Archive for the tag: Disease

Inflammatory Bowel Disease – Crohns and Ulcerative Colitits

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Inflammatory Bowel Disease Clinical essentials – Dr. Kiran Peddi MRCP(UK), FRCP(London), CCT(Gastro)

Inflammatory bowel disease (IBD) is an idiopathic chronic relapsing inflammation of the bowel that presents with recurrent episodes of abdominal pain and diarrhea. There are two sub-types of IBD: Crohn’s disease and ulcerative colitis.

Interestingly, while smoking is associated with an increased risk of Crohn’s disease, it is protective for the development of ulcerative colitis.

IBD subtypes can be differentiated based on the pattern of inflammation:
โ€ข Crohn’s disease is associated with transmural inflammation. Histopathology reveals lymphoid aggregates with noncaseating granulomas.
โ€ข Ulcerative colitis is associated with mucosal inflammation (superficial submucosa may also be affected). Histopathology reveals crypt abscesses with neutrophils, but no granulomas.

IBD subtypes can be differentiated based on the affected location within the GI tract:
โ€ข Crohn’s disease begins anywhere from the mouth to anus with “skip lesions”.The terminal ileum is most commonly involved while the rectum is rarely involved.
โ€ข Ulcerative colitis begins in the rectum (always involved) and can extend up to the cecum, with continuous involvement (and sparing of the remainder of the GI tract).

IBD subtypes can be differentiated based on gross morphological appearance:
โ€ข In Crohn disease there is “cobblestone” mucosa, strictures, and creeping fat
โ€ข In ulcerative colitis, there are pseudopolyps

IBD subtypes can be differentiated based on imaging with barium contrast:
โ€ข Crohn disease may present with “string sign” (due to narrowing of the lumen)
โ€ข Ulcerative colitis may present with “lead pipe sign” (loss of haustra)

IBD subtypes can be differentiated based on associations with certain extraintestinal disorders:
โ€ข Crohn disease is associated with calcium oxalate kidney stones and gallstones
โ€ข Ulcerative colitis is associated with primary sclerosing cholangitis (p-ANCA positive)
Both subtypes are associated (to varying degrees) with the following disorders:
โ€ข Pyoderma gangrenosum
โ€ข Erythema nodosum
โ€ข Ankylosing spondylitis
โ€ข Uveitis
โ€ข Aphthous ulcers
โ€ข Arthritis

Serologic studies for the presence of anti-Saccharomyces cerevisiae antibodies (ASCA) and perinuclear anti-neutrophil cytoplasmic antibodies (p-ANCA) can contribute to the differentiation of IBD subtypes. Helpful patterns are:
โ€ข Crohn disease: ASCA-positive, p-ANCA negative
โ€ข Ulcerative colitis: ASCA-negative, p-ANCA positive

Systemic complications of both IBD subtypes include:
โ€ข Malnutrition due to intestinal inflammation. This is particularly common in patients with Crohn’s disease (which most commonly involves the terminal ileum) since the absorption of both vitamin B12 and bile salts occurs in the terminal ileum.

โ€ข Adenocarcinoma of the large colon due to persistent inflammation. This can be seen in both inflammatory bowel diseases but is more common in ulcerative colitis since ulcerative colitis always involves the colon.

The risk of developing inflammatory bowel disease-associated adenocarcinoma is proportional to:
โ€ข Disease duration (increased risk at 8-10 years)
โ€ข Extent of colonic involvement (increased risk with pancolitis)
โ€ข Frequency and intensity of inflammation (increased risk with more intense and frequent relapses)

There are several important GI complications more closely associated with Crohn disease, most notably the following:
โ€ข Obstruction caused by stricture formation
โ€ข Fistula formation
โ€ข Perianal disease
โ€ข Cholelithiasis

There are several important GI complications more closely associated with ulcerative colitis, most notably:
โ€ข Toxic megacolon
โ€ข Sclerosing cholangitis

Cutaneous pathologies that are associated with inflammatory bowel diseases include erythema nodosum and pyoderma gangrenosum.

Pyoderma gangrenosum is a neutrophilic dermatosis that appears as a purulent ulcer with a violaceous edge. The majority of patients with pyoderma gangrenosum have an associated systemic disease, most commonly inflammatory bowel disease.

Treatments for ulcerative colitis include:
โ€ข 5-aminosalicylic acid formulations (e.g. sulfasalazine, mesalamine)
โ€ข 6-mercaptopurine (purine synthesis inhibitor)
โ€ข Infliximab (anti-TNFฮฑ antibody)
โ€ข Colectomy

Treatments for Crohn disease include:
โ€ข Corticosteroids
โ€ข Azathioprine (purine synthesis inhibitor)
โ€ข Infliximab (anti-TNFฮฑ antibody)
โ€ข Adalimumab (anti-TNFฮฑ antibody)
โ€ข Antibiotics (ciprofloxacin, metronidazole)

#inflammatoryboweldisease #clinicalessentials #gastroentrology #pathology #internalmedicine #Crohndisease #Crohnsdisease #ulcerativecolitis

The Disease Model of Addiction

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Addiction needs to be treated like a disease and we need to follow the disease model.

Sickle Cell Disease, Animation

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(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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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.
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 Cรฉsar Naoum and Alia F. M. Naoum.

A Sรฃo Josรฉ 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 Cรฉsar Naoum, Aliรก 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

Why is Buerger Disease occurs more often in smokers than non-smokers? How can we treat it?

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Why is Buerger Disease occurs more often in smokers than non-smokers? How can we treat it?

Why is Buerger Disease (Thromboangiitis Obliterans) occurs more often in smokers than non-smokers? How can we treat it when diagnosed? Have you ever felt tingling or numbness in your hands or feet? Or that your hands or feet are pale or blue in color? Buerger’s disease is a rare disease of the arteries and veins in the arms and legs. In Buerger’s disease in which your blood vessels become inflamed, swell and can become blocked with blood clots.

RESOURCES & LINKS:
——————————————————————-

Questions discussed with Doctor Gwon (Leading doctor at Korea University Anam Hospital)
– What is thromboangiitis obliterans and which vessels are affected in this disease?
– What are the symptoms of Buerger’s disease?
– What are the causes of this disease? Is it like bad habits, or is it related to heredity, for example?
– What are the methods of diagnosis of Buerger’s disease?
– Can you tell us a little bit in detail about the modern medical or surgical treatments?
– Buerger’s disease, does it have certain complications on the legs?
– Is there any way to prevent it?

——————————————————————-

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Coeliac (Celiac) Disease – Overview (signs and symptoms, pathophysiology, diagnosis, treatment)

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Coeliac (Celiac) Disease - Overview (signs and symptoms, pathophysiology, diagnosis, treatment)

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Expert Insights: How do doctors test for Celiac disease?

May is Celiac disease awareness month. Dr. Wahid Wassef, MD, MPH, FACG, director of the Division of Gastroenterology and Hepatology at the UArizona College of Medicine โ€“ Phoenix, explains more about this autoimmune disease and how to get tested if you think you may have it.
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Buerger's Disease and Raynaud's – Medical-Surgical (Med-Surg) – Cardiovascular System – @Level Up RN

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Buerger's Disease and Raynaud's - Medical-Surgical (Med-Surg) - Cardiovascular System - @Level Up RN

Cathy Parkes BSN, RN, CWCN, PHN covers Buerger’s Disease and Raynaud’s. The Medical-Surgical (Med-Surg) – Cardiovascular System video tutorial series is intended to help RN and PN nursing students study for your nursing school exams, including the ATI, HESI and NCLEX.

In this video, Cathy discusses Buerger’s disease and Raynaud’s, including Raynaud’s disease and Raynaud’s phenomenon. She covers the pathophysiology, risk factors, signs/symptoms, diagnosis, treatment, and patient teaching associated with these conditions. At the end of the video, Cathy provides a quiz to test your understanding of some of the key points she covers in the video.

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#Cardiovascular #Buerger’s #Raynaud’s
00:00 Intro
00:26 Buerger’s Disease
2:35 Raynaud’s
4:33 Quiz time!
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Diagnosis and treatment of Celiac Disease

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Sheryl Pfeil, MD, a gastroenterologist at Ohio State, explains the symptoms of true Celiac disease and its similarity to simple gluten sensitivity or other disorders. Definitive diagnosis may require bloodwork and evaluation or sampling of the digestive tract during an endoscopy. If confirmed, patients with true Celiac disease can eliminate symptoms and effectively โ€œcureโ€ themselves with strict adherence to a gluten-free, or wheat-free diet. To learn more or to schedule an appointment, visit https://internalmedicine.osu.edu/digestivediseases/ or call (614) 293-6255.

What is the Disease Model of Addiction?

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This video describes the disease model of addiction. The disease model of addiction states that changes in the brain due to substance use greatly compromise an individualโ€™s ability to stop using drugs or alcohol. This model treats substance use disorders more like a medical condition as opposed to a โ€œdecision to stop using.โ€ Some other models of addiction more heavily weight the role of accountability, responsibility, and motivation in the recovery from substance use disorders. Many of the models offer something of value to the discussion of addiction treatment, however, it is my opinion that the disease model is currently the most useful model of addiction available.

The SIR model is one of the simplest disease models we have to explain the spread of a virus through a population. I first explain where the model comes from, including the assumptions that are made and how the equations are derived, before going on to use the results of the model to answer three important questions:

1. Will the disease spread? 6:32
2. What is the maximum number of people that will have the disease at one time? 11:00
3. How many people will catch the disease in total? 16:55

The answers to these questions are discussed in the context of the current COVID-19 (Coronavirus) outbreak. The model tells us that to reduce the impact of the disease we need to lower the โ€˜contact ratioโ€™ as much as possible โ€“ which is exactly what the current social distancing measures are designed to do.

The second video explaining Travelling Wave solutions to the SIR model is here: https://www.youtube.com/watch?v=uSLFudKBnBI

The third video including an Incubation Time in the SIR disease model is here:

Produced by Dr Tom Crawford at the University of Oxford.

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Behcet disease – causes, symptoms, diagnosis, treatment, pathology

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What is Behcet’s disease? Behcet’s disease, or Behcet disease, is a type of immune-mediated vasculitis, meaning inflammation of the blood vessels, and can affect small, medium, or large arteries or veins. Find more videos at http://osms.it/more.

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An introduction to Behcet’s Syndrome, including epidemiology, clinical features, diagnostic criteria, treatment, and prognosis. This is part of Strong Medicine’s series on Underappreciated Diseases.

There is a variety of ways in which the Behcet of Behcet’s Syndrome is pronounced around the world. In this video, I pronounce this condition with a soft ch sound (“beh-shet’s”), which is by far the most common pronunciation in the US. Internet references state that in Turkey (the home of Dr. Behcet), Behcet is pronounced with a hard ch (“Beh-chet’s”). However, the word should definitely *not* be pronounced with a silent T (“Beh-shay”).

#BehcetSyndrome #BehcetsSyndrome #BehcetDisease
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Batten Disease and Gene Therapy

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Batten disease occurs when at least one of the thirteen known ceroid lipofuscinosis (CLN) genes is mutated. Gene therapy may offer a one-time treatment to slow or ideally stop the progression of these disorders by delivering a working gene to target the cause of the disease.

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