Steatosis

Jump to: navigation, search

WikiDoc Resources for Steatosis

Articles

Most recent articles on Steatosis

Most cited articles on Steatosis

Review articles on Steatosis

Articles on Steatosis in N Eng J Med, Lancet, BMJ

Media

Powerpoint slides on Steatosis

Images of Steatosis

Photos of Steatosis

Podcasts & MP3s on Steatosis

Videos on Steatosis

Evidence Based Medicine

Cochrane Collaboration on Steatosis

Bandolier on Steatosis

TRIP on Steatosis

Clinical Trials

Ongoing Trials on Steatosis at Clinical Trials.gov

Trial results on Steatosis

Clinical Trials on Steatosis at Google

Guidelines / Policies / Govt

US National Guidelines Clearinghouse on Steatosis

NICE Guidance on Steatosis

NHS PRODIGY Guidance

FDA on Steatosis

CDC on Steatosis

Books

Books on Steatosis

News

Steatosis in the news

Be alerted to news on Steatosis

News trends on Steatosis

Commentary

Blogs on Steatosis

Definitions

Definitions of Steatosis

Patient Resources / Community

Patient resources on Steatosis

Discussion groups on Steatosis

Patient Handouts on Steatosis

Directions to Hospitals Treating Steatosis

Risk calculators and risk factors for Steatosis

Healthcare Provider Resources

Symptoms of Steatosis

Causes & Risk Factors for Steatosis

Diagnostic studies for Steatosis

Treatment of Steatosis

Continuing Medical Education (CME)

CME Programs on Steatosis

International

Steatosis en Espanol

Steatosis en Francais

Business

Steatosis in the Marketplace

Patents on Steatosis

Experimental / Informatics

List of terms related to Steatosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

Histological section of a murine liver showing severe steatosis. The clear vacuoles would have contained lipid in the living cells, however the histological fixation caused it to be dissolved and hence only empty spaces remain

In cellular pathology, steatosis (also called fatty change) is the process describing the abnormal retention of lipids within a cell. It reflects an impairment of the normal processes of synthesis and breakdown of triglyceride fat. Excess lipid accumulates in vesicles that displace the cytoplasm. When the vesicles are large enough to distort the nucleus, the condition is known as macrovesicular steatosis, otherwise the condition is known as microvesicular steatosis. Whilst not particularly detrimental to the cell in mild cases, large accumulations can disrupt cell constituents, and in severe cases the cell may even burst.

The risk factors associated with steatosis are varied, and include diabetes mellitus,[1] protein malnutrition,[2] hypertension[3] cell toxins, obesity,[4] and anoxia.[5] As the liver is the primary organ of lipid metabolism it is most often associated with steatosis, however it may occur in any organ, commonly the kidneys, heart, and muscle.[5]

Historical Perspective

Classification

Pathophysiology

Pathogenesis

No single mechanism leading to steatosis exists, rather a varied multitude of pathologies disrupt normal lipid movement through the cell and cause accumulation. These mechanisms can be separated on whether they ultimately cause an oversupply of lipid which can not be removed quickly enough (too much in), or whether they cause a failure in lipid breakdown (not enough being utilised).

Oversupply of lipid may occur due to obesity, insulin resistance, or alcoholism. Nutrient malnutrition may also cause the mobilisation of fat from adipocytes and create a local oversupply in the liver where lipid metabolism occurs. Excess alcohol over a long period of time can induce steatosis. The breakdown of large amounts of ethanol in alcoholic drinks produces large amounts of chemical energy, in the form of NADH, signalling to the cell to inhibit the breakdown of fatty acids (which also produces energy) and simultaneously increase the synthesis of fatty acids. This "false sense of energy" results in more lipid being created than is needed.

Failure of lipid metabolism can also lead to the mechanisms which would normally utilise or remove lipids becoming impaired, resulting in the accumulation of unused lipids in the cell. Certain toxins, such as alcohols, carbon tetrachloride, aspirin, and diphtheria toxin, interfere with cellular machinery involved in lipid metabolism. In those with Gaucher's disease, the lysosomes fail to degrade lipids and steatosis arises from the accumulation of glycolipids. Protein malnutrition, such as that seen in kwashiorkor, results in a lack of precursor apoproteins within the cell, therefore unused lipids which would normally participate in lipoprotein synthesis begin to accumulate.

Causes

Drug Side Effect

Differentiating Steatosis from Other Diseases

Epidemiology and Demographics

Appearance

Histologically, steatosis is physically apparent as lipid within membrane bound liposomes of parenchymal cells[5]. When this tissue is fixed and stained to be better viewed under a microscope, the lipid is usually dissolved by the solvents used to prepare the sample. As such, samples prepared this way will appear to have empty holes within the cells where the lipid has been cleared. Special lipid stains, such as Sudan stains and osmium tetroxide are able to retain and show up lipid droplets, hence more conclusively indicating the presence of lipids. Other intracellular accumulations, such as water or glycogen, can also appear as clear vacuoles, therefore it becomes necessary to use stains to better decide what is accumulating.

Grossly, steatosis causes organ enlargement and lightning in colour[5]. This is due to the high lipid content increasing the organ's volume and becoming visible to the unaided eye. In severe cases, the organ may become vastly enlarged, greasy, and yellow in appearance.

Risk Factors

Screening

Natural History, Complications, and Prognosis

Diagnosis

Diagnosis Criteria

History and Symptoms

Physical Examination

Laboratory Findings

Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Prevention

Related Chapters

References

  1. Araya Q AV; et al. (2006). "Glucose tolerance alterations and frequency of metabolic syndrome among patients with non alcoholic fatty liver disease". Rev Med Chil. 134 (9): 1092-1098.
  2. Conde Martel A; et al. (1993). "Liver changes in protein malnutrition. An experimental study in rats". Nutr Hosp. 8 (6): 358-363.
  3. MJ Brookes, BT Cooper (2007). "Hypertension and fatty liver: guilty by association?". J Hum Hypertens. 21 (4): 264-270.
  4. S Saadeh (2007). "Nonalcoholic Fatty liver disease and obesity". Nutr Clin Pract. 22 (1): 1-10.
  5. 5.0 5.1 5.2 5.3 Cotran. Robbins Pathologic Basis of Disease. Philadelphia: W.B Saunders Company. 0-7216-7335-X. Unknown parameter |coauthors= ignored (help)

it:Steatosi



Linked-in.jpg