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Haemochromatosis is protean in its manifestations, i.e., often presenting with signs or symptoms suggestive of other diagnoses that affect specific organ systems.Many of the signs and symptoms below are uncommon, and most patients with the hereditary form of haemochromatosis do not show any overt signs of disease nor do they have premature morbidity, if they are diagnosed early, but, more ...
Disease progresses slowly, and lifespan is shortened. Congenital muscular dystrophy includes several disorders with a range of symptoms. Muscle degeneration may be mild or severe. Problems may be restricted to skeletal muscle, or muscle degeneration may be paired with effects on the brain and other organ systems. [14]
As muscle hypertrophy is a response to strenuous anaerobic activity, ordinary everyday activity would become strenuous in diseases that result in premature muscle fatigue (neural or metabolic), or disrupt the excitation-contraction coupling in muscle, or cause repetitive or sustained involuntary muscle contractions (fasciculations, myotonia, or ...
H&E stain. Prussian blue iron staining, highlighting the hemosiderin pigment as blue. This finding indicates mesenchymal iron overload (within Kupffer cells and/or portal macrophages) rather than parenchymal iron overload (within hepatocytes). [7] There are several methods available for diagnosing and monitoring hemosiderosis including: Serum ...
Iron overload (also known as haemochromatosis or hemochromatosis) is the abnormal and increased accumulation of total iron in the body, leading to organ damage. [1] The primary mechanism of organ damage is oxidative stress, as elevated intracellular iron levels increase free radical formation via the Fenton reaction.
It is used to show gliosis in the central nervous system, tumours of skeletal muscles, and fibrin deposits in lesions. Muscle is stained blue-black to dark brown, connective tissue is pale orange-pink to brownish red, fibrin and neuroglia stain deep blue, coarse elastic fibers show as purple, and bone and cartilage obtain yellowish to brownish ...
Glycogen storage disease type II (GSD-II), also called Pompe disease, and formerly known as GSD-IIa or Limb–girdle muscular dystrophy 2V, is an autosomal recessive metabolic disorder [1] which damages muscle and nerve cells throughout the body.
The disease is named because it is a porphyria that often presents with skin manifestations later in life. The disorder results from low levels of the enzyme responsible for the fifth step in heme production. Heme is a vital molecule for all of the body's organs. It is a component of hemoglobin, the molecule that carries oxygen in the blood.