Dry And Brittle Hair

During the summer time, we must pay special attention to our hair care, because the sun and humidity are the biggest enemies of the hair, causing various unpleasant situations: split ends, dry or brittle hair. Normally, the moisture level of a healthy hair is about 10%, but sunlight has the same harmful effects as those of warm air hair dryer.

Dry hair is usually a symptom of exposure to adverse environmental or inadequate production of sebum. Sebum is secreted by the sebaceous glands, which are associated to hair follicles. Improper production of sebum leads to a oily or a dry scalp. Wet weather and excessive heat will stimulate the sebaceous glands and hair will become oily. Low temperatures and low humidity slows down the production of sebum, and in combination with the wind will lead to a excessively dry hair. 90% of people suffer from dry, brittle or frizzy hair because it is insufficiently hydrated.

Dry Hair

There is a misconception according to which a person’s hair is dry because it suffers from a lack of natural oils. They say that vigorous brushing of the hair as many times with a natural brush or applying hot oil treatments will nourish the hair. But through these actions the hair quality will not improve in a meaningful way and the abuses of natural oil can have negative consequences.

Curly hair:

People with naturally curly hair or those who wrinkle their hair by chemical treatment will have to nourish and hydrate the hair in addition.

Chemical treatments (perms, hair dyes, etc.) will lead to a decrease in hair moisture, even up to 2%. When this happens will appear hair with split ends. If the moisture level of the hair will not be raised to 8%, then the hair will become brittle .

Those who live in areas with warm climates, prolonged exposure to sunlight or high temperatures should ensure that the hair care products they use contain substances with protection against harmful ultraviolet rays of the sun.

How to moisture your hair:

For the hair to become smoother and easy to comb, it will be added six drops of lavender oil, bay and sandalwood (six drops of each one) in 150 grams of sesame or soy oil. For applying this composition to the scalp will be used a cotton swab. Then you should wrap your hair in a towel and let the oil to act and to penetrate into the hair for about 15 minutes. Wash your hair with a normal shampoo. Alternatively you can use flax seeds that have an excellent moisturizer role.

Mosture Hair

Treatment for dry hair:

Dry, thin and brittle hair is prone to breaking and requires after washing with shampoo, the use of a conditioner, which can prevent the hair to become brittle, to repair the protein structures and to moisture the hair. Hair coloring, chemical treatments, including the stretching of the hair during styling will decreases the moisture of the hair and will damage the cellular connection between the elastic proteins.

Argan oil is naturally oil, derived from argan, a plant native to Morocco. It is believed that this is one of the best treatments available for loss of hair  moisture, it is absorbed rapidly and will provide immediate shine. If with argan oil are used extracts of  hemp seed and dimethicone, the nutritional benefits to the hair, are multiple,  the hair will not be brittle and will be protected against damage caused by heat.

Is indicated that before styling to be use products that are designed to nourish the hair: reparative gel or cream, conditioner, etc.

Jojoba oil,  mimics the natural properties of sebum and is often used in products that are cleaning and moisturize the hair. Considered to be effective when is added in its pure form to washing and cleaning hair products, jojoba oil nourishes and provides humidity to the hair.

Jojoba Oil

Emu oil used for thousands of years ago by Australians, deeply moisturize the hair,  in a natural way. It is found usually in the composition of shampoos and conditioners, but can be used separately or together with vitamin E, in a hair treatment. It has antifungal and antibacterial qualities and is often used to treat psoriasis, eczema, irritation and inflammation of the scalp.

Rice protein and corn protein are two of the most effective ingredients that act in different ways. Rice proteins penetrates the hair and its reach the hair roots and have a significant role in treatment of damaged hair. Corn proteins are focused on the protection and will add shine to the hair follicles.

Persons with brittle hair should avoiding the use of alkaline shampoos or of the shampoos that are containing alcohol. Brittle hair should be protected from excessive heat, especially from exposure to sunlight.

Cutting the tips of the hair regularly, is the best way to get rid of split ends. In addition, to this process will be used a conditioner and hair treatment at least once a week to keep hair healthy and hydrated.

During swimming, the helmet will protect hair to the harmful effect of the chlorine in the pool and the hair will be washed before and after swimming, to minimize chlorine absorption by the hair.

Dry And Brittle Hair

Diet for a healthy hair:

Body health will affect hair health. Dry hair is often a result of poor diet and of a mild dehydration. Therefore, we need to consume enough water and we need to have a balanced diet, which contain protein, fat and carbohydrates. If necessary, it will consider taking vitamin and mineral supplements. For dry hair treatment are given vitamins A, C, E and calcium. Hair state depends heavily on your overall health.

Biliary Dyskinesia

Biliary dyskinesia is a quite common disease of the gallbladder. The gallbladder stores the bile which is released by the liver. The bile reaches the small intestine where it digests the fat from aliments. To reach the small intestine, the bile must pass through the common bile duct and if the bile can not be secreted by the gallbladder or can not flow through the common bile duct, then will return in the gallbladder, leading to biliary dyskinesia.

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When a person eats, a hormone known as cholecystokinin is secreted by the cells from the intestine. The main action of cholecystokinin is activation of receptors that are distributed in the muscle of the gallbladder, thus producing contraction of gallbladder and the elimination of bile. Then, the bile is cleared from the gallbladder and will reach the small intestine. If a patient is suffering from biliary dyskinesia, then the gallbladder can not contract properly.

At the end of the common bile duct are three muscles that form the sphincter of Oddi. In its action to contract the gallbladder, cholecystokinin it binds to the receptors in the sphincter of Oddi and cause muscle relaxation. In this way the bile is eliminated from the gallbladder and will reach into the small intestine. If the sphincter of Oddi does not work properly, the bile will not pass through common bile duct and will remain in the gallbladder, which will cause biliary dyskinesia.

Biliary Dyskinesia Anatomy

Biliary Dyskinesia Causes And Symptoms

Biliary dyskinesia is often a symptom of disease rather than a disease itself. May signal the existence of gallbladder stones, acute or chronic pancreatitis and of other digestive disorders. However, symptoms can be induced by the consumption of certain types of food. Chronic inflammation may be another cause of biliary dyskinesia.

There is evidence that stress is a significant cause of biliary diskynesia. Some theorists believe that dopamine receptor dysfunction can trigger a biliary dyskinesia. Gallbladder function is likely to be damaged and can not receive appropriate signals from the brain when the bile will reach the gallbladder.

The most obvious sign of disease is the sharp pain in the right hypochondrium, intermittent cramps that are located under the right ribs. However, there are many patients who have no symptoms. Other patients may feel only a vague discomfort or a dull ache in right hypochondrium. Most often, pain occurs in approximately 40 minutes after the patient has eaten a meal high in fat. Rarely, may occur nausea and vomiting.

Biliary Dyskinesia Diagnosis, Risk Factors And Treatment

Most types of gallbladder disorders have symptoms similar to biliary dyskinesia. An extensive differential diagnosis is necessary to exclude other diseases such as cancer or gallstones. For the diagnosis, the doctor will ask, usually, blood tests and ultrasound. If the result of this  investigations is negative, will be done other tests or ultrasound that evaluate the gallbladder function.

Gallbladder

If is necessary a detailed investigation, then will be done colecistography. This involves the injection of a contrast substance into the bloodstream which will be transported to the liver cells and excreted trough gallbladder, which will allow the visualization of the gallbladder on a X-ray examination.

Although there are several risk factors for gallbladder disease in general, few of them are quite specific. Obesity, age and sex are known factors. Older women who are overweight are more likely to suffer from biliary dyskinesia than men. Treatment usually involves laparoscopic cholecystectomy (gallbladder removal complete).

Biliary Dyskinesia Herbal Remedies

Herbal remedies for biliary dyskinesia are using plants that are producing the contraction and relaxation of gallbladder and are regulating the liver secretion of bile. There are a number of plants with choleretic action and cholagogue effect (contributing to the contraction of gallbladder and evacuation of bile into the duodenum). 

• Artichokes – from this plant, with a good colecistokinetic effect, can be made teas. However, the taste is quite bitter, which is why many people avoid to drink it. The resulting liquid should be consumed with small sips, unsweetened, in the morning on an empty stomach. Then, the patient should stay on the right side about 30 minutes for maximum effect of the tea. The alternative would be capsules with artichokes, which can taken half an hour before each meal.
• Yarrow – infusion may have a slightly sweet taste, according to some. Drink a cup of tea from this plant with a half hour before every meal to stimulate the evacuation of the bile. The infusion is prepared from a teaspoon of dried herb to a cup of boiling water. Cover the infusion and leave it untouched for 5 minutes. This is a very good tea for hyperacid gastritis, gastric and duodenal ulcer, hepatitis, abdominal bloating, nausea and loss of appetite.
• Dandelion – is one of the most effective herbs for liver drainage and evacuation of bile in the digestive tract. Represents an excellent way to stimulate liver activity. For a cup of infusion will be use 2 teaspoons of herb. Drink 2-3 cups a day. You can follow a diet with fresh dandelion stems (10-15 strains per day) if you have hepatitis or biliary dyskinesi.

Biliary Dyskinesia Treatment

•  St. John’s Wort – the use of oil or tea from this plant will relieve the symptoms of biliary dyskinesia. The infusion is prepared by adding a teaspoon of crushed herb per cup of boiling water. The infusion should be served in 15-20 minutes after boiling. To treat lazy gallbladder (hypotonic biliary dyskinesia ), you should drink daily 2-3 cups of unsweetened tea or you should take a teaspoon of rattle oil after each meal. The plant is stimulating the liver function and has beneficial effects in gastritis and gastric hyperacidity.
• Celandine – reduce the pain caused by the contractions of the gallbladder. Drink a cup of infusion of celandine per day (one teaspoon of herb per cup of water).

Biliary Dyskinesia

Other recommendations:

• Because biliary dyskinesia can be triggered by the nervous system, try to be calm, at least until the pain relieves.
• Take regular 4-5 meals per day and avoid foods with high level of fats.
• Avoid fried foods, sauces and stews; prefer boiled or baked foods.
• Stop smoking and try not to have a sedentary lifestyle.
• For proper disposal of the bile, is indicated that after meals to lie on the right side for 30 minutes.

Diet in the case of biliary dyskinesia is not very strict. You should just avoid the wrong foods for you.

Sources

1. https://www.ncbi.nlm.nih.gov/pubmed/12095476

2. www.gallstoneadvice.com

Deep Venous Thrombosis

Deep venous thrombosis is represented by the formation of a blood clot (thrombus) in the deep veins of the lower limbs, pelvis or upper limbs. Thrombi can form in the superficial veins ( the condition is called thrombophlebitis or more simply, phlebitis) or in deep veins. Thrombi in superficial veins rarely cause problems, while those in the deep veins require immediate medical evaluation.

Thrombi from deep veins can be large in size and may move into the blood torrent up to the lungs, causing pulmonary embolism, which can be life-threatening. Deep venous thrombosis may have other long-term complications. In about 25% of cases, deep venous thrombosis can cause venous wall damaging, leading to chronic post-thrombotic syndrome. This syndrome is responsible for the appearance of pain, leg swelling, abnormal pigmentation of the leg skin (depigmentation) and limb injuries. Most of the thrombi develop in lower leg and thigh veins and less frequently in the upper limb or in pelvic veins.

Deep Venous Thrombosis

Deep Venous Thrombosis Causes

There are three major causes that increase the risk of developing deep venous thrombosis:

• Slowed blood flow. After certain surgical procedures or after a period of inactivity (for example after prolonged period of immobilization in bed or in long time airplane flights), blood flow from the veins of the legs is slowed and this represents a factor which can favor the formation of thrombi.
• Damage to the blood vessels. Blood vessels can be damaged by certain surgical procedures or by trauma.
• Changes in blood composition. Cancer or certain inherited disorders can cause the formation of clots faster than usual.

Deep Venous Thrombosis Risk Factors

There are several factors that increase the risk of developing deep venous thrombosis. Some risk factors can not be modified (eg. congenital disorders), while others are transiently and depend on certain circumstances (eg. pregnancy). The risk factors for deep venous thrombosis can be divided in major and minor.

Major risk factors for deep venous thrombosis are:

1. Bed rest for a period longer than 3 days.
2. Coagulation disorders (hypercoagulable state, in which clots forms faster), as a result of inherited genetic disorders, like deficiency of S protein, C protein deficiency, antithrombin III deficiency and factor V Leiden deficiency.
3. Major trauma.
4. Surgical procedures, especially for the knee or hip, neurosurgery or thoracic or abdominal surgical intervensions.
5. Procedures and therapies used for cancer treatment.
6. Paralysis due to spinal cord damage.
7. Introduction of a central venous catheter.

Deep Venous Thrombosis causes

Minor risk factors for deep venous thrombosis are:

Most of these factors have minimal effect if they appear alone, but in combination increase the risk for developing deep venous thrombosis. The risk of developing deep venous throbosis is increased by:

1. Certain diseases: varicose vein, myocardial infarction, heart failure or stroke.
2. A long journey by plane or by car, because of prolonged immobilization.
3. Pregnancy, especially after normal birth or after cesarean section.
4. Age. People older than 40 years have a higher risk of developing deep venous thrombosis.
5. Obesity.
6. The use of contraceptives. A recent study showed that the risk of pulmonary embolism as a complication of deep venous thrombosis is higher in women who are taking birth control pills. Contraceptive used before the appearance of thrombosis seems not to increase the risk of pulmonary embolism.
7. Hormonal therapies, such as estrogen substitutes, raloxifene for osteoporosis or tamoxifen for breast cancer treatment. Some studies have shown that the estrogen-progesterone combination have a lower risk for developing deep venous thrombosis.
8. Smoking.

Deep Venous Thrombosis Symptoms

In general, deep venous thrombosis causes minimal symptoms. If the symptoms appear, it may include:

• Edema, which can be generalized or localized to the affected limb, or only to the affected blood vessel and will give the aspect of a inflamed cord, which can be felt on palpation.
• Increased local temperature.
• Pain or tenderness. Pain may be continuous in the lower limb or in thigh, or can be present only at the palpation of the area or can appear in walking.
• Erythema (skin redness).

Deep Venous Thrombosis causes

There are several disorders which can have symptoms that are similar to deep venous thrombosis symptoms, such as Baker cyst or cellulitis, and can make the diagnosis to be difficult.

Sometimes the appearance of a pulmonary embolism, will raise the suspicion of a deep venous thrombosis. Pulmonary embolism is a sudden blocking of arteries in the lungs. Thrombi from deep veins of the legs are the most common cause of pulmonary embolism. Symptoms of pulmonary embolism include:

• Sudden dyspnea (shortness of breath);
• Chest pain that gets worse in inspiration;
• Cough that can be bloody (with streaks of blood);
• Tachycardia (increased heart rate).

Pulmonary Embolism

Deep Venous Thrombosis Diagnosis

Deep venous thrombosis is suspected by history of the patient and by physical examination. The data obtained after the initial investigations will allow the physician to determine if the risk of developing deep venous thrombosis is low, medium or high. Establishment of risk will help the physician to determine the appropriate investigations to diagnose deep vein thrombosis.

Investigations commonly used in the diagnosis of deep vein thrombosis are:

Ultrasound represents the most used test to diagnose deep venous thrombosis. This test allows the visualization of blood flow in the veins. Sequence of investigations for deep venous thrombosis is influenced by risk level and by ultrasound results. If further investigations are need, these include:

• Ultrasound repetition, usually after a period of several days;
• Venography. This test involves injecting a contrast substance in the veins, which allow their visualization on X-ray examination.

Venography is useful if ultrasound examination does not provide an accurate diagnosis of deep venous thrombosis. Ultrasound examination does not provide accurate results if it is performed to determine the existence of a thrombus in deep veins of the lower leg. Although, thrombi at this level are not, usually, dangerous, they can grow in size and can extend to the thigh and can become dangerous. Thrombi from the leg veins have increased risk for the occurrence of pulmonary embolism. For this reason are needed  repeated ultrasound examinations, venographies or other tests to identify thrombi that can be overlooked in one ultrasound.

Additional tests:

Aditonale tests are useful in cases in where the ultrasound results are unclear, venography is not available or the result of venography can not establish the diagnosis of deep venous thrombosis. These additional tests can diagnose a thrombus or can exclude a deep venous thrombosis, but are not usually used.

Additional tests may include:

• Determination of D-dimers. This blood test is done before or after the ultrasound examination, if results are not clear enough to exclude deep venous thrombosis in individuals at low risk.
• MRI;
• Computed tomography (CT).
• Certain blood tests can diagnose a inherited coagulation disorders that can increase the risk of thrombus formation. However, screening of these diseases is not usual.

Deep Venous Thrombosis Ultrasound

Screening is indicated in individuals who had one or more of the following events:

1. Thrombus in a vein that has a precise cause.
2. Thrombosis occurred in a person younger than 45 years.
3. Presence of  deep venous thrombosis in a first degree relatives (mother, father, brother, sister). Family history of clots in the arteries does not increase the risk of developing deep venous thrombosis.
4. Thrombus with unusual location, such as: gastrointestinal region, brain or upper limbs.

Some experts believe that routine screening can prevent the onset of a deep venous thrombosis in patients with high risk or who are in a situation with high risk, for example, are subjected to a major surgical intervention.

People treated with anticoagulants need regular blood tests to monitor the effects of anticoagulants.These tests include:

• The activated partial thromboplastin time (APTT) for monitoring therapy with unfractionated standrad heparin;
• Prothrombin time for monitoring warfarin therapy;
• If pulmonary embolism is suspected, will be performed chest X-ray, computed tomography or pulmonary angiogram.

Disc Herniation

Disc herniation is a neurological disorder which is characterized by the sliding of nucleus pulposus along the spinal cord and spine, which translates clinically by the appearance of a very intense back pain in that area.

Disc Herniation Treatment

The diagnosis of a disc herniation can be made sometimes, only by the symptoms if the intensity and nature of the pain are high. Complete history of the patient have to be centered on the character of the pain and its evolution in time and physical examination can highlight disturbances in neurological reflexes, muscle strength and sensory disturbances.

Some characters of the pain may suggest a disc herniation:

• Pain that is localized to the lumbar region and gluteal areas (buttock) is often associated with disc herniation;
• Pain associated with sciatic radiculopathy, which radiates along the leg, below the knee;
• Pain that appear on flexion, rotation of the leg or in prolonged standing and have a sharp character is suggestive of a disc herniation.

Other information suggestive for the diagnosis of disc herniation are:

1. Acute onset of the symptoms, usually after a traumatism;
2. Pain that is  localized unilateral, which is aggravated by movement and relieved by resting in a certain position.

From the patient’s medical history is important to know if there have been recent trauma, if the patient have a profession that is requiring intense physical activity or if in his family exist other members with this condition.

Physical examination may reveal:

1. Reduced physiological curvature of the spine in the area that is involved in the disease process;
2. Abnormal position of the patient;
3. Pain in the leg that appeare after the patient lift the leg as high as he can.

Lumbar Disc Herniation

Also, can be performed a series of specific tests that may suggest cervical and lumbar radiculopathy. For example, the patient is asked to tilt the head forward and then to the sides while the doctor applies a slight pressure on top of the head. If the patient will experience pain or any sensory change in this test, the patient is suspected of cervical radiculopathy.There are several tests that can be practiced for the discovery of lumbar radiculopathy.

For a certain diagnosis of disc herniation are indicated imaging studies like, X-rays, computer tomography (CT), magnetic resonance imaging (MRI) and myelography.

X-ray of the spine is especially indicated to exclude other diseases which may have symptoms like disc herniation. The most common diseases that enter in the differential diagnosis are: pelvic fractures, horse tail syndrome, spinal infection, epidural and subdural infections, spinal stenosis and spondylolisthesis. Radiographic examination is limited, because it can not offer useful information about the state of the soft tissue that is surrounding the spine.

Computer tomography (CT) can provide useful information about the diameter of the spinal canal and about the soft tissue that is surrounding the spine.

Magnetic resonance imaging (MRI) is more indicated than CT in diagnosing pathologies of the spine, because has a greater accuracy. Three-dimensional images are obtained and in this way are very well visualized both spine and nerve roots, the nucleus pulposus and it can be determine the degree of the condition. Currently, MRI is the imaging method of first intention for diagnosing disc herniation and can be used even in patients without clinical symptoms. Studies have shown that over 60% of asymptomatic patients who did an MRI, have some degree of disc herniation.

Disc Herniation MRI

Myelography is a very accurate paraclinical examination, which can reveal the diagnosis of disc herniation, but is an invasive technique, because is requiring a lumbar puncture and the injection of a contrast substance. After the injection of contrast agents is made a radiography of the spinal canal and depending on the aspect can be determine if there are processes that are applying pressure on spinal nerves, if there are hernias and what is their degrees, if there are other pathological processes of the spine. Myelography has better results when is combined with CT.

Other specific tests are the electromyogram (EMG) and tests that determine the conduction velocity of a nerve impulses. EMG is done to determine exactly the nerve root that is involved in disc herniation. EMG can be performed simultaneously with tests that determine the conduction velocity of a nerve impulses and purpose of the two methods is to determine if there is an active pathological process which is affecting the nerves, the nerve roots or the muscles.

In general, patients with symptoms that are suggestive for disc herniation do not require further investigation. But if the patients are elderly, have symptoms that are not improving at the administration of a correct treatment and the pain is atypical, the specialst may request some laboratory tests, like: complete blood count, erythrocyte sedimentation rate (ESR), the level of alkaline phosphatase, serum calcium level and serum protein electrophoresis.

EMG

Treatment:

The goal of disc herniation treatment is pain relief and stop the evolution of etiopathogenic process. For this is indicated a period of rest, administration of NSAIDs and physiotherapy. Most patients respond well to these combined treatments and they can resume their daily activities, because the symptoms are adequately controlled. There are a relatively small percentage of patients who need long-term treatment, corticosteroids or even surgery.

Pharmacologic treatment

Pharmacological treatment includes the use of general analgesics or opioids, of muscle relaxants and anti-inflammatory drugs. The goal of pharmacological treatment is to reduce local pain and inflammation and restoring the patient’s freedom of movement.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are mainly indicated for moderate pain relief. Among NSAID, ibuprofen is best, if the patient has no contraindications. It is administrated 200-400 mg, but not exceeding 2 or 3 grams / day. Is not indicated in patients with peptic ulcer, renal failure and coagulation disorders.

Besides ibuprofen can be used other analgesics such as ketoprofen, naproxen or acetaminophen. Acetaminophen is not an NSAID, it has a different mechanism of action and has no side effects so important as NSAIDs (in particular on the stomach) but it has no anti-inflammatory activity. Opioid analgesics can be administered to patients with severe pain that can not be controlled by analgesics. The administration of opioid medication must be done under medical supervision because exist the risk of addiction. Unlike treatment with NSAIDs that can be administrated for a long period of time, opioids are administered only in short periods. Their indications are limited, like a disc herniation which is secondary to a severe trauma.

Muscle relaxants are given only if the patient has muscle spasms. Some patients may receive, corticosteroids (oral or intravenous) if the inflammation is important and it can not be reduced by the treatment with NSAIDs.

Epidural cortisone injections

A therapeutic option used to control pain and inflammation in disc herniation is represented by the injection of corticosteroids into the affected area. The beneficial effects are lasting several months. The procedure has some risks because it is invasive.  For a good localization of the affected area, the injections are performed under radiological control.

Surgical treatment:

Surgery is rarely used for uncomplicated disc herniation. Surgery should be considered as a measure of treatment, only if symptoms persist and are greatly affecting patient’s quality of life, by limiting daily activities and movements.

Lumbar Discectomy

The most used and indicated surgical procedures are:

1. Discectomy and micro-discectomy represents the removal of a disc that is protruding. The procedure is performed under general anesthesia and the patient remains hospitalized 3-4 days or until health status will allow discharge. To avoid the risk of blood clots, patients are stimulated to mobilize even in the first day, postoperative. Full recovery takes several weeks. If the disc herniation was not unique or whether there are other disorders that have to be treated, recovery will be difficult and longer. Micro-discectomy represents the removal of a fragment of disc which is involved in very small hernia, through a small incision;
2. Laminectomy and hemi-laminectomy, involves to relieve spinal stenosis or nerve compression;
3. Chemonucleolysis, is a procedure that involves injecting an enzyme (chimopapain) inside the herniated disc in order to dissolve the gelatinous substance (nucleus pulposus) that is responsible for the symptoms. In some cases chemonucleolysis can be an alternative to discectomy.

Disc Herniation

Disc herniation is a neurological disorder which is characterized by the sliding of nucleus pulposus along the spinal cord and spine, which translates clinically by the appearance of a very intense back pain in that area. This condition occurs when a part or the entire nucleus pulposus herniates through a weakened area of  the fibrous ring of intervertebral disc.

Disc herniation is often located posterior and on the same side of the defect. The intervertebral disc is located between the vertebral bodies. It is designed to absorb the shock waves which are being put on the vertebral column while are performed sudden movements during strenuous activities.

Disc Herniation Patient

The intervertebral disc is composed of a central area with the consistency of a gel substance, called the nucleus pulposus which is surrounded by a fibrous capsule, called the fibrous ring. This structure is held in place by a strong ligament, called anterior longitudinal ligament (which is located anterior to the spine vertebral bodies) and posterior longitudinal ligament (located posterior to the spine vertebral bodies). Besides these two ligaments, the structures are kept fixed also by the paravertebral muscles.

Disc herniation can occur at any level of the intervertebral discs, but the two most common locations are the cervical and the lumbar discs. Lumbar disc herniation is the one that produces most chronic back pain which is radiating into the leg. Lumbar disc herniation is more common than the cervical disc herniation and occurs especially in the segments L5-S1 of the spine, because in this area ligaments are weaker and more slender.

Frequency of disc herniation is relatively high, varying between 1-10% of the adult population. The most affected group of population is between 25-45 years.

Stages of Disc Herniation

Causes:

Spinal column is formed by the overlapping of the vertebrae and has many roles, including to support the trunk, to protect the spinal cord and nerves that emerge from it and which are distribute to the periphery. Despite the fact that it look rigid, spinal column has some flexibility and vertebrae are overlapping through some spaces which are connected by a fibrous rings, which have in the center a very fine viscous gel, called the nucleus pulposus.

The function of fibrous ring is to equal distribute pressure in all area of the spine and not to overload one area of the spine. Thus, are amortized a lot of shock waves. The spine column is divided into several regions: cervical spine, dorsal spine, lumbar spine, sacral spine and coccygial spine.

Disc herniation occur when in the fibrous ring, a structure that is surrounding the nucleus pulposus, appear fissures that allows the nucleus pulposus to mobilize from its usual place and reach between vertebral corpus. Then, the nucleus pulposus will reach in the spinal canal and will press on the spinal nerve roots and will cause symptoms.

These fractures occur as a result of trauma, in some professions that require some very intense physical activity or in patients who are sitting very much in the chair. If the patient is compiling of persistent pain, but not a very intense pain, this is a sign of dulling of the intervertebral disc and not a sign of trauma.

Lumbar Disc Herniation

Risk Factors

A very important risk factor in the occurrence of a disc herniation is smoking because it interferes with proper oxygenation of the column and thus of the intervertebral disc. In this way, may appear dehydration and degeneration of the intervertebral disc, which, in time, will cause a disc herniation.

Scientists believe that in the appearance of a disc herniation, an important role is taken by genetic component, especially in patients with lumbar disc herniation.

Other risk factors are represented by:

• Age;
• Vigorous physical activity at work;
• Obesity;
• Sedentary lifestyle;
• Excessive vibration on which is subjected the spine column;
• Birth defects of the spine and spinal canal.

Most hernias occur in the lower back. This location is 15 times more common than the neck and is one of the most common causes of back pain. Cervical disc herniation appear in 8% of cases and in 1-2% of the cases appear high thoracic disc herniation. Cervical hernias occur mostly in the C5 – C6 and C6 – C7 segments of the spine and most often, in this type of disc herniation are involved cervical and brachial plexus.

In some disc herniation are affected the nerve roots and the clinical picture is important and more violent, because the patient will presenting symptoms of both motor and sensitive nature.
Disc herniation affects mostly middle-aged population and young adults with active occupations.

Herniated disc

Symptoms

Symptoms are greatly depending on the exact location of the disc herniation and on the soft tissue involved and affected. The pain felt by the patient can vary from moderate to very intense and can radiate along the nerve tracts. Often, disc herniation is not diagnosed immediately, because patients delay the presentation to the doctor or the symptoms are non-specific.
Sometimes, patients with disc herniation are asymptomatic and this situation is possible if the nucleus pulposus is not pressing on the soft tissue or on the nerves.

Symptoms of lumbar disc herniation:

The most common location of lumbar disc herniation is between L4 – L5 or between L5 – S1 segments of the spine. In this case, the most important symptom is the pain, which can affect the lower lumbar area, buttocks, thighs and may radiate to the leg and foot. Of all the nerves, the most often involved is the sciatic nerve, which is causing classic clinical appearance of the pain, but the femoral nerve may be also affected.

Symptoms described by patients include:

1. Muscle spasm;
2. Hypotrophy and muscular atrophy in the affected territory;
3. Pain which is irradiating along nerves track;
4. Pain which become worse when the patient is coughing, sneezing, laughing, because this actions are increasing the pressure in the spinal canal;
5. Paresthesia and other sensory disturbances in the leg.

Lumbar Disc Herniation

Symptoms of cervical disc herniation:

Symptoms may be localized to the posterior region of the skull, neck, pectoral arch, shoulder and upper limb and if there exist cervical and brachial plexus damage, the intensity of the pain is increased.

The most common symptoms are:

1. Asthenia of the muscles of the upper limbs;
2. Intense pain in the shoulder;
3. Pain in the nuchal region;
4. Failure to turn the head or making sudden movements;
5. Pain which is Irradiating in the shoulder, arm, forearm, and rarely in the hand and fingers;
6. Spasm of the superior vertebral muscles;
7. Sharp pain which appear in laughing, coughing and sneezing.

Cervical Disc Herniation

There are several characteristics of the pain from a disc herniation:

• Is unilateral;
• The pain has a continuous character, not a pulsating character;
• Appears when the patient is adopting a specific position.

Oral Antidiabetic Medication

Oral antidiabetic medication includes a multitude of substances, grouped as follows: sulfonylureas, biguanides, meglitinides, thiazolidinediones, alpha-glucosidase inhibitors and new antidiabetic drugs.

The main indications of oral antidiabetic medication include: type 2 diabetes mellitus, which is not regulated only with properly prescribed and rigorously observed diet.

Contraindications of oral antidiabetic medication:

1. Diabetic ketoacidosis;
2. Type 1 diabetes mellitus;
3. Associated infections;
4. Pregnancy, because oral antidiabetic medication have teratogenic effect;
5. Before, during and after surgical interventions (until the recovery);
6. Type 2 diabetes mellitus, which can be balanced with diet, but because the patient is undisciplined, this goal can not be achieved (the medication does not improve glucose balance).

Type 2 diabetes

Classification of oral antidiabetic medication:

• Sulfonylureas:

1. Generation I: Tolbutamide, Chlorpropamide, Tolazamide.
2. Generation II: Glibenclamide, Glipizide, Gliclazide, Gliquidone.
3. Generation III: Glimepiride.

• Biguanides: Metformin, Buformin.

• Thiazolidinediones: Pioglitazone, Rosiglitazone.

• Meglitinides: Repaglinide, Nateglinide.

• Alpha glucosidase inhibitors: Acarbose, Miglitol, Voglibose.

• New antidiabetic drugs: Exenatide (Byetta), Sitagliptin (Januvia).

• Combinations: Glibomet (metformin + glibenclamide), Avandamet (rosiglitazone + metformin), Competact (pioglitazone + metformin), Janumet (sitagliptin + metformin).

Sulfonylureas:

Sulphonylurea drugs used by almost half a century, to treat type 2 diabetes, are indicate in normal weight patients who have type 2 diabetes and in obese patients if they can not tolerate metformin.

After ingestion, sulphonylurea drugs are rapidly absorbed in the intestine, pass into the bloodstream, where they bind to specific proteins (albumin, in particular) and reach the liver where they are metabolized into inactive byproducts. Elimination is predominantly renal, with the exception of gliquidone that is eliminated in the bile in proportion of 95%.

Mechanism of action. Sulphonylureas are fixing on specific receptors and acts through the potassium channel from the pancreatic and the extra-pancreatic level. At pancreatic level, increase insulin secretion and at the level of pancreatic beta cells, they increase the number of insulin receptors. At extra-pancreatic sulphonylurea drugs decrease hepatic gluconeogenesis (glucose synthesis from non-carbohydrate sources), increased glycolysis and enhances insulin action in skeletal muscle and in adipose tissue.

Adverse effects. The main side effect of sulphonylureas is hypoglycaemia (favored by a high dose, kidney failure, liver failure, alcohol consumption, intense physical effort, age over 70 years). Other adverse effects consist of digestive manifestations (nausea, epigastric pain, liver pain) and of haematological manifestations (pancytopenia, autoimmune hemolytic anemia, thrombocytopenia).

Sulphonylureas can not be associate with each other, but may be associated with biguanides, thiazolidinediones, and even with insulin therapy.

Sulfonylureas

Biguanides:

Biguanides are used to treat type 2 diabetes with obesity. The most used drug in this class is metformin.

After ingestion, metformin is absorbed at intestinal level, disseminate in the body and is excreted in urine and faeces, unchanged.

Mechanism of action. Biguanides increase insulin action by binding to specific receptors, decrease intestinal absorption of carbohydrates and decrease anaerobic gluconeogenesis.

Adverse effects. Digestive manifestations, especially epigastric pain and diarrhea, occur in approximately 20% of cases and it is requiring a dose reduction or even quitting to this class of oral antidiabetic medication. Lactic acidosis is another adverse effect.

Biguanides may be associated with sulphonylureas, with thiazolidinediones and with insulin in both type 2 and type 1 diabetes.

Metformin

Thiazolidinediones:

Thiazolidinediones have been introduced in the treatment of type 2 diabetes in 1999.

Mechanism of action. Thiazolidinediones lower blood glucose levels by reducing insulinresistance in adipose tissue, in the muscle and in the liver, thus increasing insulin sensitivity, in this way it favors the hypoglycemic action of insulin.

Adverse effects. Before and during treatment with thiazolidinediones, is necessary to control liver enzymes (AST, ALT in particular). This class of oral antidiabetic medication is well tolerated in general, however, sometimes may occur mild edema of the lower limbs, through the loss of elimination of salt and water, which, on the one hand, may decrease hemoglobin, with the appearance of anemia, and on the other hand, requires to be administered with caution to patients with type 2 diabetes and heart failure. Thiazolidinediones can cause hypercholesterolemia and triglycerides disorders and for this reason, blood fats should be checked periodically.

The two used thiazolidinediones are pioglitazone and rosiglitazone, the latter being less used these days, because it is considered that increase the risk of cardiovascular complications.

Pioglitazone

Meglitinides:

After oral administration, meglitinides are absorbed at intestinal level, are metabolized in the liver and will result inactive byproducts, which are excreted into the bile.

Mechanism of action. This drugs are fixing on specific sites of potassium channels and increase insulin secretion stimulated by glucose level if there is a residual function of pancreatic beta cells.

Adverse effects. Rarely can cause hypoglycemia.

Considering that this class of oral antidiabetic medication has a short half-life, meglitinides are useful in correcting postprandial hyperglycemia. The tablets of this class are given after every meal (“one meal-one dose”).

Alpha glucosidase inhibitors:

Alpha glucosidase inhibitors are used to treat type 2 diabetes, which is inadequately controlled by diet.

Mechanism of action. Alpha glucosidase inhibitors are reversibly binding to alpha-glucosidase enzymes of small intestine cells, enzymes that are designed to split disaccharides and oligosaccharides, thus preventing the digestion and absorption of carbohydrates, along the small intestine. Thus, carbohydrates reach into the colon and are metabolized by bacteria, found at this level, in short-chain fatty acids and then are eliminated.

Adverse effects. Alpha glucosidase inhibitors can cause a slight weight gain, abdominal bloating, flatulence, abdominal discomfort, diarrhea, and rarely can cause liver test abnormalities.

Glucobay

New antidiabetic drugs:

1. Byetta (exenatide) is a synthetic analogue of GLP-1. GLP-1 is a substance secreted by the body that stimulates insulin secretion, but has other beneficial effects such as delayed passage of food from the stomach into the small intestine and stimulating satiety. The administration of this drug is by subcutaneous injection, like insulin, in a fixed dose, 2 times a day with pre-filled pen, initially every 5 micrograms twice a day, then 10 micrograms twice a day. Possible side effects include nausea, vomiting and rarely hypoglycemia.
2. Januvia (sitagliptin), a drug that inhibits the destruction of GLP-1 blood levels, so will extended the action of GLP-1 and will increase the insulin secretion. Daily dose is 100 mg. This drug is used in combinations with metformin.

Byetta

Sudden Cardiac Death – Causes, Diagnosis And Treatment

Sudden cardiac death is a unexpected death, which occurs in less than an hour after the onset of warning symptoms. Sudden cardiac death is caused by known or unknown heart conditions. Most cases of sudden cardiac death are caused by arrhythmias, but sometimes can be the first expression of a heart disease, unknown until that moment.

Sudden Cardiac Death

Causes:

Sudden cardiac death main causes are:

1. Ischemic heart disease, especially myocardial infarction, sudden cardiac death occurs in 80% of patients with massive myocardial infarction.
2. Arrhythmias:  ventricular tachycardia, paroxysmal supraventricular tachycardia, ventricular fibrillation, ventricular flutter.
3. Valvulopathies: mitral stenosis, aortic stenosis, mitral regurgitation, aortic regurgitation, prosthetic valves, infective endocarditis.
4. Right or left ventricular hypertrophy.
5. Myocardial diseases: myocarditis, cardiomyopathy.
6. Congenital heart malformations: patent ductus arteriosus, tetralogy of Fallot, interatrial septal defect, ventricular septal defect, atrioventricular septal defect, coarctation of the aorta.
7. Other heart diseases: cardiac tamponade, cardiac tumors.

Sudden cardiac death occurs mainly in patients with heart diseases that have been mentioned above, in the presence of precipitating factors, such as myocardial ischemia, electrolyte disturbances (hypokalemia, hypomagnesaemia), acid-base disturbances, hypoxia, anemia, drug toxicity (digoxin, antiarrhythmics).

Sudden Cardiac Death Causes

Ways in which sudden cardiac death occurs are:

• Malignant ventricular arrhythmias (sustained ventricular tachycardia or ventricular fibrillation), where exist a ventricular electrical activity, but mechanical ventricular contractions are inefficient.
• Asystole, the heart’s electrical activity and mechanical heart activity are missing.
• Electromechanical dissociation, involving a electrical activity which is present and systematized but mechanical activity of the heart is completely absent or ineffective.

Diagnosis:

Patient history obtained from the caregivers, may reveal a history of heart disease and may indicate what patient was compiling for, in the minutes preceding sudden cardiac death.

Physical examination detects changes that are caused by the loss of pump function of the heart: the abolition of consciousness, lack of response to painful stimuli, cyanosis, respiratory arrest, seizures, bilateral mydriasis which does not respond to light stimuli (fixed mydriasis).

ECG is the main paraclinical investigation that can determine the way in which sudden cardiac death occurred.

Sudden Cardiac Death ECG

Criteria for diagnosis of sudden cardiac death are represented by:

• Absence of heart sounds;
• The absence of central arterial pulse (in carotid arteries) and peripheral pulse ( in radial arteries);
• The lack of respiratory movements.

The presence of fixed mydriasis certify brain death and makes useless to undertake or to continue the resuscitation maneuvers.

Evolution and prognosis:

If it is not a prompt and competent intervention, sudden cardiac death lead to death or loss of brain function. The prognosis depends primarily on promptness with which the saviors intervened and also on the disease that caused sudden cardiac death.

Treatment:

Prophylaxis. Given that the prognosis is reserved, the most effective measure is to prevent sudden cardiac death. Prevention of sudden cardiac death refers to proper treatment of the patients with heart disease who are at risk for sudden cardiac death and hospitalization in the coronary unit immediately after the appearance of preceding symptoms of sudden cardiac death.

Measures of treatment. Diagnosis of sudden cardiac death requires the adoption of therapeutic measures of maximum emergency, which must be started even outside of the hospital:

• Placing the patient on a horizontal, solid plane;
• Control and release of upper respiratory tract;
• Starting cardiopulmonary resuscitation maneuvers (mouth to mouth breathing and external heart massage, in a ratio of 1 to 5);
• Oro-tracheal intubation;
• Getting an emergency venous access;
• Continuous monitoring of the pulse (carotid, femoral);
• ECG monitoring;
• Specific measures of treatment, adapted to the ways of production of cardiac sudden death:

1. 200-360 joules external electric shock, in repeated administration;
2. Adrenaline 1 mg intravenously (repeated boluses every 3 minutes);
3. Atropine 1 mg intravenously (repeated every 3-5 minutes, until a dose of 0.04 mg / kg).

CPR-Procedure

Cardiogenic Acute Pulmonary Edema – Causes, Symptoms, Diagnosis And Treatment

Acute pulmonary edema is a pathological condition defined by the presence of large amounts of fluid in pulmonary alveoli and in pulmonary interstitium. Cardiogenic acute pulmonary edema is an acute form of heart failure caused by increased pressure in the pulmonary capillary.

Acute Pulmonary Edema

Causes:

The mechanisms of production of acute pulmonary edema are:

1. Increased pressure in pulmonary capillary
2. Cardiogenic acute pulmonary edema by decreasing blood evacuation from the left atrium: atrial fibrillation, acute mitral regurgitation, mitral stenosis, thrombus or myxoma in the left atrium.
3. Cardiogenic acute pulmonary edema caused by left ventricular diastolic dysfunction: aortic stenosis, hypertension, hypertrophic cardiomyopathy, acute myocardial ischemia.
4. Cardiogenic acute pulmonary edema caused by left ventricular systolic dysfunction: acute myocardial ischemia, myocarditis, dilated cardiomyopathy, heart failure.
5. Non-cardiogenic acute pulmonary edema: parenteral hyperhydration.
6. Decreased oncotic pressure: nephrotic syndrome, cirrhosis.
7. Increased capillary permeability (acute respiratory distress syndrome): pneumonia, aspiration syndrome, inhalation of toxic gases, disseminated intravascular coagulation, anaphylaxis shock, acute pancreatitis.
8. Altered lymphatic drainage: pulmonary carcinomatosis
9. Incompletely understood causes: altitude acute pulmonary edema, neurogenic acute pulmonary edema, eclamsie, post anesthesia and post cardio-conversion.

Acute Pulmonary Edema Mechanism

Cardiogenic acute pulmonary edema is caused due to the increase pulmonary capillary pressure from 8-12 mm Hg (normal) to over 18 mm Hg.

Symptoms:

The main symptoms of acute pulmonary edema are the shortness of breath, cough, marked anxiety, cold and increased sweating and symptoms of the background heart disease.

Dyspnea is very intense, may occur in a patient who had until then no charge of this symptom (for example, a acute pulmonary edema that occurs after the onset of a myocardial infarction), or can overlap with the symptoms of preexisting heart failure . Dyspnea become worse when the patient is lying down.

Coughing can sometimes be the main charge of the patient. Cough may be dry or may be accompanied by the elimination of airy, pink sputum.

Physical examination revealed the following:

1. A patient that is restless, anxious or confused with sweaty, pale or mottled skin, with central type cyanosis, the patient is breathing typically standing at the edge of the bed and using accessory respiratory muscles.
2. Marked dyspnea, possibly vesicular murmur and prolonged expiration, rales crackles, of which level increases from the bases of the lungs to tops and can include the entire lung field.
3. Tachycardia, hypertension or hypotension and, depending on the case, rhythm disturbances or different heart murmurs.
4. In some cases, may appear signs of right heart failure: hepatomegaly, jugular turgor, hepato-jugular reflux, lower limb edema.

Acute Pulmonary Edema Symptoms

Paraclinical investigations:

Chest radiography shows pulmonary hilum, which are increased in volume and with wiped contours, that have the appearance of “butterfly wings” and in case of chronic heart failure, will appear cardiomegaly and pleural liquid. Radiological changes do not occur at the onset of a acute pulmonary edema.

Oximetry indicates hypoxia and hypocapnia. In severe forms may be present hypercapnia and respiratory acidosis, which constitute signs of gravity.

Other useful tests are:

• Electrocardiogram can detect: various arrhythmias, left ventricular hypertrophy or letf atrial hypertrophy, myocardial ischemia or myocardial infarction;
• Echocardiography can detect the presence of valvulopathies, of thrombus or myxoma in the left atrium, impaired function of the left ventricle.

Positive diagnosis of cardiogenic acute pulmonary edema is relatively simple, it is based on patient history and symptoms.

Acute Pulmonary Edema Ragiography

Evolution and prognosis:

Evolution of cardiogenic acute pulmonary edema is unpredictable. In a patient treated properly and quickly, acut pulmonary edema can be remitted. Sometimes, however, death occurs.

Treatment:

Treatment of acute pulmonary edema requires the following measures:

1. General measures: keep the patient in a sitting position, administration of oxygen on mask or nasal tube, dyspnea sedation with morphine.
2. Furosemide, administrated intravenous in dose of 80-120 mg or more, divided into four doses of 40 mg, each, is the primary mean of treatment of cardiogenic acute pulmonary edema. Its beneficial effects are explained by the occurrence of venous dilation, which will lead to decreased preload (quickly installed) and diuresis (which occurs in 20-90 minutes after the administration of furosemide).
3. Nitroglycerin, vasodilator with rapid effect, administrated sublingual (0.5 mg tablets, the dose can be repeated in 5-10 minutes) or intravenously, in the conditions of systolic blood pressure higher than 100 mm Hg.
4. Administration of digoxin can bring benefits by improving the cardiac tonus or by decreasing the heart rate in case of atrial fibrillation. Digoxin administration is contraindicated in cardiogenic acute pulmonary edema associated with mitral stenosis or with acute myocardial infarction.
5. Other therapeutic measures in cardiogenic acute pulmonary edema are: miofilin administration or the administration of angiotensin converting enzyme inhibitors, assisted ventilation, circulatory support with counterpulsation balloon and the treatment of the cause that led to the installation of cardiogenic acute pulmonary edema.

Metabolic Syndrome Increases The Incidence Of Liver Cancer

A team of researchers found that metabolic syndrome, a condition that increases the risk for cardiovascular disorders and diabetes, seems to be related to liver cancer. This results are based on a study, which was applied to a large number of people and the result was that metabolic syndrome is associated with an increased risk for developing hepatocellular carcinoma and intrahepatic cholangiocarcinoma.

The researchers found that metabolic syndrome was more common in patients who developed hepatocellular carcionoma (37.1%) and intrahepatic cholangiocarcinoma (29.7%) than in general population.

Incidence of  hepatocellular carcinoma and of intrahepatic cholangiocarcinoma have been rising world wide. Chronic infection with hepatitis B virus and hepatitis C virus and alcohol consumption are recognized as risk factors for this types of cancer in industrialized nations. The exact cause of this types of cancer is not know and 20- 50% of all cases of liver cancer are idiopathic.

Metabolic Syndrome

Although, intrahepatic colangiocarcinoma was associated with a number of the biliary tract or liver diseases, the exact risk factors for this type of cancer are not known, because many cases of intrahepatic cholangiocarcinoma appear to be unrelated to any of the known risk factors.

In general, the prognosis of liver cancer is quite bad. If it was diagnosed in early stages, survival at 5 years is about 30%, and if liver cancer was diagnosed in late stages, when are present metastasis to other organs, then the life expectancy to 5 years is approximately 5 -10%.

Nonalcoholic steatohepatitis have been associated with metabolic syndrome. The researchers highlight that, with the increased incidence of obesity and metabolic syndrome, worldwide, will increase the incidence of nonalcoholic steatohepatitis, that can evolve to cirrhosis and may also represent a risk factor for developing liver cancer.

Considering the high and increasing rates of obesity,  of metabolic syndrome and nonalcoholic steatohepatitis, this is a very important study because it shows that the rate of  liver cancer is higher in patients with metabolic syndrome. This study is important for physicians, because they should be aware of these associations, because people with metabolic syndrome are not generally viewed as being at high risk for these type of cancers.