DIP Episode 344 - USMLE Step 2CK/3 Rapid Review Series 65 (+10/4-8 2CK/3 Course Reminder)

Source / episode info

• Episode: 344
• Title: Divine Intervention Episode 344 – USMLE Step 2 CK/3 Rapid Review Series 65 (+10/4-8 2 CK/3 Course Reminder).
• Published: 2021-10-03
• Source: Episode page

One-liner

This episode provides a rapid review of high-yield topics including the sequelae of Group A Strep infections (Erysipelas), differentiating IgAN from PIGN based on timing, recognizing diverse causes of Thrombotic Microangiopathy (TMA), and distinguishing between pseudogout and gout based on crystal morphology.

High-yield summary

• Erysipelas Sequelae: Following a Group A Strep skin infection (e.g., Erysipelas), the most likely potential sequela is Post-infectious Glomerulonephritis (PIGN); Rheumatic fever cannot occur after a strep skin infection.
• Nephritic Syndrome Timing: If hematuria occurs 1–6 days after an upper respiratory infection, suspect IgA Nephropathy (IgAN). If it occurs > 1 week later, suspect PIGN. Both are nephritic syndromes (< 3.5 g/day proteinuria).
• TMA Pathophysiology: TMA is characterized by microthrombi formation due to endothelial damage and platelet activation; causes include malignant hypertension, SLE flare, DIC, HUS, and TTP.
• Pseudogout vs. Gout: Pseudogout involves the deposition of calcium pyrophosphate dihydrate (CPPD) crystals, which are typically rhomboid-shaped and positively bi-refringent. Gout involves monosodium urate (MSU) crystals, which are needle-shaped and negatively bi-refringent.
• FSGS in HIV: In HIV patients with nephrotic syndrome due to FSGS (especially the collapsing variant), protein loss includes antithrombin III, leading to a hypercoagulable state and increased risk of PE/DVT.

Learning objectives

• Differentiate between IgA Nephropathy and Post-infectious Glomerulonephritis based on the timing of hematuria post-URI.
• Identify the specific crystal morphology (rhomboid vs. needle) and birefringence pattern for pseudogout versus gout.
• Recognize the risk factors and underlying pathophysiology leading to a hypercoagulable state in nephrotic syndrome, particularly FSGS in HIV.
• Classify different causes of Thrombotic Microangiopathy (TMA), including those related to hypertension or complement deficiencies.
• Interpret classic histological findings on kidney biopsies, such as thyroidization of the kidneys.

Board exam buzzwords

Rapid review table

Board-speak -> diagnosis

Differential diagnosis / distinguishing features

Gout vs Pseudogout

Thrombotic Microangiopathy (TMA)

Management pearls

• Pseudogout Management: First line is NSAI Ds (e.g., Ketorolac, Ibuprofen); Second line is corticosteroids; Third line is Colchicine. Oral steroids are often preferred over IV when possible.
• TMA Workup: Always check for schistocytes and thrombocytopenia in the setting of unexplained renal failure/hemoglobinuria. Differential includes HUS, TTP, DIC, and vasculitis.
• FSGS Management (HIV): Aggressive management of proteinuria is key; monitor coagulation status due to loss of natural anticoagulants like Antithrombin III.
• Acute Pyelonephritis: If a kidney biopsy shows "thyroidization," strongly suspect chronic pyelonephritis, which requires long-term urinary culture and potentially antibiotics/drainage.

Don't miss

Integration & clinical reasoning

• Renal Physiology & Coagulation: The kidney plays a role in regulating coagulation by excreting anticoagulant proteins like Antithrombin III. Nephrotic syndrome can thus precipitate thrombotic events.
• Infectious Disease & Autoimmunity: Group A Strep infections are classic triggers for both skin infections (Erysipelas) and autoimmune sequelae (PIGN, Rheumatic Fever).
• Vascular Pathology: Both malignant hypertension and certain systemic vasculitides can cause endothelial damage leading to TMA, emphasizing that the endothelium is the primary target.

Concept connections / cross-references

• No explicit cross-references.

High-yield association table

Key terms glossary

Study optimization

Question pattern recognition

• Pattern: Hematuria 1–6 days post-URI -> IgA Nephropathy. This timing is the single most important clue to distinguish it from PIGN or other causes.
• Pattern: Schistocytes + Thrombocytopenia + Renal failure -> TMA. Always consider HUS, TTP, and Malignant HTN first.
• Pattern: Rhomboid crystals + Positive birefringence -> Pseudogout. If associated with hypercalcemia or metabolic syndrome (e.g., Hemochromatosis), the suspicion is even higher.

Test yourself

Common mistakes to avoid

Common traps

OMM / COMLEX integration

• Renal & Ureteral Viscerosomatic Reflexes (T10–L2): Kidneys and upper ureters receive sympathetic innervation from T10–T11 (aorticorenal ganglion), with Vagus nerve parasympathetics. Lower ureters and bladder receive sympathetics from T12–L2, with Pelvic Splanchnic parasympathetics (S2–S4). Acute nephrolithiasis causes intense paraspinal spasm from T10 to L2.
• Chapman Reflex Points: Kidney anterior point is 1 inch superior and 1 inch lateral to the umbilicus (posterior: T12–L1 intertransverse space). Bladder anterior point is periumbilical and over the pubic symphysis.
• Psoas Spasm in Ureteral Colic: The ureter courses along the anterior surface of the psoas major muscle. A passing calculus irritates the psoas, inducing secondary psoas spasm, pelvic sidebending, and compensatory non-neutral lumbar somatic dysfunction (L1–L2 flexed, sidebent, and rotated).