Test Your Knowledge of ATTR Amyloidosis
Reviewed by: HU Medical Review Board | Last reviewed: August 2026 | Last updated: August 2026
Transthyretin amyloidosis (ATTR) presents along a spectrum – from a progressive, length-dependent polyneuropathy to an infiltrative cardiomyopathy – and both wild-type and hereditary forms are now treatable, which makes early recognition the highest-value clinical skill.
This 5-question ATTR amyloidosis quiz spans the knowledge that most directly shapes recognition and diagnosis across the nerve and the heart: polyneuropathy red-flag clustering, the chronic inflammatory demyelinating polyneuropathy (CIDP) differential, the mechanism of disease-modifying therapy, the cardiac presentation that should prompt evaluation, and the mandatory step in noninvasive cardiac diagnosis. See how sharp your diagnostic and therapeutic reasoning is.
Clinical Challenge
In progressive idiopathic axonal polyneuropathy, which combination of features should most prompt transthyretin (TTR) genetic testing?
Clinical Challenge
When a CIDP diagnosis does not respond to immunotherapy and warrants reconsideration, which electrophysiologic and clinical findings most point toward hereditary transthyretin amyloidosis with polyneuropathy (hATTR-PN) instead?
Clinical Challenge
TTR silencer therapies and TTR stabilizers act by fundamentally different mechanisms. How do the silencer classes, RNA interference (RNAi) and antisense oligonucleotide (ASO), act compared with stabilizers?
Clinical Challenge
A patient presents with heart failure with preserved ejection fraction (HFpEF). Which additional clinical and electrocardiographic (ECG) constellation should most prompt evaluation for transthyretin amyloid cardiomyopathy (ATTR-CM), in both wild-type and hereditary disease?
Clinical Challenge
When technetium-based bone scintigraphy shows grade 2 cardiac uptake in suspected ATTR-CM, which step is mandatory before the diagnosis can be made noninvasively?