Thrombotic microangiopathies (TMAs) love to show up as “anemia + low platelets + sick patient” on exams—then the question asks you to separate TTP vs HUS in one breath. Here’s a fast, shareable visual hack plus the handful of high-yield facts that actually move the needle on USMLE.
The 10‑second snapshot (what both have in common)
Both TTP and HUS are TMAs → platelet-rich microthrombi shear RBCs in small vessels.
Expect:
- Microangiopathic hemolytic anemia (MAHA)
- ↑ LDH, ↑ indirect bilirubin, ↓ haptoglobin
- Schistocytes on smear
- Thrombocytopenia
- Normal PT/PTT (key contrast vs DIC)
Visual hack: “Brain vs Bathroom”
Picture a stick figure with two giant labels:
- TTP = Think (brain)
- HUS = Hygiene/Toilet (bathroom)
One-liners
- TTP: “Low ADAMTS13 → ultra-large vWF multimers → platelet microthrombi → MAHA + thrombocytopenia, classically neuro symptoms.”
- HUS: “Shiga(-like) toxin after bloody diarrhea → endothelial damage → MAHA + thrombocytopenia, classically renal failure.”
Side-by-side: the exam table you’ll actually use
| Feature | TTP | HUS (typical) |
|---|---|---|
| Classic association | ADAMTS13 deficiency (often acquired autoantibody) | EHEC O157:H7 (Shiga toxin), sometimes Shigella |
| Trigger clue | Adult, autoimmune/idiopathic; can be drug-related | Child after bloody diarrhea (undercooked beef, unpasteurized foods) |
| “Organ preference” | Neuro > renal | Renal > neuro |
| Key mechanism | ↓ ADAMTS13 → ↑ ultra-large vWF → platelet aggregation | Shiga toxin → endothelial injury (esp. kidney) |
| Coags (PT/PTT) | Normal | Normal |
| Smear | Schistocytes | Schistocytes |
| Treatment priority | Plasma exchange (PLEX) + steroids (don’t wait) | Supportive (fluids, dialysis PRN); avoid antibiotics/antimotility in typical Shiga HUS |
| Buzzword | “Pentad” | Post-diarrheal AKI |
The classic “pentad” (and how Step questions really test it)
TTP pentad (traditionally):
- MAHA
- Thrombocytopenia
- Neurologic symptoms (confusion, headache, seizures)
- Renal dysfunction
- Fever
Reality for exams/clinics: you don’t need all five—MAHA + thrombocytopenia with neuro symptoms should scream TTP.
High-yield decision rule: when to start plasma exchange
If you suspect TTP, the most important test is actually your reflex:
- Start plasma exchange immediately when there’s strong suspicion (MAHA + thrombocytopenia ± neuro signs), because mortality is high without treatment.
- ADAMTS13 activity testing is helpful but should not delay PLEX.
Why PLEX works: removes the inhibitor and replenishes functional ADAMTS13.
What about “atypical HUS” (quick Step 2 add-on)
Not every HUS is diarrheal:
- Atypical HUS is often due to complement dysregulation (alternative pathway)
- Can be triggered by pregnancy, infections, certain meds
- Treatment may involve eculizumab (C5 inhibitor), depending on the scenario
(But if the stem screams “bloody diarrhea + kid + renal failure,” think typical Shiga HUS first.)
Mini-mnemonics you can drop into flashcards
TTP: “A DAMN brain problem”
- ADAMTS13 deficiency
- Decreased platelets
- Anemia (MAHA)
- Mental status changes (neuro)
- Normal PT/PTT
HUS: “Hamburger → Uremia → Schistocytes”
- Undercooked beef exposure → post-diarrheal AKI → MAHA
The “don’t get tricked” checklist
- PT/PTT normal? → pushes you toward TTP/HUS, away from DIC
- Neuro symptoms prominent? → TTP
- Recent bloody diarrhea + child + AKI? → HUS
- Treatment urgency: TTP = PLEX now; typical HUS = supportive care
Rapid-fire self-test (30 seconds)
- Adult with confusion, petechiae, schistocytes, normal PT/PTT → TTP → plasma exchange
- Child after bloody diarrhea with rising creatinine, schistocytes, normal PT/PTT → HUS → supportive; avoid antimotility/antibiotics (typical Shiga HUS)