Atrophy, aplasia, and hypoplasia

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Atrophy, aplasia, and hypoplasia

1H Exam

1H Exam

Bones of the lower limb
Anatomy of the anterior and medial thigh
Vessels and nerves of the gluteal region and posterior thigh
Anatomy of the leg
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Fascia, vessels and nerves of the lower limb
Muscles of the gluteal region and posterior thigh
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Anatomy of the brachial plexus
Anatomy of the arm
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Anatomy of the sternoclavicular and acromioclavicular joints
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Anatomy of the pectoral and scapular regions
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Atrophy, aplasia, and hypoplasia
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Content Reviewers

Growing is an important part of living.

In fact, everything from an individual muscle cell, to a baby blue whale - strives to grow, in order to live and perhaps replicate or reproduce.

Sometimes, however, growth fails to occur, or even reverts back, and we call that atrophy, aplasia, or hypoplasia, depending on the situation.

Let’s break down these words. Atrophy, “a” means “no”, and “trophy”, means nourishment. So, atrophy means “no nourishment”.

Aplasia, “a” means “no” and “plasia” means development. So aplasia means “no development”, and “hypo” means “under” so hypoplasia is “under formation”.

In a nutshell, atrophy is the reduction in size of a cell, organ, or tissue, after it has attained its normal, matured growth.

This happens either through decrease in cell number or decrease in cell size.

Decrease in cell number most commonly happens due to apoptosis, which is controlled type of cell death - a bit like cellular suicide.

An example would be weight loss. In the first few weeks to months of eating healthy and losing weight, the fat cells or adipocytes get smaller but are ready to fill up again with fat.

Over months to years of eating healthy, however, the adipocytes undergo apoptosis - and at that point it’s a bit more difficult to gain back the weight.

Decrease in cell size, however, is a bit more complex.

Usually, the first step is the loss of nerve or hormonal supply, both of which provide nourishment to cells.

Then there’s something called the ubiquitin proteasome pathway.

You see, cells have a cytoskeleton, which is a framework of various filaments that keep the cell propped up.

As cells start getting less nourishment, those filaments get “tagged” for demolition with a protein called ubiquitin.

Ubiquitin proteins start to attach to one another - a process known as polyubiquitination.

And then an intracellular protein complex called a proteasome comes in to destroy all polyubiquitinated filaments, causing the cell to decrease in size.

Some organelles can also be tagged with ubiquitin; and when that happens, a bubble of phospholipid bilayer membrane forms around the organelle, creating a vacuole.

Next, lysosomal vesicles which are filled with degradative enzymes, fuse with the vacuole; destroying the unfortunate organelle. Like being sent off to the firing squad.

An example is muscle atrophy.

Anytime there’s long-standing disuse of muscles, like extended bedrest, zero gravity, or during long study sessions, there can be a loss of muscle mass and strength.

Key Takeaways

Atrophy, aplasia, and hypoplasia all refer to degeneration or poor growth of cells and tissues. Atrophy refers to the reduction in size of a tissue, or organ, after it had been normally formed and attained its normal growth. With aplasia there is a complete congenital lack of the cells, tissue or organ, whereas in hypoplasia, precursor cells are present, but they do not develop into their intended organs during embryogenesis. All three conditions can be caused by a variety of factors, including disease, injury, or genetic abnormalities

Sources

  1. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  2. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  3. "Yen & Jaffe's Reproductive Endocrinology" Saunders W.B. (2018)
  4. "Bates' Guide to Physical Examination and History Taking" LWW (2016)
  5. "Robbins Basic Pathology" Elsevier (2017)
  6. "Mergla K <sup>+</sup> channel induces skeletal muscle atrophy by activating the ubiquitin proteasome pathway" The FASEB Journal (2006)
  7. "Cancer cachexia" International Journal of Cardiology (2002)
  8. "Nutritional Considerations in Preventing Muscle Atrophy" Advances in Experimental Medicine and Biology (2018)
  9. "Genetic causes of optic nerve hypoplasia" Journal of Medical Genetics (2017)