Sharon M. Donovan PhD RD’s Post

Shigellosis is caused by Shigella species, which are a non-flagellated, non-lactose-fermenting gram negative rod. Pathogenesis involves the shig toxin which is neurotoxic, cytotoxic, and enterotoxic. Patients present with fatigue, malaise, and watery diarrhea leading to bloody diarrhea. On physical exam patients have fever, abdominal tenderness, and signs of dehydration. Treatment is largely conservative through rehydration and antibiotics can be used in severe cases with TMP-SMX or ceftriaxone. Learn more high yield-concepts about Shigellosis on our DAILY Medbullets Step 2 & 3 podcast. Listen wherever you listen to podcasts! https://bit.ly/3t0iJ5M

More from AHA including SGLT2 inhibitors, blood transfusion after MI; cracks in the armor of Factor XI inhibitors; and renal denervation are the topics John Mandrola, MD, covers in this week's podcast.

Pseudohypoparathyroidism (PHP) is a condition characterized by symptoms of hypoparathyroidism despite normal or elevated parathyroid hormone (PTH) levels due to end-organ resistance to PTH. Patients have physical exam features of Albright hereditary osteodystrophy but no symptoms of hypocalcemia, and normal PTH levels with no end-organ PTH resistance. Presenting symptoms include shortened 4th and 5th digits, short stature, obesity, developmental delay, and soft tissue calcification. Treatment is aimed at normalization of calcium levels with supplementation and calcitriol. Learn more high yield-concepts about Pseudohypoparathyroidism on our DAILY Medbullets Step 2 & 3 podcast. Listen wherever you listen to podcasts! https://bit.ly/485pXpg

Fibrous Dysplasia is a developmental abnormality caused by a GS alpha protein mutation that leads to failure of the production of normal lamellar bone. The condition usually presents in patients who are less than 30 years of age with an asymptomatic lesion that is found incidentally on radiographs. Diagnosis is made with radiographs showing a lesion with ground glass appearance or a "punched-out" lesion with a well-defined margin of sclerotic bone. Treatment is usually nonoperative with bisphosphonates for pain control. Surgical management is indicated for lesions that lead to bone deformities such as scoliosis or coxa vara. Learn more high yield-concepts about Fibrous Dysplasia on our DAILY Orthobullets podcast. Listen wherever you listen to podcasts! https://bit.ly/3P6cpSR

Testing for early onset inflammatory bowel disease can not only help establish the diagnosis but also guide therapy. Learn more in this test-specific episode of our "Answers From the Lab" podcast. https://bit.ly/4bbDlJt

Fanconi Syndrome is a type of renal tubular acidosis (type 2) in the proximal convoluted tubules (PCT). Patients typically present with polyuria/polydipsia, bone pain and pathological fractures, myalgias and weight loss, and failure to thrive or developmental delay. On physical exam they show signs of rickets such as bowed legs, scoliosis, or teeth abnormalities. Treatment is supportive care with fluid/electrolyte repletion and vitamin D if osteomalacia is present and bicarbonate supplementation for metabolic acidosis. Learn more high yield-concepts about Fanconi Syndrome on our DAILY Medbullets Step 2 & 3 podcast. Listen wherever you listen to podcasts! https://bit.ly/3QYThaf

Nutcracker Esophagus is the high-amplitude but coordinated contraction of the esophagus, also known as hyperperistalsis, it is associated with metabolic syndrome and GERD. Patients are often asymptomatic but can present with chest pain and dysphagia. First-line treatment is with calcium channel blockers, nitrates, and trazodone. Heller myotomy is indicated for cases refractory to medical treatments. Learn more high yield-concepts about Nutcracker Esophagus on our DAILY Medbullets Step 2 & 3 podcast. Listen wherever you listen to podcasts! https://bit.ly/3LfUW8b

 Questions of the month:  ---  1. What if we could use genetic evolution and modifying the ubiquitin-proteasome pathway for more targeted therapy in proteinopathies, for example utilizing directed evolution and protein engineering with ubiquitin or regions of the proteasome complex, to include antisense mRNA for key motifs apart of amyloid precursor protein (APP), PSEN1 or SNCA? Could we better target the histopathological hallmarks associated with Alzheimer’s disease, such as the plaques of amyloid-beta, that are indicated in Alzheimer’s disease progression? 2.  What if we could use different modified tRNA, or agents in the protein translation pathway, to facilitate therapy for NDD proteinopathies. In reference to question 1, check out this article on the UPS system in the body: The Ubiquitin–Proteasome System in Immune Cells .

Our MI-Heart Ceramides assay goes beyond standard testing to guide the management of patients with mildly to moderately high cholesterol. Learn more in this test-specific episode of our "Answers From the Lab" podcast. https://bit.ly/4cIHzt2

There are two types of ketone bodies, acetoacetate and β-hydroxybutyrate. β-hydroxybutyrate + NAD+ is converted into acetoacetate + NADH, and 1 ketone body is equal to 2 acetyl-CoA. Ketone bodies are produced by the liver and can be used by the brain for fuel if glucose supplies fall, they are used in prolonged starvation for energy needs. Clinically, in ketoacidosis, usually in Type 1 diabetes mellitus, ketone levels rise and patients have hypokalemia and decrease in plasma HCO3. Learn more high yield-concepts about Ketone Bodies on our DAILY Medbullets Step 1 podcast. Listen wherever you listen to podcasts! https://bit.ly/49hPcoK