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The MORE subscribers we have the MORE unintentional ASMR videos we can post, so please SUBSCRIBE http://bit.ly/UASMR, hit that 🔔 and LIKE this video for more medical exam ASMR like this! So... here is the BEST medical exam ASMR on YouTube edited specifically for unintentional ASMR to become the best video to help fall asleep at night. Our medical exam ASMR playlist: http://bit.ly/MedicalASMR
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This hour long medical exam has a quiet doctor performing a routine medical exam with minimal talking. The video is 100% accidental ASMR and features a real doctor doing a head to toe assessment. This is honestly one of the best medical exam ASMR videos and on my all time favourite unintentional ASMR videos. This audio for this video has been significantly edited for maximum ASMR.
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Original un-edited videos:
Part 1: https://youtu.be/S5tK3Ikb7ug
Part 2: https://youtu.be/m_-ALfUmmiA
WHAT IS UNINTENTIONAL ASMR?
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NOTE: This video is being shared for #unintentionalASMR reasons only. The video has been edited from its original format for this purpose.
WHAT IS ASMR? http://ineedtosleepnow.com/what-is-asmr
ASMR definition: http://ineedtosleepnow.com/asmr-definition-what-is-the-definition-for-asmr
http://iNeedToSleepNow.com is a YouTube channel and website that curates calm softly spoken voices that serve as great unintentional #ASMR. This channel focuses primarily on soft speaking, calm softly spoken voices, unintentional ASMR interviews, relaxing voices, ASMR tingles and anything that helps you sleep.
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Selective immunoglobulin A deficiency (SIgAD) is a primary immunodeficiency disease and is the most common of the primary antibody deficiencies.[1] Total immunoglobulin A deficiency (IgAD) is defined as an undetectable serum immunoglobulin A (IgA) level at a value < 5 mg/dL (0.05 g/L) in humans. Partial IgAD refers to detectable but decreased IgA levels that are more than 2 standard deviations below normal age-adjusted means.[2, 3] IgAD is commonly associated with normal B lymphocytes in peripheral blood, normal CD4+ and CD8+ T cells, and, usually, normal neutrophil and lymphocyte counts. Anti-IgA autoantibodies of the IgG and/or IgE isotype may be present. Peripheral blood may also be affected by autoimmune cytopenias, eg, autoimmune thrombocytopenia,[4, 5] and patients may have other autoimmune phenomena. IgA was first identified by Graber and Williams in 1952; ten years later, the first patients with IgAD were described. IgAD is a heterogeneous disorder, and the results of intensive study are beginning to elucidate genetic loci and molecular pathogenesis that contribute to various subtypes of this disorder. Several lines of evidence suggest that, in many cases, IgAD and common variable immunodeficiency (CVID) have a common pathogenesis, which is discussed further in Pathophysiology. Other data indicate different genetic risk factors. Family studies show variable inheritance patterns. Familial inheritance of IgAD occurs in approximately 20% of cases,[6] and, within families, IgAD and CVID are associated.[7, 8] Many IgAD patients are asymptomatic (ie, "normal" blood donors) and are identified by finding a laboratory abnormality, without any apparent associated clinical disease. Some patients with IgAD may have the following associated conditions: (1) deficits in one or more immunoglobulin G (IgG) subclasses (this accounts for 20-30% of IgA-deficient patients, many of whom may have total IgG levels within the normal range) or (2) a deficient antibody response to pneumococcal immunization (specific polysaccharide antibody deficiency [SPAD]). Some patients with IgAD later develop CVID, and family members of patients with CVID may have only selective IgAD. Characterization of the receptor for the transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI), encoded by the gene TNFRSF13B ( tumor necrosis factor receptor superfamily member 13B), suggests that people with the C104, A181E, and ins204A variants may be at risk for IgAD that progresses to CVID.[9] Primary IgAD is permanent, and below-normal levels have been noted to remain static and persist after 20 years of observation.[10] A recent report documents a rare case of reversion.[11] Environmental factors such as drugs or infections can cause IgAD, but this form is reversible in more than half the cases (see Causes). Although individuals with IgAD have largely been considered healthy, recent studies indicate a higher rate of symptoms. A 20-year follow-up study that compared 204 healthy blood donors with incidentally identified IgAD to 237 healthy subjects with normal IgA levels demonstrated that 80% of IgAD donors and 50% of control subjects had episodes of infections, drug allergy, or autoimmune or atopic disease. Severe respiratory tract infections occurred in 26% of IgAD subjects, in 24% of subjects with decreased IgA levels, and in 8% of control subjects; however, the incidence of life-threatening infections was not increased. IgAD is more common in adult patients with chronic lung disease than in healthy age-matched control subjects.[12] Patients with IgAD are at some increased risk of developing severe reactions after receiving blood products.[13, 14, 15] IgG anti-IgA antibodies may cause severe transfusion reactions if patients with IgAD are given whole blood; therefore, IgA-poor blood or washed red cells are preferred for those patients. IgA-deficient patients with immunoglobulin E (IgE)–class anti-IgA antibodies are at risk for anaphylaxis if they receive blood or intravenous immunoglobulin, but this situation is extremely rare. Individuals with such an unusual profile should receive only low IgA intravenous immunoglobulin preparations. However, caution must be used when administering IGIV to patients with IgAD if their anti-IgA status is unknown. A history devoid of previous blood product administration does not exclude the possibility of anti-IgA antibodies or adverse reactions. Fortunately, appropriate precautions can significantly reduce morbidity (see Treatment). Blood banks can use a simple ELISA screening approach to establish an IgAD blood donor poo
This video provides a demonstration of how to assess for transillumination when assessing scrotal swelling.
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An abscess is an infectious process characterized by a collection of pus surrounded by inflamed tissue. [1, 2] Abscesses can form anywhere in the body, from a superficial skin (subcutaneous) abscess to deep abscesses in muscle, organs, or body cavities. Patients with subcutaneous skin abscesses present clinically as a firm, localized, painful, erythematous swelling that becomes fluctuant (see the image below).
An ectopic pregnancy (EP) is a condition in which a fertilized egg settles and grows in any location other than the inner lining of the uterus. The vast majority of ectopic pregnancies are so-called tubal pregnancies and occur in the Fallopian tube.
Sex reassignment surgery for male-to-female involves reshaping the male genitals into a form with the appearance of, and, as far as possible, the function of female genitalia. Prior to any surgeries, patients usually undergo hormone replacement therapy (HRT), and, depending on the age at which HRT begins, facial hair removal. There are associated surgeries patients may elect to, including facial feminization surgery, breast augmentation, and various other procedures.
Butt implants are a popular plastic surgery procedure among those who wish to enhance the appearance, shape, and size of their rear ends. Buttock augmentation involves the surgical insertion of artificial body implants into a patient’s buttocks to create a larger, shapelier, and more sensuous rear end. Patients who have underdeveloped buttocks can achieve a more proportionate figure with butt implants. Women who wish to achieve an “hour glass” figure or are unhappy with the size of their buttocks can benefit from female butt implants. Men with flat or poorly developed buttocks can enhance the shape of the area to their liking with male butt implants. Many buttock augmentation patients say that their clothes fit better, they feel more attractive, and their confidence levels have improved.
This video is brought to you by the Stanford Medicine 25 to teach you the common causes of shoulder pain and how to diagnose them by the physical exam.
The Stanford Medicine 25 program for bedside medicine at the Stanford School of Medicine aims to promote the culture of bedside medicine to make current and future clinicians and other healthcare provides better at the art of physical diagnosis and more confident at the bedside of their patients.
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Website: http://stanfordmedicine25.stanford.edu/
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Diagnoses covered in this video:
Rotator Cuff Pathology
Impingement Syndrome
Biceps Tendinopathy
Adhesive Capsulitis (Frozen Shoulder)
Acromioclavicular (AC) Joint Disease
Shoulder Instability
Labral Tears (SLAP Lesions)