Symptoms, epidemiology, pathophysiology, diagnosis and treatment. For patient education. This video is available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/all-animations/microbiology-videos/-/medias/f9bc98ae-8008-40c3-8952-99c6def7864b-infectious-mononucleosis-narrated-animation
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Infectious mononucleosis, or mono, is a very common syndrome characterized by the triad of fever, swollen lymph nodes (lymphadenopathy) – most frequently in the neck, and sore throat with inflamed tonsils (tonsillar pharyngitis). Patients may also present with headache, fatigue, and enlarged spleen upon physical examination. The syndrome can be caused by several different agents, but the most common is Epstein-Barr virus, EBV; and the term “mononucleosis” usually refers to the disease caused by EBV.
EBV is ubiquitous in human. About 95% of all adults have antibodies against EBV, likely from an infection during childhood. Symptomatic infections are most prevalent in older teens and young adults, especially among college students. Infected young children are often asymptomatic or have mild symptoms. Older adults are either immune to the disease thanks to an earlier infection, or have atypical presentations that are misdiagnosed.
EBV is transmitted mainly via infected saliva. The virus is not very contagious, it takes several exposures to high viral loads to acquire EBV. Hence, kissing is the major route of transmission and mono is colloquially known as “the kissing disease”.
The incubation period is typically 3 to 5 weeks. The disease is self-limited and patients usually recover after 2 to 6 weeks, but the virus may remain in the saliva for months. Recovered patients may also shed virus periodically for life without developing symptoms. This is why most people get infected by an asymptomatic person and often cannot recall being exposed to EBV.
After infecting the oral epithelial cells, EBV attacks lymphocytes, in particular B-cells, in the tonsils. Infection then spreads throughout the lymphatic system, causing a massive immune response that is responsible for most of the symptoms. The immune response produces antibodies against EBV, providing lifelong immunity to EBV. At the same time, infection by EBV causes B-cells to proliferate and become antibody-producing plasma cells. Because B-cells are the source of antibodies of all kinds, NON-specific antibodies that do not react to EBV antigens are also produced. These so-called heterophile antibodies may be responsible for the mild thrombocytopenia, generalized rash, and antibiotic-related rash that are occasionally associated with mononucleosis.
As part of the immune defense, cytotoxic T-cells are increased in numbers and activated to kill EBV-infected B-cells. These T-cells have atypical morphology; they are known as Downey cells and are part of the diagnostic workup.
There are 2 antibody tests for mono: monospot test for heterophile antibodies, and EBV-specific antibody test. The monospot test is highly specific, but may give false-negative results in the first week of illness, and has low sensitivity, especially in children. EBV antibody test is performed when monospot test is negative but mono is still suspected.
Mononucleosis is often misdiagnosed as strep throat, and antibiotics may be given inappropriately. Antibiotic treatment can cause a rash to develop and this is often mistaken for antibiotic allergy.
Mononucleosis is self-limited, most patients fully recover after a few weeks, although fatigue may persist for months. Complications are rare but can be severe, sometimes life-threatening.
Treatment is supportive and includes bed rest, hydration, and fever and inflammation reducer. Heavy lifting and active sports must be avoided for a month to prevent splenic rupture. Corticosteroids can be helpful in certain complications, such as impending airway obstruction, but are not usually recommended for uncomplicated disease.
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Could having mononucleosis, otherwise known as mono or “The Kissing Disease,” lead to developing other possibly harmful autoimmune health concerns like lupus and celiac disease?

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(USMLE topics) Pathophysiology of HDN, Signs and Symptoms, Prevention and Treatment options.
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Voice by Ashley Fleming

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Hemolytic disease of the newborn, HDN, is a condition in which red blood cells of a newborn infant, or a perinatal fetus, are destroyed prematurely, resulting in anemia. HDN occurs when the blood types of the mother and baby are incompatible. A blood type refers to the presence or absence of a certain antigen, on the surface of a person’s red blood cells. Incompatibility happens when the baby has an antigen that the mother does not have. The mother’s immune system interprets the antigen as “foreign” and produces antibodies to target the cells carrying it for destruction.
While in principle HDN may occur with mismatch in any blood group, severe cases most commonly involve D-antigen of the Rh system. Specifically, HDN may develop if an Rh-negative mother, having no D-antigen, carries an Rh-positive fetus, with D-antigen. The first mismatch pregnancy, however, is usually not at risk. This is because the placenta normally does a good job separating the mother’s blood from the fetal blood, preventing the fetal red blood cells from being exposed to the mother’s immune system. However, at birth, or if a miscarriage or abortion occurs, the tearing of the placenta exposes fetal blood to the mother, who then responds by producing anti-D antibodies. Because antibody production takes some time, it does not affect the first baby; but if the mother is again pregnant with another Rh-positive fetus, her antibodies, being small enough to cross the placenta, can now cause hemolysis.
The first mismatch pregnancy may be at risk if the mother has previously been exposed to the antigen in other ways, such as through blood transfusion or sharing needles, or if the placental barrier is breached because of trauma, or medical procedures early in the pregnancy.
Anemia can cause heart failure, respiratory distress, and edema. Infants born with HDN also develop jaundice due to the accumulation of bilirubin, a yellow product of hemoglobin breakdown. Because red blood cells are destroyed rapidly and infants are unable to excrete bilirubin effectively, its levels rise quickly within 24h of birth. Bilirubin is toxic for brain tissues and may cause irreversible brain damage in a condition known as kernicterus. Other signs of HDN include enlarged liver, spleen, and presence of immature red blood cells, erythroblasts, in the blood. Some of these signs can be detected before birth, with ultrasound imaging.
HDN that involves D-antigen can now be effectively prevented with anti-D antibody. It is given to Rh-negative mothers during and soon after the first mismatch pregnancy. The antibody binds to fetal blood cells that leak into the mother’s blood, either destroying them, or hiding them from the mother’s immune system, thus preempting the mother’s immune response.
Infants born with HDN are usually treated with intravenous fluid, and phototherapy, a procedure in which a certain spectrum of light is used to convert bilirubin to a form that is easier for the infant to excrete.
Severe anemia may be treated with:
– blood transfusion,
– intravenous immunoglobulin G therapy, which works by blocking the destruction of antibody-coated red blood cells.
– and exchange transfusion, where the baby’s blood is essentially replaced with Rh-negative donor blood. This procedure is very effective at removing bilirubin and reducing the destructive effect of the mother’s antibody, but may have adverse effects.
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(USMLE topics, cardiology) Life and death of erythrocytes, anemia and polycythemia. This video is available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/all-animations/heart-and-blood-circulation-videos/-/medias/5519909f-97f9-44f6-a806-0c87af9addb7-red-blood-cell-disorders-narrated-animation
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Voice by Ashley Fleming
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Production of red blood cells occurs in the red bone marrow, and is stimulated by erythropoietin, EPO. EPO is secreted predominantly by the kidneys. The kidneys sense oxygen levels in the blood and adjust EPO secretion accordingly to the body’s needs.
Red cells live about 100 to 120 days. With age, the cells lose their elasticity. Without protein synthesis, they are unable to repair themselves. Worn-out red cells are detected in the spleen, which serves as a quality control center. The spleen has a network of very narrow channels which test the agility of erythrocytes. Healthy cells can bend and fold to squeeze through, while old cells, being rigid and fragile, get stuck and are destroyed by macrophages. Parts of the dead cells are salvaged to make new cells. Part of the heme is secreted into bile and disposed in feces.
The number of red blood cells is strictly regulated and has important clinical significance. Common measurements include red blood cell count, hematocrit, and hemoglobin concentration.
An imbalance between the rate of red cell production and death can result in their deficiency, known as anemia, or excess, known as polycythemia.
Anemia can be caused by blood loss, insufficient erythrocyte production, or their premature destruction.
Insufficient red cell production can result from:
+ deficiency of any of the nutrients that are required for their formation,
+ impaired kidney function, which leads to lower secretion of EPO,
+ or destruction of the bone marrow tissue responsible for red cell production. This can happen because of inherited mutations, autoimmune diseases, or exposure to chemicals, drugs or radiation; but causes are unknown for many cases. Reduced erythropoiesis is known as hypoplastic anemia, while complete cessation of red cell production is called aplastic anemia.
Inappropriate destruction of red blood cells, also called hemolytic anemia, can be inherited or acquired. The inherited forms are usually due to defects within red cells themselves, such as abnormalities in hemoglobin structure, while acquired hemolytic anemia can be caused by toxins, drugs, autoimmune diseases, infection, overactive spleen, or blood group mismatch.
Anemia results in low oxygen levels in the blood, known as hypoxemia. Mild anemia causes weakness and confusion, while severe anemia may lead to organ failure due to lack of oxygen and is life-threatening.
Excess red cell production, or polycythemia, can be primary or secondary. Primary polycythemia, or polycythemia vera, is a form of blood cancer, where the bone marrow produces too many blood cells. Secondary polycythemia, on the other hand, is a consequence of low oxygen state, which induces the kidneys to produce more erythropoietin, subsequently leading to more erythrocytes. Causes include smoking, air pollution, emphysema, living at high altitudes, and physical strenuous conditioning in athletes.
Excess red cells may increase blood volume, blood pressure, and viscosity. This augments the risks for blood clot formation, which may lead to heart attacks, strokes, and pulmonary embolism. The heart also has to work harder to manage larger amount of thicker blood and heart failures may result.

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Created on Dec 12, 2012
This video looks at diabetic retinopathy, the most common eye disease among working-age adults in the U.S. and a leading cause of blindness in people with diabetes.
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