Atrophy, aplasia, and hypoplasia

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Atrophy, aplasia, and hypoplasia

Foundations

Foundations

Introduction to the immune system
Innate immune system
Complement system
Contracting the immune response and peripheral tolerance
Cytokines
Monoclonal antibodies
Antibody classes
Bacterial structure and functions
B-cell development
B-cell activation, differentiation, and contraction
T-cell development
T-cell activation
B- and T-cell memory
MHC class I and MHC class II molecules
Thymus histology
Cell cycle
Mitosis and meiosis
DNA replication
DNA damage and repair
DNA mutations
Cell membrane
Free radicals and cellular injury
Hypoxia
Necrosis and apoptosis
Inflammation
Crohn disease
Gout
Gout and pseudogout: Pathology review
Inclusion body myopathy
Inflammatory bowel disease: Pathology review
Papulosquamous and inflammatory skin disorders: Pathology review
Myasthenia gravis
Systemic lupus erythematosus
Type I hypersensitivity
Type II hypersensitivity
Type III hypersensitivity
Type IV hypersensitivity
Serum sickness
Anaphylaxis
Graft-versus-host disease
Systemic lupus erythematosus (SLE): Pathology review
Pemphigus vulgaris
Stevens-Johnson syndrome
Rheumatic heart disease
Heart failure: Pathology review
Thrombosis syndromes (hypercoagulability): Pathology review
Body fluid compartments
Movement of water between body compartments
Hyponatremia
Pulmonary edema
Lymphedema
Coagulation (secondary hemostasis)
Platelet plug formation (primary hemostasis)
Erythropoietin
Hemophilia
Coagulation disorders: Pathology review
Platelet disorders: Pathology review
Blood components
Protein C deficiency
Protein S deficiency
Metaplasia and dysplasia
Multiple endocrine neoplasia: Pathology review
Oncogenes and tumor suppressor genes
Amyloidosis
Atrophy, aplasia, and hypoplasia
Environmental and chemical toxicities: Pathology review
Medication overdoses and toxicities: Pathology review
Multiple endocrine neoplasia
Substance misuse and addiction: Clinical
Toxidromes: Clinical
Deep vein thrombosis and pulmonary embolism: Pathology review
Heparin-induced thrombocytopenia
Myocardial infarction
Shock
Arterial disease
Atherosclerosis and arteriosclerosis: Pathology review
Carbohydrates and sugars
Childhood nutrition and obesity: Information for patients and families (The Primary School)
Fat-soluble vitamin deficiency and toxicity: Pathology review
Folate (Vitamin B9) deficiency
Iron deficiency anemia
Osteomalacia and rickets
Vitamin B12 deficiency
Water-soluble vitamin deficiency and toxicity: B1-B7: Pathology review
Wernicke-Korsakoff syndrome
Zinc deficiency and protein-energy malnutrition: Pathology review
Burns: Clinical
Burns
Hyperplasia and hypertrophy
Down syndrome (Trisomy 21)
Edwards syndrome (Trisomy 18)
Patau syndrome (Trisomy 13)
Klinefelter syndrome
Turner syndrome
Angelman syndrome
Prader-Willi syndrome
Fragile X syndrome
DiGeorge syndrome
Phenylketonuria (NORD)
Homocystinuria
Maple syrup urine disease
Disorders of fatty acid metabolism: Pathology review
Ornithine transcarbamylase deficiency
Post-transplant lymphoproliferative disorders (NORD)
Cytomegalovirus infection after transplant (NORD)
Epigenetics
Gene regulation
Independent assortment of genes and linkage
Inheritance patterns
Mendelian genetics and punnett squares
Evolution and natural selection
Antiphospholipid syndrome
Celiac disease
Graves disease
Multiple sclerosis
Diabetes mellitus
Chronic granulomatous disease
Immunodeficiencies: Clinical
Immunodeficiencies: Phagocyte and complement dysfunction: Pathology review
Immunodeficiencies: Combined T-cell and B-cell disorders: Pathology review
Immunodeficiencies: T-cell and B-cell disorders: Pathology review
Candida
Mycobacterium tuberculosis (Tuberculosis)
Tuberculosis: Pathology review
Pneumonia: Pathology review
Pneumonia
Salmonella (non-typhoidal)
Viral structure and functions
Hepatitis medications
Herpesvirus medications
Neuraminidase inhibitors
HIV (AIDS)
Nucleoside reverse transcriptase inhibitors (NRTIs)
Integrase and entry inhibitors
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Protease inhibitors
Vaccinations: Clinical
The flu vaccine: Information for patients and families
Vaccinations

Transcript

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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

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  2. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
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  4. "Bates' Guide to Physical Examination and History Taking" LWW (2016)
  5. "Robbins Basic Pathology" Elsevier (2017)
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  9. "Genetic causes of optic nerve hypoplasia" Journal of Medical Genetics (2017)