Let's start with an initial problem representation:
A 75 y/o M w/ a PMH of COPD, CAD, & aortic valve replacement p/w 2 weeks of dyspnea on exertion, 1 month of LE edema, 20 lb weight loss & recent onset PND and Orthopnea
invoke the dyspnea pyramid (cardiac, pulmonary, anemia, metabolic) but addition of progressive edema and weight gain concerning for cardiac pathology
whenever we see dyspnea on exertion and bilateral LE edema we jump straight to CHF
more features concerning for CHF but thinking also about liver and kidney leading to excess fluid as well
possible mechanical hemolysis from bio prosthetic valve contributing to dyspnea from anemia
Does the SOB improve when sitting up? concern also for hepatopulmonary syndrome
Prence of constitutional symptoms to suggest inflammation
How long after sitting up can he lie back down - very important in defining PND.
(PND) is a sensation of SOB that awakens the pt, often after 1- hours of sleep, and is usually relieved in the upright position.
alcoholism/liver dysfunction could lead to third spacing?? = weight gain
There are many reasons to awake at night and sit up. COPD, sleep apnea, both allow immediate recumbency -
Add to the PR physical exam: BP 170/90, he is chronically ill appearing, peri-orbital edema, exp wheezes, 2+ pitting edema, 2-3 cm gluteal mass & 4-5 cm thigh mass
The preorbital edema suggests nephrotic syndrome or thyroid disease
He looks volume overloaded but there are no signs of volume overload in the lungs. hmmm
Would want to see the albumin, u/a, urine protein/creatinine if albumin decreased
Don't forget about amlodipine assoc LE edema
also wondering if that mass is some kind of sarcoid/amyloid/malignancy that contributes to nephrotic syndrome
subcutaneous nodules + volume overload, also consider Rheumatic disease
isn’t there a weird parasitic infection that can cause periorbital edema from eating pork?
A soft tissue sarcoma- can originate from cardiac and are soft. In the heart can cause congestion/pericardium
Add to the PR some labs: Nml WBC, hgb 9.7, nml plts, elevated Cr from baseline at 1.63, a Gamma gap, NT-BNP of 8000, nml trop, UA: 3+ protein, 24 hr urine 9g
CXR: left pleural effusion with nodules in the left lung
We have renal dysfunction, anemia, volume overload, & a protein gap. will want to determine monoclonal from polyclonal
And we know that 3 + protein has a strong association with increased ACR or PCR
Conversion of Urine Protein–Creatinine Ratio or Urine Dipstick Protein to Urine Albumin–Creatinine Ratio for
Use in Chronic Kidney Disease Screening and Prognosis: An Individual Participant–Based Meta-analysis: Annals of Internal Medicine: Vol 0, No 0 acpjournals.org/doi/10.7326/M2…
Is this amyloid? autoinflammatory disease? Waldenstrom’s? any history of hep C?
he would be in the age group that has increased risk of chronic HCV infection
He does have a PMH of IV drug abuse and that can also result in amyloidosis
Can we get some BCx...
They were negative on admission
Echo showed no evidence of endocarditis but the presence of diastolic dysfunction
PET scan showed hypermetabolic gluteal mass
And you guessed it. We need a biopsy.
And the final Dx is Minimal Change Disease secondary to an extranodal marginal b cell lymphoma
MCD occurs in only ~0.4% of lymphomas, so incredibly rare, but always taught on UWorld
The pathogenesis of this disorder remains poorly understood; but there is evidence to suggest an immune origin
MCNS is caused by a putative circulating factor, which increases glomerular capillary permeability and leads to podocyte cytoskeleton disorganization and proteinuria
Hematogenous dissemination then can occur typically 4 to 10 weeks later, giving rise to secondary syphilis. <40% of pts w/ syphilis have primary syphilis diagnosed. These “Secondary” lesions last for several weeks before spontaneously resolving. Coined “early, latent infection”
What does late infection mean? When syphilitic lesions recur after 1 year from the initial eruption, or seropositivity is detected more than 1 year after the initial eruption, it is termed late latent syphilis.
Some optics neuritis pearls in a short #Medtweetorial 🧵…. We all know that optic neuritis is frequently associated with multiple sclerosis (MS). But optic nerve inflammation can exist from autoimmunity, infection, granulomatous disease, paraneoplastic disorders, & demyelination
Classical ON from MS is unilateral, moderate, painful color vision loss with an afferent pupillary defect & normal fundus examination.
In those with ON, 95% of patients showed unilateral vision loss & 92% had associated retroorbital pain that frequently worsened w/ eye movement.
If you have not listened to the @CuriousClinPod most recent podcast (Episode 10: Why does metronidazole treat both bacterial and parasitic infections?) then I suggest you tune in.
I'll summarize their show notes here in short #medtweetorial
First a question:
Was metronidazole first used as an antibiotic or as an antiparasitic?
If you guessed antiparasitic, then you would be correct!
It was developed in the 1950s to treat the parasite trichomonas & then was used in the 1960s to treat other parasitic infections, like giardia and amoebiasis.
A 31-year-old M born and raised in Brazil w/ no PMH presented with a 3 mon history of worsening DOE, orthopnea, 7kg weight loss, abdominal distention, dry cough, and syncope
An interesting fact from @3owllearning : Depending on the clinical problems, the studies of disease probability for differential diagnosis often show 10 - 25% of cases are unexplained, even after careful examination and testing.