The 30 facts you need for Step 1.
We extracted the highest-yield concepts from years of practice exams. 10 subjects, 10 facts each, with practice questions and explanations for when you get stuck.
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We're med students who got tired of 10,000-page resources and endless Anki decks. So we distilled everything down to the 30 concepts that actually show up on Step 1.
Each fact has a clear explanation, clinical correlation, memory trick, and practice questions.
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Renal
NSAID-Induced Prerenal Azotemia via Prostaglandin Inhibition
Key Concept
NSAIDs inhibit cyclooxygenase enzymes, reducing prostaglandin E2 (PGE2) and prostacyclin (PGI2) synthesis. These prostaglandins normally maintain renal blood flow by dilating afferent arterioles, so NSAID use can cause prerenal azotemia. Decreased renal perfusion subsequently triggers renin release through the juxtaglomerular apparatus.
Clinical Pearl
Patients at highest risk include elderly individuals, those with pre-existing kidney disease, heart failure, cirrhosis, or volume depletion. Clinical presentation includes elevated serum creatinine and BUN, oliguria, and signs of fluid retention. This is particularly concerning in hospitalized patients receiving NSAIDs for pain control or anti-inflammatory effects. The condition is typically reversible upon NSAID discontinuation, but prolonged use can lead to acute tubular necrosis and irreversible kidney damage.
Memory Trick
Remember 'PGE-2-DILATE': Prostaglandin E2 DILATEs the afferent arteriole. When NSAIDs block PGE2, think 'NO-SAID to dilation' - the arteriole constricts, reducing kidney flow and triggering renin. Visualize a garden hose (afferent arteriole) being squeezed shut when you take away the prostaglandin 'dilator muscle.'
1 of 30 high-yield facts