(USMLE topics, cardiology, blood disorders) Genetics, different forms of SCD, pathophysiology, and treatment. This video is available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/all-animations/heart-and-blood-circulation-videos/-/medias/20d89e5d-4da4-4e1d-8f53-5a293088ad11-sickle-cell-disease-narrated-animation
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Voice by Ashley Fleming
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Sickle cell disease is a group of inherited blood disorders in which the body produces abnormally-shaped red blood cells that look like crescent moons or sickles. Sickle cells have a shorter-than-normal life span; their premature destruction results in shortage of red cells, known as anemia. Signs of anemia include shortness of breath, fatigue, and delayed growth in children. Unlike normal red cells which are pliant, sickle cells are rigid and also sticky. They may clump together and stick to the walls of blood vessels, causing obstruction in small vessels and subsequent reduced oxygen supply to various organs. This happens repeatedly and manifests as periodic episodes of pain, called crises, which can last hours to days, and may result in organ damage, especially in the eyes, lungs, kidneys, bones and brain. The spleen has to handle large numbers of dead red cells and becomes enlarged and fibrous, its immune function declines, making the body more vulnerable to infections. In an attempt to compensate for blood cell loss, the bone marrow tries to produce more cells and grows larger, causing bones to weaken. Other signs include jaundice, a result of rapid destruction of heme.
Hemoglobin is the major component of red blood cells and is responsible for oxygen transport. The adult hemoglobin, or hemoglobin A, is composed of 4 protein chains: 2 alpha and 2 beta. The beta subunit is encoded by the HBB gene. Several mutations in HBB gene are responsible for the disease. Each individual has two copies of HBB gene. The disease develops when both copies are mutated, producing no normal beta globin. The 2 copies may be mutated differently, producing two different forms of abnormal beta subunits in the same person. Various combinations of these mutations produce different forms of sickle cell disease, but the most common and also most severe, called sickle cell anemia, is caused by 2 copies of the same mutation producing the mutated hemoglobin S. Each copy comes from a parent. The 2 parents each carry one copy of the mutated gene, but they typically do not show any symptoms. This pattern of inheritance is called autosomal recessive.
Hemoglobin S has the tendency to form polymers under low oxygen conditions. This process is called sickling, or gelation, for the gel-like consistency of the resulting polymer. As the polymer filaments grow, they eventually involve the cell membrane and distort the cell into the characteristic crescent shape. Apart from oxygen tension, the presence of other hemoglobins also seems to affect the sickling process. Normal adult hemoglobin inhibits sickling and this explains why heterozygous parents, who produce both mutated hemoglobin S and normal hemoglobin A, do not usually develop the disease. Fetal hemoglobin F, which has 2 gamma chains in place of 2 beta chains, also suppresses sickling. Infants born with the condition seem to benefit from high levels of fetal hemoglobin in the first few months of life: they do not develop symptoms until the age of 6 months or so, when fetal hemoglobin levels drop.
Bone marrow transplantation is currently the only known cure for sickle cell disease. It involves replacing the diseased stem cells in the bone marrow with healthy cells from an eligible donor, usually a relative. The procedure however is complex and finding a suitable donor can be difficult. In most cases, treatments aim to avoid crises, relieve symptoms and prevent complications.
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Sickle Cell Anemia. Written by Paulo César Naoum and Alia F. M. Naoum.

A São José do Rio Preto’s Science and Technology Academy video.
www.ciencianews.com.br

Animated by Birdo Studio
www.birdo.com.br

Full Credits:
Production: Birdo
Script: Dr. Paulo César Naoum, Aliá F. M. Naoum
Direction: Luciana Eguti, Paulo Muppet
Storyboard: Paulo Muppet
Design: Rafael Gallardo
Animation and additional design: Antonio Linhares, Fernando Finamore, Pedro Eboli, Rafael Gallardo, William Iamazi Ferro
Sound design: Rafael Gallardo, Antonio Linhares

2011

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(USMLE topics) Crohn disease: pathophysiology, symptoms, causes, risk factors, complications, diagnosis and treatments. This video is available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/narrated-videos-by-topics/digestive-diseases/-/medias/47f8d399-6671-487c-909c-2ed1eb5b6a77-crohn-s-disease-narrated-animation
Voice by: Ashley Fleming
©Alila Medical Media. All rights reserved.
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All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition.
Crohn’s disease is one of the 2 major forms of inflammatory bowel disease. Inflammation caused by Crohn’s disease may affect any parts of the gastrointestinal tract, but it most commonly involves the end of the small bowel, the ileum, and the beginning of the colon. The inflammation is not continuous, inflamed segments are usually interrupted by normal healthy tissues.
Most people experience recurrent flares, when the disease is active, followed by symptom-free periods of remission.
Symptoms may differ depending on the parts of the digestive tract that are affected. Most common signs include diarrhea, abdominal pain and tenderness, loss of appetite, weight loss, fatigue and fever. Blood in stools occurs when the colon is involved; nausea and vomiting are usually the signs that the stomach or the first part of the small intestine is affected. About one third of patients present with perianal disease, including abscess, fistulas and ulcers. The disease also often manifests outside the intestine, especially in the joints, skin, and eyes.
Inflammation in Crohn’s disease extends to the entire thickness of the intestinal wall. Deep lesions in the mucosa often alternate with areas of mucosal swelling, creating a characteristic cobblestoned appearance. Extensive inflammation may cause thickening of the bowel wall and hypertrophy of the mesenteric fat that wraps around the intestine (creeping fat). Intestinal wall thickening, together with scar formation, may block the flow of digestive content, leading to bowel obstruction. Ulcers can extend through the bowel wall and form tunnels, called fistulas, which may connect to other loops of the intestine, to abdominal organs, muscles and even skin. A fistula may become infected and form abscesses, which can be life-threatening if not treated. In the long-term, Crohn’s disease may increase risks for colon cancers.
The disease has a major peak of onset between the age of 20 and 30, and a smaller peak later in life. White individuals, people with family history, and smokers are at higher risks.
The exact mechanism of Crohn’s disease is not fully understood, but it likely involves both genetic and environmental factors. Multiple genes are identified, most of which act in the immune system, or in maintaining the gastrointestinal epithelial barrier. This barrier separates the gut content from the underlying immune system, preventing the body from reacting to dietary antigens and resident bacteria of the gut. A crack in the barrier may increase the chance that the immune system overreacts to non-pathogenic antigens from the gut content.
Involvement of environmental factors is evidenced by higher disease incidence in developed countries, especially urban areas.
Diagnosis is made based on a combination of tests and imaging procedures.
Treatments start with dietary management to maintain good nutrition but avoid foods that may exacerbate symptoms. Some patients may benefit from nutrition therapy, a special diet given via a feeding tube or injected into a vein. The therapy provides nutrition while allowing the bowel to rest, reducing inflammation.
A number of medications can be prescribed depending on disease severity and the patient’s response to different drugs. These may include: antidiarrheals, anti-inflammatories, antibiotics, corticosteroids, immunomodulators and biologics.
Abscesses and fistulas are drained and treated with antibiotics.
Nearly half of patients require at least one surgery to manage recurrent intestinal obstructions or complicated fistulas or abscesses. Surgical removal of the diseased parts of the bowel may improve symptoms temporarily, but is not a cure, because the disease is likely to recur, usually near the reconnected tissue.
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Crohn’s disease is difficult to diagnose, because the symptoms overlap with other diseases. Physicals, x-rays, colonoscopies and biopsies aid in diagnosis.
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Crowdfunding Sex and Taxes: https://sexandtaxes.georgeoughttohelp.com/

Based on an essay by Roderick T. Long: http://www.freenation.org/a/f12l3.html

A facebook page about my video work: https://www.facebook.com/georgeoughttohelp/

Please feel free to provide caption translations.

If you’d like to dub the video with narration in a different language, please use the files I’ve posted here for a higher quality result than downloading the original material from YouTube:
https://archive.org/details/hgsthc

Roderick T. Long’s bibliography:

David T. Beito. “The ‘Lodge Practice Evil’ Reconsidered: Medical Care Through Fraternal Societies, 1900-1930.” (unpublished)

David T. Beito. “Mutual Aid for Social Welfare: The Case of American Fraternal Societies.” Critical Review, Vol. 4, no. 4 (Fall 1990).

David Green. Reinventing Civil Society: The Rediscovery of Welfare Without Politics. Institute of Economic Affairs, London, 1993.

David Green. Working Class Patients and the Medical Establishment: Self-Help in Britain from the Mid-Nineteenth Century to 1948. St. Martin’s Press, New York, 1985.

David Green & Lawrence Cromwell. Mutual Aid or Welfare State: Australia’s Friendly Societies. Allen & Unwin, Sydney, 1984.

P. Gosden. The Friendly Societies in England, 1815-1875. Manchester University Press, Manchester, 1961.

P. Gosden. Self-Help: Voluntary Associations in the 19th Century. Batsford Press, London, 1973.

Albert Loan. “Institutional Bases of the Spontaneous Order: Surety and Assurance.” Humane Studies Review, Vol. 7, no. 1, 1991/92.

Leslie Siddeley. “The Rise and Fall of Fraternal Insurance Organizations.” Humane Studies Review, Vol. 7, no. 2, 1992.

S. David Young. The Rule of Experts: Occupational Licensing in America. Cato Institute, Washington, 1987.
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Dr Reality brings you the data showing India and Spain have now achieved herd immunity, as Dave predicted on Sept 8th.

Dave wonders whether ‘government health experts’ are fools or liars when they claim not to understand readily discernible dynamics of how a virus operates in society.

Why we need to change the language we use when discussing “herd immunity”.

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