 2.4-4 million people in the US are estimated to be living with HepC. Only 1 in 3 of those diagnosed have actually been cured.

Those with HepC are those least likely to engage meaningfully with the outpatient healthcare system and include those who are homeless, incarcerated, or who use injection drugs. 

New models bring care to these patients rather than expecting them to come to the clinic. Examples including treating patients at opioid treatment programs.

FDA recently approved a point-of-care hepatitis C RNA finger-stick test that gets results within an hour.

Future treatments may include long-acting injectables to bypass issues of adherence and follow up. True elimination will likely require a vaccine.

Goal is to find it, confirm active viremia, stage liver disease, treat with pan-genotypic direct-acting antiviral (DAA), and keep people from getting reinfected

If you consistently reflex-confirm viremia, stage fibrosis noninvasively, pick a pan-genotypic DAA with interactions in mind, and ensure SVR12 (sustained virologic response at 12 weeks) documentation plus cirrhosis-appropriate surveillance, you’ll cure the vast majority of your patients and prevent most long-term complications.

Genotyping is no longer routinely required for treatment naive patient

For most treatment-naïve adults without decompensated cirrhosis, two regimens cover nearly everyone: 

glecaprevir/pibrentasvir for eight weeks (extend to 12 weeks in compensated cirrhosis)

sofosbuvir/velpatasvir for 12 weeks. 

Before treating, send baseline labs and check for interactions

When treatment is complete, check HCV RNA quant 12 weeks after the last dose to document sustained virologic response which means there is a cure

There is no post-exposure prophylaxis for HCV

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Orthostatic Hypotension (CORE IM)

⚕️September IM and Hospitalist Recap!⚕️

All things HFpEF!

Glad this one got revisited! Opportunity to review the literature behind a new "GDMT" taking shape.

Check out the linked @thecurbsiders post, and then some of my top takeaways below.

https://x.com/thecurbsiders/status/1974136346345381897

Are you sure the symptoms are actually from HFpEF? 

Similar symptoms can arise from a wide array of diseases, such as cirrhosis, renal failure, nephrotic syndrome, or venous insufficiency.

Due to the stiff, non-compliant nature of the ventricle in HFpEF, small changes in volume can lead to large swings in filling pressures, making patients particularly sensitive to dietary sodium.

A normal BNP in an obese patient with compelling symptoms of volume overload shouldn't completely rule out HFpEF

Tools like the H2F-PEF score can be useful to estimate the probability of HFpEF.

Don't miss mimics including cardiac amyloidosis, which may be present in up to 15% of older adults hospitalized for HFpEF and now actually has treatments

Early mitral inflow velocity / mitral annular early diastolic velocity (E/e’) ratio is a surrogate for left ventricular (LV) filling pressure and can help to diagnose HFpEF

“E” is obtained with pulsed-wave doppler across the mitral valve and reflects trans mitral flow in early diastole

“e′” is measured with tissue doppler at the mitral annulus and reflects the rate of myocardial relaxation.

Because E rises with higher left atrial (LA) pressure while e′ falls with impaired relaxation, a higher E/e′ implies higher LV filling pressures, the hemodynamic signature of HFpEF.

An average E/e′ ≥ 14–15 at rest is generally considered abnormal and supports elevated LV filling pressure; an average ≤ 8 suggests normal pressure; and 9–14 is a gray zone that needs additional data.

The cornerstone of management of HFpEF involves addressing the comorbidities that are associated with it, including HTN, AFib, CKD, obesity, and sleep apnea.

I've started to see more HFpEF patients on "GDMT" medications

Sodium-glucose cotransporter-2 (SGLT2) inhibitors were the first drug class to meet primary endpoints in RCTs, reducing the composite of cardiovascular death and heart failure hospitalizations. (EMPEROR-Preserved Trial) 


Mineralocorticoid Receptor Antagonists (MRAs) like spironolactone hold a class 2b recommendation; TOPCAT trial was neutral but subgroup analyses of patients from the Americas showed a benefit in reducing hospitalizations; the Jury is still out though


Angiotensin Receptor-Neprilysin Inhibitors (ARNIs) - Entresto - also have a class 2b recommendation, having missed the primary endpoint in the PARAGON-HF trial. However, episode suggests it may be considered, particularly for patients with lower-range ejection fractions or persistent hypertension.


Lively debate over the last week! @AnilMakam 

I've seen more patients with HFpEF (or HFmrEF) on Entresto recently, so interesting to think through why.

https://x.com/AnilMakam/status/1981845086431486380

STEP-HFpEF trial demonstrated that Glucagon-like peptide-1 (GLP-1) receptor agonists significantly improve symptoms, physical function, and weight in patients with obesity-related HFpEF.

Safe to say these medicines (and losing weight, really) are going to be effective for most major cardiovascular and metabolic co-morbidities.

Check out the @pointofcaremed pages to learn more about ADHF and inpatient diuresis!

https://www.pointofcaremedicine.com/cardiology/adhf

https://www.pointofcaremedicine.com/blog-post/diuresis-201

Thread Source: 

https://thecurbsiders.com/curbsiders-podcast/460-heart-failure-with-preserved-ejection-fraction


⚕️September IM and Hospitalist Recap!⚕️

One Detail Completely Changed This Case (An Unexpected Outcome) - Conan Liu MD

@EGSuppy - really enjoyed this case!

My takeaways, and additional thoughts on approaching hypoalbuminemia below!

https://www.youtube.com/watch?v=KB_0BbKQAMQ&t=1s


Patient presented with chief complaint of swelling in the face and neck leading to difficulty swallowing and sleeping. Given this type of swelling is atypical and possibly life threatening, along with the assumption that it was an acute change, clinicians anchored on angioedema and didn’t immediately realize that the patient had more diffuse body swelling.

A miscommunication (language barrier) led to the team misunderstanding the time course and location of the patient’s swelling.

A re-framing of the illness script to anasarca led to realization the patient had low albumin and high lipids. This led to eventual diagnosis of proteinuria and minimal change disease

Highlights the importance of taking each piece of information on its own. Many patients have low albumin from malnutrition or chronic illness, but in a patient who doesn’t necessarily fit those typical phenotypes, should be thinking about proteinuria or protein-losing enteropathy.

Hypoalbuminemia can be broken into three buckets - decreased synthesis (cirrhosis, malnutrition), increased loss (nephrotic syndrome, protein-losing enteropathy, severe burns), and inflammation-mediated (sepsis, malignancy) where albumin acts as a negative acute-phase reactant.

The most common clinical sign of hypoalbuminemia is peripheral edema or anasarca due to loss of plasma oncotic pressure.

Giving IV albumin is only valuable in limited clinical settings - SBP, HRS, and large-volume paracentesis where the goal is to stabilize circulation. It is not an effective treatment for correcting a low serum albumin level, as it does not address the underlying cause - it will immediately be lost in the urine or stool like the albumin before it.

Though historically some have tried using albumin to augment diuresis in nephrotic patients, the effect is modest and short-lived.

Anasarca and edema due to low albumin in tough-to-reverse disease (cancer, malnutrition, sepsis and ICU level care) should address sodium restriction, avoiding unnecessary fluids, and creating steady natriuresis with loop diuretics with a modest and sustainable goal of net negative 1-2 liters per day.

Promote elevation, ambulation, properly fitted compression wraps or stockings to augment lymphatic return. Provide adequate protein and calories to reduce catabolism, but focus mostly on what the patient will actually take in.

In sum, with hypoalbuminemia and edema, stop adding salt and water, help the kidneys remove what’s already there, improve lymphatic return mechanically, drain symptomatic compartments, and treat any fixable outflow obstruction. Everything else, including albumin, plays only a supporting role.

⚕️September IM and Hospitalist Recap!⚕️

DOAC Failure (Curbsiders)

I've seen this a few times recently, and could have really used these insights!

Check out the linked @thecurbsiders post, and then some of my top takeaways below.


https://x.com/thecurbsiders/status/1970184628636913849

True anticoagulation failure, defined as definitive evidence of a new thrombus despite adequate anticoagulation, is exceptionally rare

Confirm patient adherence, not just by asking the patient if they are taking their medicine, but by verifying pharmacy fill histories to ensure consistent access

It is also essential to review the specific administration details; for example, rivaroxaban requires co-administration with food for optimal absorption, and apixaban is dosed twice-daily. 

Radiologists can often identify features on ultrasound or CT that distinguish an acute thrombus from a chronic, organized one - ask!

During the initial 1-3 months following a new VTE, some degree of asymptomatic clot propagation or remodeling can occur and does not necessarily represent treatment failure

A normal D-dimer can provide reassurance that a new, significant thrombotic process is less likely, especially when clinical symptoms are chronic or unchanged.

If true failure, active malignancy or an underlying condition like antiphospholipid syndrome (APS) or anatomic factors like May-Thurner or thoracic outlet syndrome should be considered as possible reasons

Its reasonable to temporarily switch to low-molecular-weight heparin (lovenox) while a full investigation is completed.

Switching to warfarin should not be a reflexive decision; it represents a significant lifestyle change and requires a motivated patient - given the added challenges with adherence, it’s unlikely to be more successful than a DOAC especially if adherence was uncertain to begin with

In patients with obesity with BMI > 50-60, data on DOAC efficacy are scarce

For patients with severe renal dysfunction, including those on dialysis, apixaban is often the preferred agent due to its lower degree of renal clearance

Thread Source(s): 

https://thecurbsiders.com/curbsiders-podcast/499-inpatient-doac-dilemmas-with-dr-jori-may


⚕️September IM and Hospitalist Recap!⚕️

Orthostatic Hypotension (Core IM)

Despite taking care of at least 1-2 patients with orthostasis each week, I still learned so much! 

Check out the linked @COREIMpodcast threads, and then some of my top takeaways below.


https://x.com/COREIMpodcast/status/1966094950548099333

Recommend lying flat for 5 minutes to get stable BP baseline. Check BP at least twice at both the sitting and standing intervals. It may require waiting 5-10 minutes after standing to catch early neurogenic disease which can have a delayed drop in BP.

HR response can give clue to etiology - ratio of change in HR to change in systolic BP - if HR does not increase by at least one beat per two point drop in SBP (in other words, a ratio of less than 0.5), this strongly suggests blunted autonomic response, such as in diabetic neuropathy

Treatment should focus on symptoms and functionality and not fixing the orthostatic BP given this may not be possible; that being said, ideally an SBP of 100 when standing should be goal to ensure adequate brain perfusion

Orthostasis symptoms may also include weakness, blurry vision, mental fog, or "coat hanger pain" in neck and shoulders caused by poor blood flow to the trapezius muscles

Promote motility, especially in the hospital - avoid deconditioning just because a patient is a fall risk

Deprescribe alpha blockers (tamsulosin), beta blockers, nitrates, and alpha-2 agonists (tizanidine) when able

Thigh-high compression stockings or abdominal binders are the best lifestyle intervention; a significant amount of blood pools in the abdominal circulation upon standing; abdominal binders are often easier to manage in frail adults than compression stockings (don’t have to lean over)

“Water bolus” trick: having a patient rapidly drink about 16 ounces of cool water can raise their blood pressure for about 30 minutes, acting as a quick rescue measure before beginning activity.

Patients should be counseled to avoid hot showers and large carbohydrate-heavy meals that can cause postprandial hypotension

Viewing medications to address orthostasis not as permanent additions, but as a temporary bridge to facilitate mobility and participation in physical therapy can help reframe the clinical decision to start them

Midodrine is often first line - induces vasoconstriction and raises baseline BP; avoid taking while supine, or when expecting to be supine in next 4 hours to prevent supine hypertension - best in AM or before PT/activity

Midodrine onset is ~60 minutes, and lasts for 3-4 hours; can check BP at 1 hour mark to see if it is efficacious

Midodrine can cause urinary retention

Fludrocortisone helps with volume retention, but may not be the best option in patients with heart failure or baseline HTN; it can also cause hypokalemia; may be a good choice in those with baseline hypotension

Droxidopa is a prodrug converted into norepinephrine (basically oral levophed), and is approved for neurogenic orthostatic hypotension (in my experience, it is often limited by insurance coverage)

Patients can have orthostasis symptoms without hypotension if they have HTN at baseline - the BP drop leads to symptoms because the brain is used to the higher pressures, so it experiences relative hypoperfusion

Severe BP swings are more common in those with neurogenic etiologies - to avoid supine hypertension, recommend sleeping with head of bed elevated

Supine hypertension can lead to a pressure natriuresis overnight leading to loss of salt and water and this can worsen orthostasis in the AM

Check out the @pointofcaremed page to learn more about syncope and LOC for guidance on HPI intake, treatment, and pearls!

https://www.pointofcaremedicine.com/inpatient/syncope

And listen to our podcast episode on the topic!

https://creators.spotify.com/pod/profile/pointofcarepodcast/episodes/Syncope-and-Loss-of-Consciousness-Inpatient-e1t7uf9/a-a959pud

Thread Source(s): 

https://www.coreimpodcast.com/2025/09/11/orthostasis-part-1-gray-matters/

https://www.coreimpodcast.com/2025/09/22/orthostatic-hypotension-part-2-gray-matters/


Some practical tips for taking care of patients with CKD and ESKD in the hospital! 

Collected these from during my recent deep dive into CKD, and threw in a bunch of lessons from experience!

- Thread - 


Many admissions involve being too wet or too dry, and the kidney doesn’t like either.

If diuresing, you often need higher doses of loop diuretics, and augmentation is commonly needed.

Electrolyte derangements (like HyperK) may require lower threshold for action.

Magnesium-containing laxatives and antacids and phosphate enemas can swing electrolytes dangerously in patients with CKD.

Discuss dose adjustments with pharmacy. Avoid or dose-adjust baclofen, gabapentin/pregabalin, cefepime, morphine.

Unfractionated heparin is easiest to start and stop when GFR<30. Apixaban is usually the best DOAC option for long-term AC needs.

Vancomycin usually requires "dosing by level". 

Cefazolin given after dialysis is a common MSSA treatment. 

Insulin clearance falls as GFR drops making hypoglycemia a serious risk.

In general, if a contrasted scan is needed, get it. If its not needed, avoid it. 

Hydrate as able if you are using contrast. 

Iron deficiency is common and IV iron can be helpful.

Uremia can cause encephalopathy. 

Uremic platelet dysfunction may present as mucosal bleeding or oozing - desmopressin may be needed if a procedure can’t wait.

Pruritis and restless leg syndrome (RLS) may indicate high phosphorus.

Phosphate binders should be continued if the patient is eating.

Vascular access is sacred - avoid PICCs in Stage 4-5 CKD in case fistulas are needed. 

Never place IVs, draw blood, or take BPs on the same arm as a fistula/graft.

The RIJ is the preferred dialysis catheter site; needed central access should favor femoral or left-side of the neck.

In peritoneal dialysis, abdominal pain is peritonitis until proven otherwise.

ESKD patients should have their next chair time confirmed on DC.

Read the full September Recap on Substack! 

Subscribe for more monthly recap posts like this!

https://rokeefemd.substack.com/p/september-im-and-hospitalist-recap?r=4zig6


CKD - Tips for Hospitalists

⚕️September IM and Hospitalist Recap!⚕️

Chronic Kidney Disease (Annals of IM)

A majority of patients with CKD will die from cardiovascular disease rather than progressing to ESKD.

Here are some of my takeaways, from staging, to the 4 pillars, anemia, and inpatient pitfalls.

- Thread 🧵 - 

#MedEd #IMRecaps


CKD is staged by GFR and albuminuria which together predict the risk of progression and mortality.

Image Source: 
https://www.ahajournals.org/doi/10.1161/JAHA.123.030131

CKD requires evidence of kidney damage or decreased function for at least 3 months (not a one time measurement)

Most commonly based on estimated glomerular filtration rate (eGFR) less than 60 mL/min/1.73 m2 OR a urine albumin-to-creatinine ratio (UACR) > 30 mg/g.

In cases of abnormal muscle mass or for more precise staging, combined creatinine-cystatin C equation is the most accurate method of calculating eGFR.

Image Source: https://www.coreimpodcast.com/2023/11/08/ckd-staging-cr-vs-cystatin-c/


In the hospital, creatinine-based eGFR is an unreliable measure of kidney function. 

Acute illness, inflammation, and muscle wasting reduce creatinine and thus eGFR likely overestimates actual kidney function which can lead to dangerous dosing errors in anticoagulants and antibiotics that are renally cleared. 

Cystatin C can provide more accurate estimation.

Management is based on 4 pillars to slow progression and reduce cardiovascular risk

- RAAS inhibition
- SGLT2 inhibitors
- Nonsteroidal MRAs (nsMRA)
- GLP-1 receptor agonists

Patients with albuminuria should begin with a RAAS inhibitor such as ACE or ARB. These reduce intraglomerular pressure and proteinuria.

SGLT2i are started regardless of T2DM status

nsMRAs like finerinone reduce CKD progression and cardiovascular events through anti-inflammatory and anti-fibrotic mechanisms and have a lower risk of hyperkalemia than steroidal MRAs (spironolactone)


Systolic BP target of <120 is guideline recommendation for most patients with CKD based on the SPRINT trial.


Guidelines recommend statins for nearly all CKD or ESRD patients over age 50, regardless of baseline cholesterol based on the SHARP trial

Note that it evaluated simvastatin and ezetimibe


Anemia is a near universal complication of advanced CKD, driven by decreased EPO production and impaired iron metabolism.

Image Source: https://www.ccjm.org/content/83/8/613

Anemia of CKD requires iron repletion before considering erythropoiesis-stimulating agents (ESAs), as they are not effective without adequate iron.

Oral iron is usually started, but IV iron is often necessary. 

Goal of ESA treatment is to address symptoms. 

The TREAT trial showed Hgb >13 did not lead to reduction in cardiovascular events, but did increase risk of stroke. 

Thus, general goal is Hgb level between 10-11.5 and NOT normalization of Hgb levels. Its a balance between addressing symptoms while maintaining safety.


CKD patients have reduced renal reserve making them highly susceptible to AKI from NSAIDs, IV contrast, aminoglycosides and insults like hypovolemia or hypotension.

Check out the @pointofcaremed page to learn more about outpatient CKD intake, treatment, and pearls!

https://www.pointofcaremedicine.com/outpatient/chronic-kidney-disease


Thread Source: 

https://www.acpjournals.org/doi/10.7326/ANNALS-25-02684


CKD Review

⚕️September IM and Hospitalist Recap!⚕️

Hypertrophic Cardiomyopathy Review (NEJM)

Turns out there's more to know than STEP 1 would have you believe (Valsalva anyone?) 

Just took care of a patient with HCM on the wards, and this came in handy!

Here are some of my favorite lessons and pearls for clinical practice!

- Thread 🧵 - 

#MedEd #IMRecaps


Obstructive HCM is defined by a dynamic LVOT gradient caused by septal hypertrophy and systolic anterior motion (SAM) of the mitral valve.

The interventricular septum bulges into LVOT and anterior mitral valve leaflet moves toward septum during systole

Image Source: https://professional.heart.org/en/science-news/2024-guideline-for-the-management-of-hypertrophic-cardiomyopathy

70% of HCM is the obstructive form; however the obstruction is not fixed, but is rather a dynamic process

Obstruction worsens with any maneuver or medication that decreases preload 

- Valsalva
- Dehydration
- Standing
- Vasodilators like nitrates
- Dihydropyridine calcium channel blockers

Obstruction worsens with increased contractility

- Exercise
- Sympathomimetics like the pure inotrope digoxin

Medical treatment is geared towards alleviating the LVOT gradient, and improving symptoms

First-line includes beta blockers, non-dihydropyridine calcium channel blockers (verapamil, diltiazem)

Next, cardiac myosin inhibitors can be considered. 

Mavacamten and aficamten directly target the underlying HCM mechanism (mutations of sarcomeric proteins that lead to excess of actin-myosin cross-bridges and hypercontractility). 

These drugs inhibit cardiac myosin ATPase, reducing the number of cross-bridges which decreases contractility and alleviates the LVOT obstruction.

Image Source: Wikipedia


Landmark clinical trials like EXPLORER-HCM (mavacamten) and SEQUOIA-HCM (aficamten) demonstrated significant improvements in LVOT gradients, exercise capacity, and symptoms. 

The primary side effect to watch for is a decrease in EF which requires monitoring.

AFib develops in 1/4 of HCM patients and can lead to issues with hemodynamics due to loss of the coordinated atrial kick, reducing filling of the stiff LV. 

HCM patients should be on AC regardless of CHADS-VASc score given there is often left atrial enlargement which is prothrombotic.

Septal reduction therapy (SRT) via myectomy (or alcohol ablation in older/frailer patients) is definitive treatment for medically refractory disease.

Alcohol ablation injects ethanol into septal perforator coronary artery to induce a controlled MI and thus scarring and thinning of the basal septum.

Image Source: https://thoracickey.com/ethanol-septal-ablation/

Key factors that strongly favor ICD placement include: 

1) A family history of SCD attributed to HCM

2) Massive left ventricular hypertrophy (wall thickness ≥30 mm)

3) Recent unexplained syncope

4) The presence of an LV apical aneurysm

5) An EF <50%. 

Other important, though less definitive, markers include multiple or prolonged runs of NSVT on ambulatory monitoring and extensive late gadolinium enhancement (LGE) on cardiac MRI, which signifies myocardial fibrosis and scarring.

Here are some practical tips for the hospitalist taking care of patients with HCM: 

- Take care to avoid tachycardia, hypovolemia, and sudden drops in afterload.

- Practically, this means maintaining hydration, being more ginger with diuresis, avoid vasodilators, control pain/anxiety and fevers, and prioritize continuing rate control medication. 

- If a pressor is needed, phenylephrine can raise afterload without stimulating the heart. 

- Dobutamine and dopamine can worsen obstruction. 

- Myosin inhibitors have a number of drug-drug interactions including azoles, macrolides, anticonvulsants; discuss with pharmacy when continuing them.

Source: https://www.nejm.org/doi/full/10.1056/NEJMra2413445


HCM Review

⚕️September IM and Hospitalist Recap!⚕️

Hypothyroidism: A Review (JAMA)

This one is absolutely LOADED with pearls!

Read on for some of my favorite lessons for clinical practice!

- Thread 🧵 - 

#MedEd #IMRecaps


Diagnosis is established with a high TSH level with low free T4.

When the thyroid gland fails, the pituitary compensates by increasing TSH, often before free thyroxine (fT4) levels fall below normal range

Overt hypothyroidism has low T4 whereas subclinical hypothyroidism has normal T4

T3 has no role in the initial diagnostic workup - levels are often maintained until severe hypothyroidism

Anti-thyroid peroxidase (TPO) antibodies can confirm Hashimoto thyroiditis, but is not necessary to start treatment with levothyroxine

Central hypothyroidism (less than 1% of cases) should be suspected in patients with low T4 and INAPPROPRIATELTY normal or low TSH

It is often accompanied by other signs of pituitary dysfunction like adrenal insufficiency or hypogonadism

Treatment monitoring in this case is based on T4 level instead of TSH which will ALWAYS be low/normal. 

Also be mindful that TSH with reflex T4 screens may not be adequate to effectively diagnose, as TSH levels may be normal and it won't auto-run the T4

Young healthy patients can start levothyroxine with full replacement doses of 1.6 mcg/kg/day; in elderly or those with CAD start at 25-50 mcg daily

The goal of treatment is to normalize the TSH without inducing iatrogenic thyrotoxicosis which can increase myocardial oxygen demand and lead to angina or arrythmias

After starting treatment, TSH levels should be checked in 6-8 weeks to allow for equilibration to a new steady state; changes should be made in increments of 12.5 to 25 mcg until TSH is within the target range

Euthyroid patients should have levels checked once a year to make sure levels are still appropriate

Overtreatment and undertreatment are both serious

Overtreatment can lead to AFib, decreased bone mineral density, increased fractures

Undertreatment can lead to dyslipidemia, HTN, CAD

Absorption and metabolism of levothyroxine is significantly affected by medications and effective treatment requires consistent absorption and metabolism. 

Calcium carbonate, iron sulfate, phosphate binders and PPIs can decrease absorption - the administration of these should be separated by at least 4 hours

Levothyroxine should be given on an empty stomach, consistently timed with respect to meals and the above interacting medications

Enteral tube feeds should be paused for ~1 hour prior to Synthroid administration when able

Hepatic enzyme inducers such as carbamazepine, phenytoin, phenobarbital, and rifampin increase T4 clearance and may raise needed dose requirements. Sertraline may also do so. 

Estrogen therapy increases thyroxine-binding globulin and also necessitates higher doses.

More binding-proteins scoops up the free T4

This is the reason pregnancy increases levothyroxine requirements

On the other hand, nephrotic syndrome or protein-losing enteropathy can REDUCE binding proteins, complicating interpretation of thyroid labs

Myxedema coma is more of a spectrum of disease than an all-or-none event.

It should be on your radar in elderly, chronically hypothyroid patients presenting with hypothermia, bradycardia, hypoventilation, hyponatremia, pericardial effusion, AMS, and some sort of trigger (infection, sedatives, cold exposure, surgery, MI).

If you’re concerned about myxedema coma, draw a cortisol if possible, then begin treatment with steroids to address possible adrenal insufficiency as treatment with just levothyroxine can precipitate shock.

Be mindful of euthyroid sick syndrome in the hospital - this is usually due to low T3, which is another reason it has no role in the initial diagnosis of hypothyroidism.

High dose biotin (common in hair and nail supplements) can interfere with thyroid assays.

It may lead to apparent low TSH and high T4, mimicking hyperthyroidism

Patients should hold supplements for up to 48 hours prior to testing

Amiodarone can impair the peripheral conversion of T4 to T3 which can cause thyroid dysfunction. 

Check baseline thyroid studies before starting 

After radiation therapy for head and neck cancer, as many as 42% of patients develop hypothyroidism over a seven-year period.

Certain immune checkpoint inhibitors (especially combination therapy with anti-PD-1, anti-PD-L1, and anti-CTLA-4 agents) can cause secondary hypothyroidism by inducing hypophysitis (inflammation of the pituitary gland), which may lead to panhypopituitarism.

Levothyroxine half-life is ~7 days

If a patient is NPO, missing a dose or two is usually safe

However, if missing considerably more than this, switch to a ~75% dose via IV

Source: https://pubmed.ncbi.nlm.nih.gov/40900603/


Hypothyroidism Review

⚕️September IM and Hospitalist Recap!⚕️

Large Vessel Vasculitis Review (The Lancet)

GCA is not just a disease of the temporal arteries, and there's more to know than just jaw claudication and vision loss!

Read on for some of my favorite lessons for clinical practice!

- Thread 🧵 - 

#MedEd #IMRecaps

The cranial phenotype presents with the classic headache, jaw claudication, scalp tenderness, visual disturbances. 

The large-vessel phenotype manifests with inflammation of the aorta and major branches which can lead to limb claudication, asymmetric BP, aortic aneurysm, FUO. 

If GCA diagnosed, recommend getting a CTA even if patient presents with purely cranial symptoms to evaluate for large-vessel disease.


The most feared complication of cranial GCA is permanent vision loss from arteritic anterior ischemic optic neuropathy (A-AION) due to occlusion of the posterior ciliary arteries of the ophthalmic artery.


Any patient over 50 with a compelling clinical picture - amaurosis fugax, diplopia, jaw claudication - should be started on pred 40-60mg daily

If presenting with active or evolving vision loss, IV methylpred 500-1000mg daily for 3 days is strongly recommended before oral steroids

You DON'T need to worry about getting a biopsy before starting steroids!

Diagnostic yield remains high for up to 2 weeks after starting steroids!

https://www.openevidence.com/ask/1f1eb17b-e21e-45ce-94a6-b8c652f24f3c

Ultrasound of the temporal and axillary arteries is a first-line imaging modality

The “halo sign” (non-compressible hypoechoic circumferential wall thickening) has high sensitivity and specificity for GCA (image below)

CTA and MRA can further reveal mural wall thickening, luminal stenosis, and aneurysmal dilation.

Image Source: https://radiopaedia.org/cases/giant-cell-arteritis-of-the-distal-superficial-femoral-artery#image-27926613

In the 2022 ACR/EULAR classification criteria, a positive “halo sign” or evidence of aortitis is weighted as heavily as a positive temporal artery biopsy, possibly allowing patient to forgo the need for an invasive procedure

When compared with Takayasu arteritis, the main difference is demographics - GCA is a disease of older adults; Takayasu is a disease of younger, often Asian patients

The GiACTA trial demonstrated efficacy of tocilizumab (IL-6 receptor inhibitor) along with steroid taper in GCA.

It showed higher rates of sustained steroid-free remission; in other words, it helps more reliably taper steroids faster and then stay off them; hopefully avoids adverse side effects of prolonged steroids (osteoporosis, diabetes, infections, etc.)

https://pubmed.ncbi.nlm.nih.gov/28745999/

Source: https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(25)01436-9/abstract
