Flashcards on Medical Ethics in Pediatric End-of-Life Care

Medical Ethics in Pediatric End-of-Life Care: A Guide

1 / 40

What are mitochondrial DNA depletion syndromes (MDDS)?

Autosomal recessive oxidative phosphorylation disorders characterized by a reduction in mitochondrial DNA leading to severe clinical symptoms.

Tap to flip · Swipe to navigate

Medical ethics

40 cards

Card 1

Question: What are mitochondrial DNA depletion syndromes (MDDS)?

Answer: Autosomal recessive oxidative phosphorylation disorders characterized by a reduction in mitochondrial DNA leading to severe clinical symptoms.

Card 2

Question: What mutation did Charlie Gard have and what protein does it affect?

Answer: A mutation in the RRM2B gene, which encodes the ribonucleotide reductase M2B subunit protein.

Card 3

Question: What were Charlie Gard's main clinical features?

Answer: Respiratory failure requiring a ventilator, tetraplegia with only occasional eye opening, epilepsy, and progressive decline leading to death.

Card 4

Question: What experimental treatment did Charlie's parents seek?

Answer: Experimental nucleoside replacement therapy previously used in patients with a different mitochondrial DNA depletion syndrome (TK2 mutation).

Card 5

Question: Why was the proposed nucleoside replacement therapy considered unproven for Charlie?

Answer: It had not been used for RRM2B-related MDDS; evidence existed only for TK2 mutations, which cause a myopathy rather than an epileptic encephalomyopath

Card 6

Question: What ethical principles are central to deciding whether to give an experimental therapy?

Answer: Beneficence (potential to benefit), nonmaleficence (avoid causing harm or prolonging suffering), and autonomy (or surrogate decision-making when the p

Card 7

Question: What does 'compassionate use' mean in this context?

Answer: Administration of an unproven therapy when efficacy for the specific condition is unclear, typically to try to help a patient with no other options.

Card 8

Question: What evidence suggested potential benefit of nucleoside replacement therapy?

Answer: In TK2 mutation cases it improved muscle strength and head support in a child and significantly prolonged lifespan in mice with TK2 deficiency.

Card 9

Question: Why might nucleoside replacement therapy not have helped Charlie despite benefits in TK2 cases?

Answer: TK2 mutations cause primarily myopathy, whereas Charlie had an RRM2B mutation causing epileptic encephalomyopathy — different disease manifestations m

Card 10

Question: What concern relates to nonmaleficence when considering experimental therapy for Charlie?

Answer: Even if the therapy had no known serious adverse effects, prolonging life could have extended Charlie's suffering given his severe, noncommunicative c