Lupus Manifestations
Diagnostic Criteria For Systemic Lupus Erythematosus, ACR
The American College of Rheumatology established eleven criteria in 1982, which were revised in 1997 as a classificatory instrument to operationalise the definition of SLE in clinical trials. They were not intended to be used to diagnose individuals and do not do well in that capacity. For the purpose of identifying patients for clinical studies, a person has SLE if any 4 out of 11 symptoms are present simultaneously or serially on two separate occasions.
1. Serositis: Pleuritis (inflammation of the membrane around the lungs) or pericarditis (inflammation of the membrane around the heart); sensitivity = 56%; specificity = 86% (pleural is more sensitive; cardiac is more specific).
2. Oral ulcers (includes oral or nasopharyngeal ulcers).
3. Arthritis: nonerosive arthritis of two or more peripheral joints, with tenderness, swelling, or effusion; sensitivity = 86%; specificity = 37%.
4. Photosensitivity (exposure to ultraviolet light causes skin rash, or other symptoms of SLE flareups); sensitivity = 43%; specificity = 96%.
5. Blood—hematologic disorder—hemolytic anemia (low red blood cell count) or leukopenia (white blood cell count<4000/µl), class="mw-redirect">lymphopenia (<1500/µl) sensitivity =" 59%;" specificity ="">
6. Renal disorder: More than 0.5g per day protein in urine or cellular casts seen in urine under a microscope; sensitivity = 51%; specificity = 94%.
7. Antinuclear antibody test positive; sensitivity = 99%; specificity = 49%.
8. Immunologic disorder: Positive anti-Smith, anti-ds DNA, antiphospholipid antibody, and/or false positive serological test for syphilis; sensitivity = 85%; specificity = 93%. Presence of anti-ss DNA in 70% of cases (though also positive with rheumatic disease and healthy persons)
9. Neurologic disorder: Seizures or psychosis; sensitivity = 20%; specificity = 98%.
10. Malar rash (rash on cheeks); sensitivity = 57%; specificity = 96%.
11. Discoid rash (red, scaly patches on skin that cause scarring); sensitivity = 18%; specificity = 99%.
The mnemonic to remember the 11 symptoms is 'SOAP BRAIN MD'.
Some people, especially those with antiphospholipid syndrome, may have SLE without four criteria, and also SLE may present with features other than those listed in the criteria.
1. Serositis: Pleuritis (inflammation of the membrane around the lungs) or pericarditis (inflammation of the membrane around the heart); sensitivity = 56%; specificity = 86% (pleural is more sensitive; cardiac is more specific).
2. Oral ulcers (includes oral or nasopharyngeal ulcers).
3. Arthritis: nonerosive arthritis of two or more peripheral joints, with tenderness, swelling, or effusion; sensitivity = 86%; specificity = 37%.
4. Photosensitivity (exposure to ultraviolet light causes skin rash, or other symptoms of SLE flareups); sensitivity = 43%; specificity = 96%.
5. Blood—hematologic disorder—hemolytic anemia (low red blood cell count) or leukopenia (white blood cell count<4000/µl), class="mw-redirect">lymphopenia (<1500/µl) sensitivity =" 59%;" specificity ="">
6. Renal disorder: More than 0.5g per day protein in urine or cellular casts seen in urine under a microscope; sensitivity = 51%; specificity = 94%.
7. Antinuclear antibody test positive; sensitivity = 99%; specificity = 49%.
8. Immunologic disorder: Positive anti-Smith, anti-ds DNA, antiphospholipid antibody, and/or false positive serological test for syphilis; sensitivity = 85%; specificity = 93%. Presence of anti-ss DNA in 70% of cases (though also positive with rheumatic disease and healthy persons)
9. Neurologic disorder: Seizures or psychosis; sensitivity = 20%; specificity = 98%.
10. Malar rash (rash on cheeks); sensitivity = 57%; specificity = 96%.
11. Discoid rash (red, scaly patches on skin that cause scarring); sensitivity = 18%; specificity = 99%.
The mnemonic to remember the 11 symptoms is 'SOAP BRAIN MD'.
Some people, especially those with antiphospholipid syndrome, may have SLE without four criteria, and also SLE may present with features other than those listed in the criteria.
Bed Bug Bites
Disease transmission
Bedbugs seem to possess all of the necessary prerequisites for being capable of passing diseases from one host to another, but there have been no known cases of bed bugs passing disease from host to host. There are at least twenty-seven known pathogens (some estimates are as high as forty-one) that are capable of living inside a bed bug or on its mouthparts. Extensive testing has been done in laboratory settings that also conclude that bed bugs are unlikely to pass disease from one person to another. Therefore bedbugs are less dangerous than some more common insects such as the flea. However, transmission of Chagas disease or hepatitis B might be possible in appropriate settings.
The salivary fluid injected by bed bugs typically causes the skin to become irritated and inflamed, although individuals can differ in their sensitivity. Anaphylactoid reactions produced by the injection of serum and other nonspecific proteins are observed and there is the possibility that the saliva of the bedbugs may cause anaphylactic shock in a small percentage of people. It is also possible that sustained feeding by bedbugs may lead to anemia. It is also important to watch for and treat any secondary bacterial infection.
Bedbugs seem to possess all of the necessary prerequisites for being capable of passing diseases from one host to another, but there have been no known cases of bed bugs passing disease from host to host. There are at least twenty-seven known pathogens (some estimates are as high as forty-one) that are capable of living inside a bed bug or on its mouthparts. Extensive testing has been done in laboratory settings that also conclude that bed bugs are unlikely to pass disease from one person to another. Therefore bedbugs are less dangerous than some more common insects such as the flea. However, transmission of Chagas disease or hepatitis B might be possible in appropriate settings.
The salivary fluid injected by bed bugs typically causes the skin to become irritated and inflamed, although individuals can differ in their sensitivity. Anaphylactoid reactions produced by the injection of serum and other nonspecific proteins are observed and there is the possibility that the saliva of the bedbugs may cause anaphylactic shock in a small percentage of people. It is also possible that sustained feeding by bedbugs may lead to anemia. It is also important to watch for and treat any secondary bacterial infection.
Top 10 Epidemics of All time
Plague
Smallpox| Measles |  | Number 10 |
| Polio | | Number 9 |
| Yellow Fever | | Number 8 |
| AIDS | | Number 7 |
| Malaria | | Number 6 |
| Tuberculosis (TB) | | Number 5 |
| Cholera | | Number 4 |
| Plague (bubonic and Pneumonic) | | Number 3 |
| Smallpox | | Number 2 |
| Influenza or “flu” | | Number 1 |
Choked Adult - How can you save him.
In a Party, An adult has something stuck to his throat, turns blue and is suffocating.
Watching this video can train you to manage and save such cases
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Myasthenia Gravis and Lambert Eaton
Myasthenia gravi
s
Ptosis of the left eye. Tensilon test
Imaging
sMyasthenia gravis (literally "serious muscle-weakness") is a neuromuscular disease leading to fluctuating muscle weakness and fatiguability. It is an autoimmune disorder, in which weakness is caused by circulating antibodies that block acetylcholine receptors at the post-synaptic neuromuscular junction, inhibiting the stimulative effect of the neurotransmitter acetylcholine. Myasthenia is treated medically with cholinesterase inhibitors or immunosuppressants, and, in selected cases, thymectomy. At 200–400 cases per million it is one of the less common autoimmune disorders.
Signs and symptoms
Ptosis of the left eye.
The hallmark of myasthenia gravis is fatiguability. Muscles become progressively weaker during periods of activity and improve after periods of rest. Muscles that control eye and eyelid movement, facial expression, chewing, talking, and swallowing are especially susceptible. The muscles that control breathing and neck and limb movements can also be affected. Often the physical examination is within normal limits.[3]
The onset of the disorder can be sudden. Often symptoms are intermittent. The diagnosis of myasthenia gravis may be delayed if the symptoms are subtle or variable.
In most cases, the first noticeable symptom is weakness of the eye muscles. In others, difficulty in swallowing and slurred speech may be the first signs. The degree of muscle weakness involved in MG varies greatly among patients, ranging from a localized form, limited to eye muscles (ocular myasthenia), to a severe or generalized form in which many muscles - sometimes including those that control breathing - are affected. Symptoms, which vary in type and severity, may include asymmetrical ptosis (a drooping of one or both eyelids), diplopia (double vision) due to weakness of the muscles that control eye movements, unstable or waddling gait, weakness in arms, hands, fingers, legs, and neck, a change in facial expression, dysphagia (difficulty in swallowing), shortness of breath and dysarthria (impaired speech, often nasal due to weakness of the velar muscles).
In myasthenic crisis a paralysis of the respiratory muscles occurs, necessitating assisted ventilation to sustain life. In patients whose respiratory muscles are already weak, crises may be triggered by infection, fever, an adverse reaction to medication, or emotional stress.[4] Since the heart muscle is stimulated differently, it is never affected by MG.
DiagnosisMyasthenia can be a difficult diagnosis, as the symptoms can be subtle and hard to distinguish from both normal variants and other neurological disorders. A thorough physical examination can reveal easy fatiguability, with the weakness improving after rest and worsening again on repeat of the exertion testing. Applying ice to weak muscle groups characteristically leads to improvement in strength of those muscles. Additional tests are often performed, as mentioned below. Furthermore, a good response to medication can also be considered a sign of autoimmune pathology.
Physical examination
Muscle fatigability can be tested for many muscles.A thorough investigation includes:
- looking upward and sidewards for 30 seconds: ptosis and diplopia.
- looking at the feet while lying on the back for 60 seconds
- keeping the arms stretched forward for 60 seconds
- 10 deep knee bends
- walking 30 steps on both the toes and the heels
- 5 situps, lying down and sitting up completely
- "Peek sign": after complete initial apposition of the lid margins, they quickly (within 30 seconds) start to separate and the sclera starts to show
Blood tests
If the diagnosis is suspected, serology can be performed in a blood test to identify certain antibodies:
- One test is for antibodies against the acetylcholine receptor. The test has a reasonable sensitivity of 80–96%, but in MG limited to the eye muscles (ocular myasthenia) the test may be negative in up to 50% of the cases.
- A proportion of the patients without antibodies against the acetylcholine receptor have antibodies against the MuSK protein.
- In specific situations (decreased reflexes which increase on facilitation, co-existing autonomic features, suspected presence of neoplasm, especially of the lung, presence of increment or facilitation on repetitive EMG testing) testing is performed for Lambert-Eaton syndrome, in which other antibodies (against a voltage-gated calcium channel) can be found.
Edrophonium test
Tensilon test
Imaging
A chest CT-scan showing a thymoma (red circle).
A chest X-ray is frequently performed; it may point towards alternative diagnoses (e.g. Lambert-Eaton due to a lung tumor) and comorbidity. It may also identify widening of the mediastinum suggestive of thymoma, but computed tomography (CT) or magnetic resonance imaging (MRI) are more sensitive ways to identify thymomas, and are generally done for this reason.
Pulmonary function test
Restrictive pattern on spirometry
Associations
Myasthenia Gravis is associated with various autoimmune diseases, including:
- Thyroid diseases, including Hashimoto's thyroiditis and Graves' disease
- Diabetes mellitus type 1
- Rheumatoid arthritis
- Lupus, and
- Demyelinating CNS diseases
Computer Eye Strain: Tips to relieve
Computer Eye Strain: 10 Steps for Relief
1. Get a computer eye exam.
2. Use proper lighting.
3. Minimize glare.4. Upgrade your display.
5. Adjust the brightness and contrast of your computer screen
7. Exercise your eyes.
8. Take frequent breaks.
9. Modify your workstation.
10. Consider computer eyewear.
Contact Dermatitis
Contact dermatitis is a localized rash or irritation of the skin caused by contact with a foreign substance. Only the superficial regions of the skin are affected in contact dermatitis. Inflammation of the affected tissue is present in the epidermis (the outermost layer of skin) and the outer dermis (the layer beneath the epidermis).Unlike contact urticaria, in which a rash appears within minutes of exposure and fades a
way within minutes to hours, contact dermatitis takes days to fade away. Even then, contact dermatitis fades only if the skin no longer comes in contact with the allergen or irritant. Contact dermatitis results in large, burning, and itchy rashes, and these can take anywhere from several days to weeks to heal. Chronic contact dermatitis can develop when the removal of the offending agent no longer provides expected relief.
Causes
In North/South America, the most common causes of allerg
ic contact dermatitis are plants of the Toxicodendron genus: poison ivy, poison oak, and poison sumac. Specific plant species that can induce
such contact dermatitis include Western Poison Oak, a widespread plant in the western USA. Common causes of irritant contact dermatitis are harsh (highly alkaline) soaps, detergents, and cleaning products.
Types of contact dermatitis
There are three types of contact dermatitis: irritant contact, allergic contact, and photocontact dermatitis. Photocontact dermatitis is divided into two categories: phototoxic and photoallergic.
Chemical irritant contact dermatitis
Physical irritant contact dermatitisPlants
Allergic contact dermatitisCommon allergens implicated include the following:
- Nickel (nickel sulfate hexahydrate) - metal frequently encountered in jewelry and clasps or buttons on clothing
- Gold (gold sodium thiosulfate) - precious metal often found in jewelry
- Balsam of Peru (Myroxylon pereirae) - a fragrance used in perfumes and skin lotions, derived from tree resin (see also Tolu balsam)
- Thimerosal - a mercury compound used in local antiseptics and in vaccines
- Neomycin - a topical antibiotic common in first aid creams and ointments, cosmetics, deodorant, soap and pet food. Found by itself, or in Polysporin or Triple Antibiotic
- Fragrance mix - a group of the eight most common fragrance allergens found in foods, cosmetic products, insecticides, antiseptics, soaps, perfumes and dental products [15]
- Formaldehyde - a preservative with multiple uses, e.g., in paper products, paints, medications, household cleaners, cosmetic products and fabric finishes
- Cobalt chloride - metal found in medical products; hair dye; antiperspirant; metal-plated objects such as snaps, buttons or tools; and in cobalt blue pigment
- Bacitracin - a topical antibiotic found by itself, or as Polysporin or Triple Antibiotic
- Quaternium-15 - preservative in cosmetic products (self-tanners, shampoo, nail polish, sunscreen) and in industrial products (polishes, paints and waxes).[16]
- Colophony (Rosin) - Rosin, sap or sawdust typically from spruce or fir trees
- Topical steroid - see steroid allergy
Photocontact Dermatitis
Sometimes termed "photoaggravated"(Bourke et al. 2001)[17], and divided into two categories, phototoxic and photoallergic, PCD is the eczematous condition which is triggered by an interaction between an otherwise unharmful or less harmful substance on the skin and ultraviolet light (320-400 nm UVA) (ESCD 2006), therefore manifesting itself only in regions where the sufferer has been exposed to such rays. Without the presence of these rays, the photosensitiser is not harmful. For this reason, this form of contact dermatitis is usually associated only with areas of skin which are left uncovered by clothing. The mechanism of action varies from toxin to toxin, but is usually due to the production of a photoproduct. Toxins which are associated with PCD include the psoralens. Psoralens are in fact used therapeutically for the treatment of psoriasis, eczema and vitiligo.
Photocontact dermatitis is another condition where the distinction between forms of contact dermatitis is not clear cut. Immunological mechanisms can also play a part, causing a response similar to ACD.
Symptoms
Allergic dermatitis is usually confined to the area where the trigger actually touched the skin, whereas irritant dermatitis may be more widespread on the skin. Symptoms of both forms include the following:
- Red rash. This is the usual reaction. The rash appears immediately in irritant contact dermatitis; in allergic contact dermatitis, the rash sometimes does not appear until 24–72 hours after exposure to the allergen.
- Blisters or wheals. Blisters, wheals (welts), and urticaria (hives) often form in a pattern where skin was directly exposed to the allergen or irritant.
- Itchy, burning skin. Irritant contact dermatitis tends to be more painful than itchy, while allergic contact dermatitis often itches.
While either form of contact dermatitis can affect any part of the body, irritant contact dermatitis often affects the hands, which have been exposed by resting in or dipping into a container (sink, pail, tub, Sun, Swimming Pools With High chlorine ), containing the irritant.
Treatment
Self-care at Home
- Immediately after exposure to a known allergen or irritant, wash with soap and cool water to remove or inactivate most of the offending substance.
- Weak acid solutions [lemon juice, vinegar] can be used to counteract the effects of dermatitis contracted by exposure to basic irritants [phenol etc.].
- If blistering develops, cold moist compresses applied for 30 minutes 3 times a day can offer relief.
- Calamine lotion and cool colloidal oatmeal baths may relieve itching.
- Oral antihistamines such as diphenhydramine (Benadryl, Ben-Allergin) can also relieve itching.
- For mild cases that cover a relatively small area, hydrocortisone cream in nonprescription strength may be sufficient.
- Avoid scratching, as this can cause secondary infections.
- A barrier cream such as those containing zinc oxide (e.g. Desitin, etc.) may help to protect the skin and retain moisture.
Medical Care
If the rash does not improve or continues to spread after 2-3 of days of self-care, or if the itching and/or pain is severe, the patient should contact a dermatologist or other physician or physician assistant. Medical treatment usually consists of lotions, creams, or oral medications.
- Corticosteroids. A corticosteroid medication similar to hydrocortisone may be prescribed to combat inflammation in a localized area. This medication may be applied to your skin as a cream or ointment. If the reaction covers a relatively large portion of the skin or is severe, a corticosteroid in pill or injection form may be prescribed.
- Antihistamines. Prescription antihistamines may be given if nonprescription strengths are inadequate.
Prevention
Since contact dermatitis relies on an irritant or an allergen to initiate the reaction, it is important for the patient to identify the responsible agent and avoid it. This can be accomplished by having patch tests, a method commonly known as allergy testing. The patient must know where the irritant or allergen is found to be able to avoid it. It is important to also note that chemicals sometimes have several different names.[18]
In an industrial setting the employer has a duty of care to the individual worker to provide the correct level of safety equipment to mitigate the exposure to harmful irritants. This can take the form of protective clothing, gloves or barrier cream depending on the working environment.
When Did AIDS Begin? How?
When Did AIDS
Begin?
Spring 1988A new study of the oldest known HIV suggests the virus jumped from animals to humans in the 1940s. By comparing the DNA of the 1959 virus with that of samples taken from the '80s and '90s. Ho and his colleagues constructed a viral family tree in which the Leopoldville isolate sits right at the juncture where three subtypes branch out. The 39-year-old specimen is also strikingly similar to the other seven subtypes. The clear implication: all the viral strains can be traced back to a single event or a closely related group of events. One theory is that AIDS started through contact with infected monkeys in a remote area and spread to the rest of the population through urbanization and mass inoculations.
The year was 1959, location: The central African city of Leopoldville, now called Kinshasa, shortly before the waves of violent rebellion that 
followed the liberation of the Belgian Congo. A seemingly healthy man walked into a hospital clinic to give blood for a Western backed study of blood diseases. He walked away and was never heard from again. Doctors analyzed his sample, froze it in a test tube and forgot about it. A quarter-century later, in the mid-1980s, researchers studying the growing AIDS epidemic took a second look at the blood and discovered that it contained HIV, the virus that causes AIDS.
And not just any HIV. The Leopoldville sample is the oldest specimen of the AIDS virus ever isolated and may now help solve the mystery of how and when the virus made the leap from animals (monkeys or chimpanzees) to humans, according to a report published last week in Nature. Dr. David Ho, director of the Aaron Diamond AIDS Research Center in New York City and one of the study's authors, says a careful genetic analysis of the sample's DNA pushes the origin of the AIDS epidemic back at least a decade, to the early '50s or even the '40s.
Over the past 15 years, scientists have identified at least 10 subtypes of the virus. But they couldn't tell whether they were seeing variations on one changeable virus or the handiwork of several different viruses that had made the jump from primates to man. A look at the genetic mutations in the Leopoldville sample strongly suggests that all it took to launch the epidemic was one unlucky turn of events.
The findings underscore how rapidly HIV can adapt to its surroundings, making it difficult to develop effective vaccines. No one knows how many more subtypes of HIV will sprout in the next 40 years, but chances are they will be every bit as lethal as the ones we see today, if not more so.
Apert Syndrome : A genetic disorder
Apert Syndrome
Introduction
Apert syndrome is a rare genetic disorder that is characterized by specific craniofacial and limb abnormalities. It is caused by a genetic mutation in the FGFR2 gene on chromosome 10. The mutation can be inherited from a parent who has Apert syndrome or it can be a spontaneous (new) mutation. Studies show that Apert syndrome tends to occur more often in children with older fathers. Furthermore, all new mutations (those that have not been inherited by an affected parent) have been shown to occur exclusively in the FGFR2 gene received by the father. Apert syndrome occurs in 1 out of 100,000 to 160,000 live births and affects males and females equally. The first reported case of the syndrome was in 1848 by S.W. Wheaton, and in 1906, a French physician named E. Apert described nine cases and defined the syndrome.
Features and Characteristics
The following characteristics have been found in children with Apert syndrome:
- Prematurely fused cranial sutures
- Retruded (or sunken) mid-face
- Fused fingers
- Fused toes
- Brachycephaly (short wide head)
- Acrocephaly (high prominent forehead)
- Flattened back of skull
- Prominent eyes - may be spaced widely apart or slant downward
- Strabismus
- Prominent mandible
- Depressed nasal bridge and small anteverted nose
- Down-turned corners of the mouth
- Low set ears (as well as hearing loss)
- Cleft palate
- Severe acne in teens
- Hydrocephalus
- Dental abnormalities (malposition of the teeth, crowding of the teeth, delayed tooth eruption, high-arched narrow palate, thickened ridges that support the teeth)
- Internal organ abnormalities including heart defects and abnormalities of the trachea,
- uterus, and brain
| Hyperhidrosis Synonychia Brittle nails Severe acne in puberty Interruption of the eyebrows Hypopigmentation Hyperkeratosis Paronychial infections of plantar skin Excessive skin wrinkling of forehead Dimples at knuckles, shoulders and elbows |
Prematurely Fused Cranial Sutures
Retruded Mid-face
Fused Fingers and Toes
Diagnosis
The diagnosis can be made by a skull x-ray, which will confirm premature closure of the skull, and by a clinical exam. The combination of the craniofacial problems and the fused fingers and toes is what distinguishes Apert syndrome from other similar syndromes. Since the defect which causes Apert syndrome has been identified, genetic testing can be provided to confirm a diagnosis.
Treatment
Treating a child with Apert syndrome is best accomplished with a team approach. This would include a craniofacial surgeon, neurosurgeon, ENT specialist, audiologist, speech pathologist, oral surgeon, psychologist, ophthalmologist, and an orthodontist. The majority of treatment methods is surgical and the individual will likely require many operations. Aside from the surgeries required to correct the craniofacial problems and the fused fingers and toes, there may be other potential surgeries to improve the upper airway, address severe eye problems, or correct dental issues.
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