Lyme Disease Causes, Symptoms, Treatment And Prevention

Lyme disease, also known as the Lyme infection is a bacterial disease transmitted by the tick (Ixodes), insect that carries a bacterium called Borrelia burgdorferi. The disease is found in North America and Europe, where it was initially described almost 100 years ago. Maximum prevalence of lyme disease is in the north-eastern states of America, half of the cases are concentrated in New York and Connecticut area.
American doctors have described the disease almoast 70 years ago. Most of those affected lived in the town of Lyme in Connecticut, hence the name “Lyme disease. “

• Fortunately, less than 5% (1 of 20) of tick bites cause Lyme infection
• Doctors have gained experience with the disease, from first cases until today. Thus, currently a treatment for Lyme disease exists.

Lyme Disease

Causes

B. burgdorferi is the bacterium that causes Lyme disease. The life cycle of this bacteria is very complex and a part of the like cycle taks place inside the tick. The rest of the life cycle, B. burgdorferi is parasitizing various mammals such as mice or deer. Humans are not part of the life cycle, but can become infected if they are bitten by a tick.

Symptoms

1. Infection. Initial infection occurs without symptoms or with minimal manifestations, often going unnoticed. Some reports of flu-like symptoms or a characteristic rash are succeeding the tick bite.
2. Flu Symptoms. These occur in the warm weather months, an atypical period for influenza.
3. Rash. It is a red annular lesion that grows from day to day and is called erythema migrans. The center of infection control and prevention (CDC) defines the eruption as a red dot that increases over a few weeks to form a round lesion of at least 5 cm in diameter. A red point that appears within a few hours after the bite is usually the body reaction. The appearance of rash at the bite site is considered the primary lession. Multiple secondary lesions may occur in response to infection. All these lesions are characteristic for Lyme disease. The rash is oval or round (circular). As it grows, the rash can get red or pale in the center, sometimes  looks like a “bullseye”, with red concentric circles alternating with healthy skin. Left untreated, the symptoms of primary infection disappear within a few weeks, but may reappear – skin eruption.
4. Later, additional symptoms may occur as a result of damage to internal organs:

• Facial nerve paralysis causing facial muscles asymmetry (can resolves itself, even without treatment)
• Meningitis with headaches, fever and neck stiffness
• Nerve inflammation with dizziness and tingling sensation in the hands and feet
• Cerebral edema (encephalitis) causes learning difficulties, confusion and dementia
• Intermittent episodes of arthritis that last about a week and affect wrists or knees. May reappear for several months in a row and without treatment, persistent knee arthritis occurs. Lyme disease can occasionally manifest with acute arthritis of the knee, in the absence of a suggestive rash.
• Inflammation of the cardiac structures (carditis – inflammation of the heart) leads to cardiac rhythm disturbances.

Lyme Disease

Diagnosis

Lyme disease diagnosis is based on a complete clinical examination and specific laboratory tests.

1. Your doctor will ask if you were bitten by a tick and if you perform outdoor activities in areas that are endemic for ticks.
2. Clinical signs are important, especially erythema migrans, as described above. If there is any doubt regarding the causal skin rash, the doctor can measure the erythema and then ask you to return to perform a second measurement after 2-3 days. Erythema migrans grows about 1 centimeter in size daily. There are specific clinical signs by which the physician can distinguish Lyme disease from other diseases.
3. Blood tests for antibodies against the bacterium Borrelia burgdorferi detection. In the first weeks after infection the antibodies can be absent, so testing can be negative. There are two blood tests that can be used to detect Lyme disease, a screening test (ELISA Lyme), and if the result is positive, a second, specific test (called “Western blot”), confirms the infection. In countries where Lyme disease is very common, patients can have positive tests for Borrelia, without having the disease. Positivation of a simple screening test is not sufficient to establish the diagnosis of Lyme disease: a Western Blot test must be also positive. Once the tests for Lyme disease become positive, they remain positive for a very period of time, even after proper treatment. Thus, repeating the test after the treatment is not necessary or useful.
4. Ticks can carry other organisms besides B. burgdorferi, which can cause diseases that can mimic Lyme disease. Therefore, liver function tests and blood counts are recommended.
5. Patients who have headaches may require lumbar puncture to determine the degree of inflammation of the nervous system and to detect the possible presence of specific Lyme disease antibodies in the cerebrospinal fluid (CSF).
6. An electrocardiogram (ECG) to identify potential cardiac complications.
7. Magnetic resonance imaging (MRI) and computed tomography may be performed to rule out other diseases with similar manifestations of Lyme disease.

Lyme Disease Diagnosis

Treatment

It is recommend that the early stages of Lyme disease are treated with antibiotics such as doxycycline, penicillin or erythromycin. Advanced stages of Lyme disease (patients with neurological, cardiac or joint complications) have to be treated during hospitalization with antibiotics administered intravenously.

Prevention
There are three ways to prevent Lyme disease.

1. Avoiding tick bites
   -Do not venture into forests unprotected, especially during summer
   -Wear socks that create barriers between the tick and the skin;
   -Insert the bottom edge of the trousers inside the socks, and wear colorful clothes, allowing quick identification of insects on the fabric.
   -Apply an insecticide, especially on the clothing and not on your skin. This product is not recommended for children as they can absorb the insecticide through the skin. Insecticide application reduces the chances of infection by reducing the risk of tick bites.
2. Removing ticks. For transmitting Borellia the ticks needs 24-48 hours to stay attached to the skin surface. Thus, after carrying out your outside activities, inspect all exposed areas of your skin. If you notice an insect sting it is very important to be aware of the associated symptoms that may occur in the next three weeks.
   – Ticks attach themselves to warm, moist areas: groin, armpits, neck and hair line implantation.
   – If you find a tick, remove it quickly. This maneuver reduces the risk of contracting the infection.
   – If you have a pair of tweezers, grasp the tick as close to the implantation site and pull it out slowly but firmly. If you do not have tweezers, grasp the tick’s body and take it out slowly.
   – Disinfect the bite site with alcohol or other antiseptic solutions.
   – If the tick does not come out easily, pull it out by twisting, pinching and pulling upward.
3. Antibiotic treatment. Treatment of tick bites in the first 72 hours with a single dose of doxycycline prevents Lyme disease. It is recommended for those that are living in an endemic area and are bitten by a tick. It is advisable to ask your doctor before administering the dose of antibiotic.

Ideal Vaginal pH

The intimate zone is the most delicate female body part. Is colonized by a variety of bacteria that form the vaginal flora. The vaginal flora creates a protective barrier that acts against the proliferation of different infections.

Among the bacteria that comprise the vaginal flora the presence of Lactobacillus is very important, beacuse it produces lactic acid and maintains an acidic vaginal pH ,creating therefore a hostile environment that prevents the growth of pathogenic microorganisms.This barrier maintains proper vaginal health. When Lactobacillus are replaced in the vaginal area the balance alters with consequent discomfort and irritation.The bacteria that make up the vaginal flora (Lactobacillus) produces lactic acid which maintains a proper vaginal pH by creating a protective barrier that prevents the growth of pathogenic microorganisms. The vaginal pH is acid, the acidity decreases as the pathogenic flora (fungi) is being established.

Vaginal Ph

The vaginal pH varies between different stages of the life cycle of women. Thus, the pH until puberty is 7.0 but since then until menopause, different situations are distinguished involving changes in vaginal pH:

• Menstrual phase pH is 6.8 to 7.2, the premenstrual phase pH is 3.8 to 4.2 and for the rest of the cycle the pH varies between 4.0 and 5.0.
• During pregnancy the vagina shows a fairly acidic pH similar to the premenstrual phase (<4.2). With the advent of menopause, the vaginal pH becomes as in the early life of women with values close to 7.0.

In addition, there are other common situations that can alter the physiological pH of the intimate zone:

• Use of chemicals or fabrics that irritate or cause local allergic reactions (spermicides, latex, synthetic fiber underwear etc.)
• Thermal factors
• Trauma (chafing by the use of tight clothing)
• Diabetes
• Use of broad spectrum antibiotics
• Birth control (condoms, IUDs, pills).

An altered vaginal pH favors the presence of discomfort such as itching, irritation and redness and the appearance of vaginal infections. The main defense against discomfort and irritation vulvovaginal proper hygiene is a daily to help maintain the proper vaginal pH.

In cases in which there is a vaginal yeast infection, vaginal pH adjustment will be beneficial in preventing and supplement the pharmacological treatment.

Myocardial Infarction Treatment

Myocardial infarction is a major cardiac emergency. Currently myocardial infarction is well standardized in terms of therapeutic means.

Prehospital Care

It starts with pain treatment, and anti-ischemic treatment:

• Nitroglycerin (given sublingually, spray or intravenously)
• Aspirin in all patients (160-325 mg)
• Oxygen if the patient is hypoxic
• Atropine in case of sinus bradycardia (decreased heart rate below 60 beats per minute in adults and less than 80 beats per minute in children) and / or hypotension
• Cardio-respiratory resuscitation
• Procainamide should not be administred  for ventricular extrasystoles prevention.

Myocardial Infarction

During prehospital care, thrombolysis is possible, given the existence of mobile coronary unit. Its benefits are increased reperfusion, reduced mortality, decreased size of infarction  zone area. The first 60 minutes elapsed the from stroke onset are considered “the golden hour” of reperfusion (resumption of circulation to the infarction zone). The agents used are Streptokinase, tissue plasminogen activator, Urokinase.

Emergency room

Emergency treatment consists of morphine, oxygen  (flow rate of 2 l / min), 325 mg Aspirin (unless it was given), and nitroglycerin (sublingual or perfusion).

If the patient shows no signs of haemodynamic deterioration and bradycardia, beta blockers are intravenously administered (metoprolol, atenolol).

Myocardial Infarction Treatment

Coronary Care Unit

• Aspirin in doses of 160-325mg / day
• Further fighting pain using common analgesics (metamizole sodium, vials 1g), opioid analgesics (morphine 20mg/1ml vials) in doses of 4-8mg intravenously, 5-15 mg at 2-8 minutes until the pain disappeares.

Beneficial effects of morfine : intense analgesic effect, reduces sympathetic tone, increase vagal tone, reduces anxiety, produces vasodilation.
Morphine contraindications: hypotension, bradycardia, inferior myocardial infarction, right ventricular infarction.Morphine side effects: hypotension, respiratory depression, nausea, vomiting.

• Oxygen therapy: 2-4 liters / minute, under the mask or nasal tube for 6-12 hours in patients with moderate hypoxemia. It is not indicated if the oxygen saturation is normal, because it can increase the peripheral vascular resistance.
• Nitrates and beta blockers can relieve pain through their coronary and anti-ischemic effect.

Cardioprotection by restoring coronary blood flow.

Cardioprotective measures include all pharmacological measures, especially thrombolysis, and non-pharmacological measures that aim for myocardial reperfusion. Myocardial reperfusion by thrombolysis is the most important measure that reduces mortality, improves ventricular function and limitates the infarct size . This measure will be continued in the coronary artery unit as early restoration of coronary blood flow (1-2 hours after onset), reduces the size of necrotic myocardium.

• Thrombolysis medication. Can be administed directly in the coronay arteries (only when coronary thrombosis occurs during an angiographic procedure) or intravenously. Streptokinase, tissue plasminogen activator are used.
  A possible evolution of coronary thrombolysisis is reocclusion of the coronary artery (approximately 10% of cases). To reduce the risk, antiplatelet therapy is required (aspirin, clopidogrel), and antithrombotic agents (low molecular weight heparin). Antiplatelet therapy increases the success rate of reperfusion, prevents intraventricular thrombus formation, prevents deep vein thrombosis and pulmonary embolism.
  The most important complication of thrombolytic therapy is bleeding (cerebral, digestive, etc.)
  Absolute contraindications of thrombolysis: Stroke (any time in history), ischemic stroke, brain neoplasm, active internal bleeding, suspected aortic dissection.

• Percutaneous transluminal coronary angioplasty (PTCA procedure) is another important method of thrombolysis and reperfusion.

• 

  Angioplasty

• Bypass surgery, is indicated in the following situations associated with myocardial infarction: PTCA procedure failure (with persistent pain or hemodynamic instability), PTCA risk procedure due to the coronary anatomy (left common trunk stenosis), coronary occlusion occurred after catheterization, cardiogenic shock.

Cardioprotection by decreasing myocardial oxygen consumption.

• Beta-blockers. Early treatment with beta blockers is associated with reduced mortality and reduced cardiac arrest risk by 15%. Their administration reduces heart rate and blood pressure decreasing myocardial oxygen consumption through these mechanisms. Beta-blockers indications: recurrent or persistent pain, ischemic tachyarrhythmias (atrial fibrillation with fast heart rate), myocardial infarction with or without ST-segment elevation, actually all patients without contraindications.
  Beta-blockers contraindications: hypotension (systolic blood pressure <90 mmHg), bradycardia (heart rate <50 beats per minute), heart blocks.
• Nitrates. Nitroglycerin can be used in the first 24-48 hours in patients with acute myocardial infarction, congestive cardiac failure, persistent ischemia, hypertension. After 48 hours, will be administered to patients with recurrent angina, or pulmonary stasis. It is administrated intravenously , blood pressure monitoring is mandatory.
  Nitroglycerin contraindications: hypotension, myocardial infarction of right ventricle.
• Angiotensin converting enzyme inhibitors have beneficial effects as it prevents ventricular remodeling after myocardial infarction, decrease the rate of occurrence of heart failure, reduce the risk of recurrence of myocardial infarction and reduce mortality. Are indicated in all patients with acute myocardial infarction, especially those with heart failure, diabetes mellitus, hypertension.
  Contraindications: hypotension, pregnancy, renal insufficiency (creatinine> 3mg%)
• Calcium channel blockers. At the onset of myocardial infarction are not recommended, nifedipine increases mortality risk. It suddenly lowers blood pressure, followed by reduction of  the coronary blood flow and tachycardia, with increased imbalance between intake and myocardial oxygen demand.
  Verapamil and diltiazem can be used, but with caution (due to the negative inotropic effect) in patients in whom beta blockers are ineffective or contraindicated (asthma patients) and for heart rate control in patients with atrial fibrillation.
• Magnesium. Can be administered in case of a demonstrated magnesium deficiency , in episodes of torsades de pointes with QT interval prolongation, in doses of 1-2g IV, magnesium sulfate (10 ml vials, 20%), bolus for 5 minutes.

Nonspecific Measures

Physical and emotional rest. In uncomplicated myocardial infarction, absolute bed rest will not exceed 12 hours, a gradual resumption of physical activity is recommended, which takes into account age, physical capacity and condition. The first two days help from another person is recommended, including when washing and feeding. The following days the patient can wash his face on his own, can go to the toilet, and movement is allowed but only supervised, inside and outside the chamber (20-200 meters). After 5 to 7 days walking (200m), three times a day, climbing stairs are allowed, under supervision, and exercise testing before hospital discharge.

• Diet: light regime, hypo-caloric, salt restriction, foods rich in potassium
• Mild laxatives will be administered if needed, .
• Correction of anemia with packed red blood cells transfusions
• Treatment of infections
• Monitoring and keeping the blood pressure within normal values.

Syphilis Symptoms And Clinical Stages

Syphilis, caused by the spirochaete Treponema pallidum is one of the most important venereal disease. It is a worldwide disease, which is transmitted almost exclusively by sexual contact (acquired syphilis). The infection is also spread from an infected mother to her fetus (congenital syphilis). Blood transfusions, direct inoculation and nonsexual contact are only rare causes of syphilis. The course of acquired syphilis is classically divided into 3 stages: primary, secondary, and tertiary syphilis.

Treponema Pallidum

Primary syphilis. The classic lesion of primary syphilis is the chancre, a characteristic ulcer located at the site of Treponema pallidum inoculation. The chancre appears usually on the external genitals (gland penis, vulva), one week to 3 months after exposure, with an average incubation period of 3 weeks. In approximately 10% of cases the chancre may be extra-genital: lips, fingers, oropharynx, anus, rectum, or some other site. In about 50% of females and 30% of males, primary lesions either never develop, or are not detected.

The chancre begins as a solitary, slowly growing, hard, pale brownish – red, usually painless nodule, that varies in size up to several centimeters in diameter. Then it superficially erodes to create a clean-based, shallow ulceration on the surface of the slightly elevated papule.

The contagious induration characteristically creates a button like mass directly subjacent to the eroded skin or mucosa, providing the basis of the designation hard chancre. When the lesion is on a mucous surface and the part is not kept clean, there may be more extensive ulceration and suppurative exudation.

The ulcer persists for 3-12 weeks, during which the inguinal lymph nodes, usually on both sides, become somewhat enlarged and hard, with nonspecific acute or chronic lymphadenitis (inguinal lymphadenopathy). The chancre heals without scaring.

Histologically, the chancre is characterized by a intense mononuclear leukocytic infiltration, chiefly of plasma cells with scattered, macrophages and lymphocytes, which are mainly responsible for the hardness and swelling. Obliterative endarteritis is present within this inflammatory reaction.

Syphilis Chancre

Secondary syphilis. The most common presentation of secondary syphilis is a rash, which appears 2 weeks to 6 months after the chancre heals, with multiple symmetrical lesions of the skin and squamous mucous membranes. The rash is erythematous (discrete red-brown lesions) and maculopapular, involving the trunk and extremities and often including the palms and soles. Reddened mucous matches may appear in the mouth or vagina; they are called mucous patches and are teem with bacteria, being highly infectious.

Papular lesions in the region of the penis or vulva may become large, elevated, broad plaques. These flat red-brown elevations (up to 2-3 cm in diameter) are designated conylomata lata (wart like lesions on the genitals). The overlying epithelium is intact and hyperplastic.

General slight enlargement of lymph nodes is also common. Characteristic changes include a thickened capsule, follicular hyperplasia, increased numbers of plasma cells and macrophages, luetic vasculitis.

The secondary lesions are usually accompanied by fever, anemia and general malaise. After some months all these features disappear spontaneously and the disease becomes latent.

Histologically, in the secondary lesions in the skin and mucous membranes, the main changes are vascular enlargement and infiltration, mainly of plasma cells, but also lymphocytes, and macrophages. When the rash is distinctly papular it is usually accompanied by thickening of the epithelium.

Secondary Syphilis

Tertiary syphilis. After the lesions of secondary syphilis have subsided, an asymptomatic period lasts for years or decades. However, during this latent period, spirochetes continue to multiply, and the deep-seated lesions of tertiary syphilis gradually develop and expand. Only a third of untreated patients with syphilis develop tertiary lesions.

Tertiary lesions appear irregularly, especially in the internal organs, skin and mucous membranes; they are few but usually much larger than the primary and secondary lesions, and lead to serious and permanent damage.

Gumma is a characteristic lesions of tertiary syphilis, which may form in any organ or tissue. It is a granulomatous lesion composed of a central area of coagulative necrosis, epithelioid histiocytes, occasional giant cells and peripheral  fibrous tissue. Gummas are most commonly found in the skin, bone and joints, although the lesion may occur in any body site. They cause extensive destruction like in the nasal bones with loss of the bridge of the nose and perforation of the palate, ulceration and destruction of the larynx, creeping ulcers in the skin.

Tertiary Syphilis

Of special importance are the cardiovascular lesions. Cardiovascular syphilis principally involving the aorta, may become manifest after several years from the initial infection. It causes inflammatory scarring of the tunica media (mesaortitis) with weakening and dilatation (aneurysm formation) and narrowing the corronary ostia (may cause myocardial infarction).

Neruosyphilis is another late manifestation. The slowly progressive infection damages the meninges, cerebral cortex, spinal cord, cranial nerves, or eyes. Tertiary syphilis involving the central nervous system is sub-classified according to predominant tissue affected. Thus, there are references to meningovascular syphilis (meninges), tabes dorsalis (spinal cord), and general paresis (cerebral cortex).

Precancerous Lesions – Early Warning Signs Of Cancer

A precancerous condition is one which can be recognized by either clinician or pathologist and which idicates that the bearer has a substantially greater risk of developing a malignant tumor than normal. The early stages of precancerous change (which presumably indicate the occurrence of the earlier mutations of a multistage conversion to malignancy) can often be recognized histologically. The signs include cell nuclear irregularity, increased mitotic activity, and abnormalities of differentiation, often combined with inflammatory infiltrates, and stromal changes. The risk of such precancerous lesions becoming malignant can be established only in the light of experience of their behaviour in each particular site in which they occur.

Cancer Cell

Precancerous lesions:

• Some benign tumors . Probably al benign tumors carry some risk of malignancy, but in most cases it is little more than that of normal tissues, while in other is considerably high. There is little obvious logic about the differences. The villous papilloma of the rectum becomes malignant more often than the adenomatous tubular polyp of the same site; similar tumors of the stomach carry a worse prognosis that other gastrointestinal segment tumors, while the uncommon similar tumors of the small intestine only very rarely become invasive (malignant). Comparable anomalies could be quoted at other sites.
• Certain chronic diseases. Carcinoma (cancer) may develop as a more or less common complication of some noncancerous diseases, such as cirrhosis of the liver, ulcerative colitis, asbestosis, and a variety of skin diseases.
• Cancer in situ. Most cancers begin as localized growths confined to the epithelium in which they arise. As long as these early cancers do not penetrate the basement membrane on which the epithelium rests, such tumors are termed cancer in situ.

Cancer Microscope

In some tissues, particularly the epidermis of the skin, the squamous epithelium of the exocervix, endometrium, and the bronchial epithelium, an area of atypical proliferation of cells occurs, affecting usually the entire thickness of the epithelium and exhibiting the cytological features similar to those of invasive cancer, but no demonstrable penetration into the subephitelial stroma was discovered. It is generally believed that this lesion, cancer in situ, is a true intraepithelial cancer that frequently becomes invasive cancer if left untreated. The lesion is also known as preinvasive carcinoma.

In this stage, it is unfortunate that carcinomas are asymptomatic, because they are invariably curable. When the in situ cancer acquires invasive potential and extends directly through the underlying basement membrane, it is in a position to compromise neighbouring tissues and to metastasize. In those situations in which cancer arises from cells that are not confined by a basemnet membrane, such as connective tissues cells, lymphoid nodes, and hepatocytes, the in situ cancer stage is not defined.

The degree of risk of developing cancer varies greatly with different lesions, and is often hard to determine with any exactness. In a few rare conditions, such as polyposis coli, and xeroderma pigmentosa, it is practically 100%. In cancer in situ of the cervix, extesively studied but still controversial, it may also be high though, a period of 20 years may elapse between the appearance of the lesion and the onset of invasive cancer. In most lesions the risk appears to be much lower.

 Osteoarthritis Symptoms, Risk Factors, Specific Joint Involvment And Treatment

Osteoarthritis is a disease that affects articular cartilages of synovial joints (mobile), accompanied by increased bone activity under the cartilage, having as consequence the formation of new bone and cartilage with joint deformity and functional limitation.

Risk factors:

• Older age
• Female sex
• Race
• Genetic factors (heredity)
• Major joint trauma (fractures, dislocations)
• Repetitive stress (occupational)
• Overweight and obesity (especially for hip arthritis and osteoarthritis)
• Congenital anomalies (congenital dislocation of the hip)
• Previous inflammatory arthropathy
• Metabolic or endocrine disorders

Osteoarthritis

Symptoms

Initial stages of the arthrosic process are clinically asymptomatic, in contrast to many physical and radiological changes. Pain is a symptom that suggests the diagnosis of osteoarthritis, affecting one joint initially then several joints. Pain is described as deep, accompanied by stiffness, and follows periods of inactivity (wake up in the morning, raising from a chair). Pain may radiate to the surrounding areas, intensify during use of these joints. In early stages of the disease, pain is relieved by rest. Once the disease progresses, pain becomes persistent, affecting normal activity and preventing sleep, sometimes even during treatment.

The most common joints affected by osteoarthritis are the big toe joint, wrist joints, hips, knees, cervical and lumbar spine.
On physical examination the patient presents deformed joints that are usually sensitive to palpation, crepitus, and mobility limitation. Joint instability occurs only in severe forms. Increased joint volume is caused by increases in bone surfaces, and sometimes the accumulation of fluid in the joint space. Patients with advanced disease often experience large deformations, sometimes accompanied by subluxation.

Osteoarthritis Stages

Specific joint involvement

Hand. Heberden nodules are present as bony growths that develop slowly in the distal interphalangeal joints. Sometimes the onset is acute with pain and redness of the affected joint. Heberden nodules can cause deformities of the joint with lateral deviation or in flexion. Another form, erosive osteoarthritis manifests with similar painful episodes but differs radiologically highlighting local erosive changes, and a tendency to bone ankylosis. Another joint affected by the hand osteoarthritis is the thumb joint, with pain at movement. A square shape of the thumb base can be present also.

Knee. Idiopathic gonarthrosis is one of the most common causes of joint pain and is directly related to the individual weight. It is more common in women than men. The most commonly affected compartment is the femurotibial with varus deformation.
In idiopathic gonarthrosis, physical examination reveals pain on pressure, crepitus, and reduced joint mobility. Accumulation of fluid is common, but in low quantity. The radiological exam highlights osteophytes.

Hip. Most cases of primitive coxarthrosis are caused by mild dysplasia of the femoral head and / or of the acetabulum, wtih incongruity of the articular surface . With time, by using the joint, progressive degeneration of cartilage occurs. Pain is localized in the inguinal arch, very rare in the anterior thigh area and knee (irradiated pain). The early sign of hip arthritis is reduced internal rotation. Once the disease progresses, mobility is reduced, with significant functional limitation.

Leg. The big toe joint is often affected, associated swelling and deformity. Much more common in women, was attributed to mechanical stress due to high heeled shoes. In extreme cases the joint space may be canceled, a process known as &quot;hallux rigidus&quot; which requires surgical correction.

Spine (spondylosis). Spine osteoarthritis refers to synovial joints that can determine localized pain and irritation of adjacent nerves. Nerve root compression, due to joint subluxation or a herniated inter-vertebral disc can cause muscle asthenia, reduced reflexes, paresthesia. Spondilosis can be located at any level of the spine.

Osteoarthritis

Treatment

The objectives of treatment in osteoarthritis are pain and inflammation reduction, mobility increase in affected joints, physical disability prevention

Removal of favoring factors: weight loss, changing jobs, if the patient has a job that affects certain joints, joint measures to protect the injury (same side cane, special shoes).
Adequate physical activity: good for improving joint mobility and prevent muscle atrophy and osteoporosis.

Drug therapy

Acetaminophen (paracetamol). Reduces arthritic pain in patients. Acetaminophen – (3g/ day), first intention medication. Recent studies have shown that efficiency of Acetominophen is equal to that of NSAIDs but with fewer severe side effects .

NSAIDs. When inflammation is present or when symptoms are not sufficiently controlled with simple analgesic medication, small doses of NSAIDs are effective, especially COX2 inhibitors (colecoxib 200 mg / day, etoricoxib 120 mg / day).

Intra-articular administration of cortisone preparations keeps under control joint symptoms, especially when inflammatory reactions are present. It must not be repeated more than three times per year due to the potential of chemical erosion of the cartilage by of the steroids.

Chondroprotective agents are theoretically and experimentally, the ideal medication for arthritis, able to prevent joint damage and restore cartilage structure . The most used chondroprotective agents: Atroflex, Dona, Flexodon A, ArthroStop, polysulphate glycosaminoglycans, Piscledine 300.

Balneophysiotherapy: warm baths, hydrotherapy, paraffin packing, diathermy, ultrasound with significant palliative effects.

Osteoarthritis Knee Surgery

Surgery. The ideal time for the surgical procedure must be chosen carefully because it can compromise the outcome if delayed (the appearance of irreversible changes like muscle atrophy, paralysis, osteoporosis).

• Debridement, tissue replacement with autologous cartilage grafts
• Osteotomies
• Resection of large bone spurs
• Arthroplasty
• Prosthetic joints

Side Effects Of Insulin Therapy And Hypoglycemia Treatment

Antidiabetic therapy is mandatory in type 1 diabetes mellitus (insulin) and necessary in type 2 diabetes, which can be treated with a correct indicated diet by the physician and fully respected by the patient (oral medication or insulin). Insulin has an absolute indication for type 1 diabetes, type 2 diabetes complicated with ketoacidosis or pregnancy. Relative indications of insulin may be permanent: type 2 diabetes requiring insulin or temporary in case of infection, myocardial infarction, during surgery.
Insulin does not cause addiction, which means that its administration in type 2 diabetes may be interrupted if the disease permits it.

Insulin Therapy

Generally any drug can cause adverse effects. It is also the case of insulin that possesses a number of adverse effects that any patient with diabetes should to be aware of.

Insulin side effects

Hypoglycemia is the most common and most serious side effect of insulin, very serious, sometimes fatal. It is defined by blood sugar levels under 65 mg % (3.6 mmol / l). Hypoglycemia may occur after any type of insulin and results in brain damage by lowering oxygen consumption of the brain, more serious the lower blood sugar levels are. Sometimes, after years of illness, intellectual capacity greatly decreases at a relatively young age (around 50 years) due to destruction of neurons, a condition called hypoglycemic encephalopathy.
Factors that favor the occurrence of hypoglycemia due to insulin are very varied.

• Insulin overdose, most commonly in the intensive treatment
• Not eating – the omission of a meal, after insulin was injected (eg, patient falls asleep)
• The long interval between the injection and the carbohydrate meal or meals containing a small quantity of carbohydrates.
• Injecting insulin into a blood vessel
• More physical activity than usual, without precautions against hypoglycemia.
• The presence of vomiting and diarrhea.
• Alcohol intake

Clinical manifestations of hypoglycemia are extremely varied, depending on blood sugar levels and individual factors, some patients handling hypoglycemia better than others.

In mild and moderate forms:

• Sweating
• Tremors
• Epigastric pain
• Extreme hunger sensation
• Mouth tingling
• Unusual fatigue which is rapidly installed
• Inattention
• Headaches, especially frontal and scheduled
• Diplopia (double vision)
• Mild agitation, disorientation

In severe forms (in addition to mild and moderate form)

• Loss of consciousness (coma) and seizures, bilateral Babinski sign.

If not recognized early, hypoglycemic coma can lead to severe brain damage and even brain death. It is important to state that some patients lose warning signs of hypoglycemia (hypoglycemia awareness), hypoglycemia is asymptomatic and is installed without any warning signs leading to coma very rapidly. Some patients remain asymptomatic at extremely low blood sugar levels (below 30 mg%), while others show signs of mild and moderate hypoglycemia at close to normal blood sugar levels.

Treatment of mild to moderate hypoglycemia: the ingestion of sugar, as such, or sweetened tea, syrups, sweet drinks. This measure is urgent, as rapid progression to coma is very probable. Therefore, all diabetics must have sugar on hand at any time of day, glucose (tablets), or soft candy.

Hypoglycemic coma. 1-2 mg of glucagon is administered (in the muscle). Glucagon increases blood sugar level by releasing glucose deposits from the liver.  If  glucagon is not available, 33% hypertonic glucose is injected intravenously until the patient recovers (sometimes more than 300ml). Because it is an emergency, treatment is started immediately after diagnosis, including family members (immediately after they called 112 / 911). If  you can not differentiate hyperglycaemic coma from hypoglycemic coma (in absence of blood glucose testing),the coma is treated as a hypoglycaemic coma. Glucose administration does not harm in case of hyperglycemia, but saves the patient in the case of hypoglycaemic coma.

Other Insulin Side Effects

• Allergy: human insulin is theoretically free of this risk, which in practice can be observed, however, extremely rare
• Insulin resistance, a condition defined by a higher necessary per day  (more than 1.5-2 units / kg or 200 units per day).
• Lipodystrophy (fat redistribution), atrophic and hypertrophic form, modifying the local reabsorption of insulin.
• Local abscess (very common among insulin side effects)
• Injection site pain
• Visual disturbances at the start of treatment (reversible within a couple of weeks)
• Insulin edema (rare in women who use high doses)

Insulin Injection

Rheumatic Fever Symptoms, Clinical Signs, Evolution And Treatment

Rheumatic fever is an inflammatory rheumatic disease, which occurs as a result of pharyngeal infection with group A streptococcus and affects the entire body’s connective tissues, but especially the joints, heart and central nervous system. Although rheumatic fever damage highlights, as a rule, joint damage , rheumatic fever is so important by affecting the heart, which can be severe, even fatal, in the acute stage, or may lead to rheumatic heart disease characterized by scarring and deformation of the heart valves, with multiple clinical and hemodynamic consequences.

Throat Infection

In developed countries the incidence of rheumatic fever has declined over the past decades, due to the prompt treatment of steptococcal pharyngitis. The most commonly affected age is between 5 and 15 years.

Rheumatic Fever Causes

Rheumatic fever is a disease caused by streptococcus group A, located exclusively in the pharynx. The relationship between this bacterium and rheumatic fever is based on multiple arguments.

• Demonstrating active streptococcal infection in the patient’s recent past (ASO growth and other antistreptococcal antibodies).
• Prevention of rheumatic fever and its relapses by prompt treatment of the streptococcal infection (primary and secondary prevention).
• Rheumatic fever occurs at a certain period of time after pharyngitis.

The mechanism by which streptococcal infection leads to rheumatic fever is still  imcompletely known. Two hypotheses are probable: imnuo-allergic and autoimmune.

• Imnuo-allergic mechanism, which consists of a hypersensitivity reaction to one or more antigens (parts of microbes) or metabolites, argued by high ASO antibody titers.
• Autoimmunity. Certain streptococcal antigens cause a  cross-immune reaction with the cardiac and vascular structures,  due to antigenic similarity between some components of streptococcal membrane ( such as M protein) and several heart “antigens” (like myosin). In simple terms some streptococcal components resemble the structure with that of human cell components (the body makes no difference, and immune system reacts against its own cells and attacks them)

Rheumatic Fever

Rheumatic Fever Risk Factors

• Environmental factors seem to be important in promoting streptococcal infection, such cold climates, high humidity climates and human congestion (schools, barracks, large families, urban communities) are conditions that favor transmission of strep throat.
• The genetic predisposition to react in a certain way, against streptococcal infection, which results in rheumatic fever.

Rheumatic Fever Signs And Symptoms

The disease progresses in stages in the attacks of 8-12 weeks, spontaneous self-limited. Prodromal stage, represented by erythematous angina, may be absent in 20-50% of cases. Latent stage of rheumatic fever covers the period of 1 to 5 weeks, from the occurrence of angina and the onset of rheumatic fever. It may be asymptomatic or have nonspecific symptoms: fever or low grade fever, joint pain, fatigue, poor appetite, sweating, palpitations, weight loss, epistaxis, abnormal behavior, and alterations in laboratory tests. State period characterized by various symptoms and signs, major (arthritis, carditis, chorea, subcutaneous nodules) and other minor signs.

Nodules

Migratory arthritis is very common manifestation of rheumatic fever, present in over 75% of cases, and has the following characters:

• Three large joints simultaneously affected with, pain, swelling, functional limitation of movement, redness and local heat.
• Affects large joints of the limbs (knee, elbow, radio-carpal, shoulder, hip), but in general can affect any joint.
• Migratory character, appearing again at the same joint.
• Heals quickly without deformation after treatment with salicylates (eg aspirin) or corticosteroids (Methylprednisolone, Prednisone.
• Lasts for 1-3 weeks, and heals spontaneously within 4-5 weeks maximum.

Rheumatic Carditis

The worst aspect of rheumatic fever is carditis, which is present in 40-60% of cases. In time, this complication occurs especially in the first two attacks, between 5th day and 15th after the onset of arthritis (arthritis rarely before).
The intensity of the manifestations of carditis  varies from a fulminant evolution – fatal to a mild inflammation, inconspicuous, up to fulminant heart failure.

• Cardiomegaly (enlargement of the heart cavities) is caused by myocarditis – very common.
• Pericarditis (5-10% of cases) may be dry, manifested by friction and pain, or exudative.
• Heart failure is the worst manifestation of carditis, involving, in varying proportions, associating manifestations of endocarditis with those of myocarditis and pericarditis.

Heart Failure

Sydenham Chorea

Syndeham chorea (chorea minor) is a neurological manifestation of rheumatic fever which occurs in less than 10% of cases at 2-7 months after  the acute episode, when most or all clinical and biological manifestations of rheumatic fever have disappeared.

Rare clinical manifestations

• Rheumatic pneumonia, which is associated with severe carditis
• Pleurisy (4-5% of cases), with small amounts of liquid, corticosteroids will lead to healing without sequelae.

Overall symptoms of rheumatic fever

• Fever is always present, can occur suddenly or gradually (3-6 days), has a moderate intensity (up to 38 degrees Celsius), fades after salicylates (aspirin), intensity depends on the severity of carditis.
• Sweating is abundant, continuous, especially overnight.
• Pallor, more pronounced than the degree of anemia is caused by infection, anemia, neuro-vegetative disorders.
• Asthenia is very pronounced in the case of carditis
• Epistaxis (nosebleeds), rarely present in 10% of cases, can be discreet or abundant.

Rheumatic Fever Evolution And Prognosis

Rheumatic fever evolution is varied and difficult to apreciate at the onset of disease. Approximately 75% of rheumatic attacks resolve in 6 weeks, 90% in 12 weeks and persist for over 6 moths in less than 5% of the cases. The latter are cases of severe rheumatic carditis with rebel attacks or prolonged Sydenham chorea symptoms.
Once rheumatic fever is remitted and more than two months have passed after interrupting treatment with salicylates or cortisone, rheumatic fever symptoms do not occur again. Only the presence of a new streptococcal infection can trigger the onset of symptoms.
The prognosis depends entirely on carditis severity. During attacks, death can occur through severe myocarditis, or heart failure, and later due to valve damage. The main causes of death in adults are: heart failure, bacterial endocarditis, systemic and pulmonary embolism.

Rheumatic Fever Treatment

Penicillin

Although there is no specific treatment for rheumatic fever and there are no measures that may influence the intesity of an attack, treatment is mandatory.

1. Bed rest and diet. Bed rest at the hospital, it is mandatory for all patients, at least for three weeks, during which carditis usually occurs. Duration must be greater for those with medium and severe carditis (2-6 months, depending on the evolution) . Limiting physical activity depends on the carditis severity. Resumption of normal activity is done after 3 months (mild carditis), 6 months (avreage severity carditis) and much later or never in case of severe carditis.
2. Antibiotic treatment. Administration of antibiotics is one essential part of the conventional treatment of rheumatic fever and aims for the eradication of group A streptococcal throat infection. Penicillin is administrated, amoxicillin for children. If the patient is allergic to penicillin, erythromycin or second generation cephalosporins are recommended.
3. Anti-inflammatory treatment (suppressive, anti-rheumatic). It represents the treatment of clinical manifestations, which aims to fight inflamation. It does not heal and does not prevent long-term evolution of rheumatic Fever. Generally, aspirin and corticosteroids (prednisone) are used to treat rheumatic fever

Prevention of rheumatic fever is represented by early and correct treatment of throat infection and prevention of further attacks.

Cataracts – Types, Symptoms, Diagnosis And Treatment

Cataracts is defined by abnormal lens transparency, the clear cause of cataracts is unknown.

Types of cataracts

There are two types of cataracts: congenital and acquired. Acquired cataracts (primitive) may occur on a healthy eye, which has not suffered from any illness, or after an injury (traumatic cataracts).
Primitive cataracts (aquired) are always bilateral (affecting both eyes). At first one eye and then the other. This does not mean the eye affected last is in any relationship with the first, on the contrary there is no connection. Congenital cataracts can occur in one eye or in both eyes. A child may be born with this disorder, which inherits it. In some cases, changes in lens structure of the newborn can occur  if the woman suffered an infection during pregnancy.

Cataracts

Symptoms

Symptoms of cataracts should not frighten the patient. Symptoms of cataracts are easy to identify: Cataracts is gradually  installed and starts to affect vision at first only slightly. You can have a blurred vision or you can percieve light as very sharp.  Other symptoms may also ocuur like double vision, the need to frequently change lenses, or even improved vision (close vision) – in the early stages. Vision fades and diminishes gradually, never abruptly (only the case of traumatic cataracts).

Cataract Vision

Diagnosis

Diagnosis of congenital cataracts in made following a simple consultation: for newborns some eye drops are administrated on the eye and an ophthalmoscope is used to determine the condition. Child’s only chance to see is surgery as soon as possible, immediately after birth. Frequently, children who develop cataracts are operated in the first three months of life. Generally, the diagnosis of cataracts can be made only by an ophthalmologist. Investigations are not very complex. The patient undergoes slit lamp exam. There are situations in which the image is identical for a patient with advanced cataracts and for one without cataracts. This can create confusion, therefore, best suited for patients is to ask the ophthalmologist. The onset of disease, cataracts can be seen by the ophthalmologist even without using an instrument. Before surgery, after certain measurements (biometrics), ophthalmologists tell patients what type of lens they have to buy. In addition, the patient undergoes a sugar blood test and blood pressure is measured. There are situations in which patients have high blood sugar levels, suffer from diabetes, and they do not know about it. High blood sugar levels are a contraindication for surgery , the risk of bleeding beeing very high. Blood pressure is measured. If the blood pressure is high only in the day of surgery, the anesthesiologist can bring it to normal values. If the hypertension is chronic (most cases), the patient is sent to a cardiovascular diseases specialist and will return when blood pressure values are constant and normal.

Cataracts Diagnosis

Treatment

Treatment of traumatic cataracts is still surgery. These cataracts occur by hitting, pinching or work accidents. Complicated cataracts are the result of ocular complications. The only effective treatment that can solve this disease is surgery. It is relatively simple: the opacified lens is replaced with an artificial lens, the operation being done under local anesthesia. Surgery can be done ambulatory or during hospitalization (1-2 days). Methods of operation are very modern. The surgery takes about 20 minutes. Generally it is better to operate when eyesight is weak. Any kind of operation has its risks. It is wrong to assume that risk when vision is still good, useful. Secondly, it is a big mistake to operate on one eye, in its early stages of cataracts. Operation in early stages, has low chances of success. Normally, immediately after surgery the patient must see. After surgery, a bandage is applied for one day. In total, the patient is not kept in hospital longer than two days for a cataract surgery. Postoperative treatment consists of placing drops. Treatment is not very expensive. After surgery, various complications can occur, such as postoperative inflammation, corneal lesions, which are generally resolved with further treatment. If surgery is performed by doctors who are competent and experienced, success rate is over 98%. Bleeding during surgery can occur in some cases (most patients with cataracts are older people and vascularization is not very good).

Cataract Treatment

Prevention

There is no way to prevent cataracts. There is one drug that can stop the evolution of the disease, but not all patients develop the desired effect. Also, there are no drugs that can cure the disease, surgery remains the only option.

Hypercholesterolemia – Why Is My Cholesterol So High?

Hypercholesterolemia is affecting about 42 million Americans, and more than 63 million have borderline high cholesterol. Hypercholesterolemia causes are varied, including family history and diet. Colestrol level is measured by a blood test: Total Cholesterol (blood)

For adults:

• High cholesterol reaches a level equal to or greater than 240 mg / dl;
• Limit cholesterol (borderline high) values range from 200 to 239 mg / dl;
• A good level of cholesterol below 200 mg / dl;

For children:

• High cholesterol reaches a level equal to or greater than 200 mg / dl;
• Limit cholesterol (borderline high) values range from 170-199 mg / dl;
• A good level of cholesterol is below 170 mg / dl;

Cholesterol Foods

Here are some of the most common causes of hypercholesterolemia

1. Nutrition. Choosing a diet rich in saturated fats (like a fried egg-based breakfast) can be the main cause of increased cholesterol.
   Unhealthy fats are often found in: beef fat, pork, milk, eggs, butter or some types of margarine, cheese, also in many prepared foods, biscuits, chips and other snacks like that kind (this kind of food favours hypercholesterolemia). On the other side, monounsaturated and polyunsaturated fats can be found in nuts and fish and can help lower LDL cholesterol, you gain the same benefit consuming fibers usually found in fruits, oats, barley and vegetables.
2. Stress. Numerous studies demonstrate the link between stress and hypercholesterolemia, stress, directly affecting the habits and lifestyle in general. For example, in tensioned moments, some people consume large amounts of fatty foods and / or sweets, developing hypercholesterolemia. Stress hormones (adrenaline and cortisol) favors the production of cholesterol, fatty substance produced by the liver to provide energy needed for the body and for repairing damaged cells.The problem is that high levels of cholesterol clog arteries and can even lead to a heart attack or stroke.
   In moments of stress, cortisol has the additional effect of producing more “sugar” – the energy source of the body for short periods of time. In recurring stressful situations, however, “sugar” is not used entirely and is converted to triglycerides or other fatty acids. Research has shown that these fat deposits are usually located on the abdomen (abdominal obesity) – increasing the risk for cardiovascular disorders or diabetes.
3. Weight. Normally, excessive weight is in direct relation with hypercholesterolemia, having in mind that the body stores excess calories and triglycerides. Obesity can raise triglyceride levels, change in the body that favors reducing good cholesterol (HDL). Weight Loss with at least 10% compared to initial weight contributes significantly to a health improvement and a better blood cholesterol level.
4. Activity Level. People who have an inactive or sedentary lifestyle, also have a increased risk of hypercholesterolemia or cardiovascular disorders. Lack of exercise can increase LDL cholesterol – bad cholesterol and decrease good cholesterol- HDL
   People who have an inactive or sedentary lifestyle, increased risk of hypercholesterolemia or cardiovascular disease. Lack of exercise can increase LDL cholesterol – bad cholesterol and decrease good cholesterol – HDL.
5. Age and sex. After  20, cholesterol level starts to grow naturally. For males, cholesterol begins to decrease after 50, and in terms of female gender, cholesterol level remains relatively low until menopause, then begins to rise, reaching close levels with those currently seen in males (equal risk of hypercholesterolemia at this stage)
6. General health status. Annual medical consultation is very important and the practitioner must be properly informed about the patient’s risk of cardiovascular disease and his hypercholesterolemia. Certain conditions such as diabetes or hypothyroidism, can increase cholesterol levels.

Increased values of total cholesterol (hypercholesterolemia) is found in:

• hypothyroidism
• pancreatic diseases: diabetes mellitus, chronic pancreatitis
• pregnancy
• alcoholism
• diet rich in fat and cholesterol (most common cause of hypercholesterolemia)
• obesity
• administration of certain drugs: progestogens, anabolic steroids, corticosteroids, certain diuretics, levodopa, phenytoin, amiodarone;
• nephrosis: chronic nephritis, renal vein thrombosis, diabetic glomerulosclerosis
• familial hypercholesterolaemia type IIa
• biliary obstruction: cholestasis, biliary cirrhosis

High Cholesterol

Other causes of hypercholesterolemia

1. Family history. In some cases, hypercholesterolemia can be present in  young patients, not caused by any illness, but due to genetics. Some inherited diseases such as hyperlipidemia or hypercholesterolemia can lead to dangerous levels of blood cholesterol, very difficult to control. For this reason, cholesterol levels should be maintained consistently low through diet and / or medication. However, some genetic abnormalities may promote increased cholesterol levels, regardless of diet or lifestyle adopted by the patient – familial hypercholesterolemia is a condition with genetic transmission, which increases the level of abnormal blood cholesterol.
2. Smoking. One of the harmful effects of tobacco is good cholesterol lowering. Smoking lowers HDL cholesterol levels and is directly responsible for approximately 20% of deaths caused by heart diseases. When a person quits smoking, in a few weeks – months (depends for each person) reaches the normal level of HDL reducing the risk of hypercholesterolemia. HDL is affected not only by active smoking, but also by passive smoking too. High cholesterol (LDL) combined with smoking results in a increased risk of peripheral arterial disease.