New Drug For Advanced Types Of Skin Cancer

A new drug, called vemurafenib (Zelboraf) was released for the treatment of  metastatic melanoma. This drug is specifically indicated in patients with melanoma and who have mutations in the BRAF gene. About 50% of patients with melanoma have this type of BRAF mutation, which does not occur in normal cells. This drug is not indicated for use in patients with melanoma and without the BRAF mutation.

Vemurafenib is a BRAF inhibitor that blocks the function of the V600E-mutated BRAF protein. This new drug has been released  with a diagnostic test that can help to determine if the patient has melanoma cells with the BRAF V600E mutation.

This is a very important year for patients with advanced melanoma, because Zelboraf is the second new cancer drug that demonstrates an improvement in patient’s survival. In March, was released Yervoy (ipilimumab), another new cancer drug, used for late-stage melanoma that also showed an improvement in patient’s survival. Ipilimumab is an immunotherapeutic agent, which is also indicated for the treatment of metastatic melanoma and unresectable melanoma, unlike vemurafenib, which is used only in patients with advance stages melanoma and BRAF mutation.

The drug was study in clinical trials, in which it was demonstrated that vemurafenib improved overall survival and stop the progression of the disease, compared with standard chemotherapy, in patients with advanced melanoma who did not received previous treatment.

Skin Cancer

In this clinical trials, was shown that patients who were receiving vemurafenib had a reduction of 74% in the risk for progression of the disease or death, compared with patients who were receiving dacarbazine chemotherapy. Mean progression-free survival was 5.3 months in the vemurafenib group, compared with 1.6 months in the dacarbazine group. At 6 months, estimated survival was 84% in the patients who were treated with vemurafenib and 64% in the patients who were treated with dacarbazine.

In this study, which was conducted at 104 centers in 12 countries, patients who participated had advance forms of melanoma, who were previously untreated or with inoperable stage III or IV metastatic melanoma and a V600E mutation in the BRAF gene. Patients receive either vemurafenib, 960 mg, orally, twice a day or dacarbazine 1000 mg/m² of body-surface area, in intravenously infusion, every 3 weeks.

Common adverse effects which were associated with vemurafenib were arthralgia, rash, fatigue, alopecia, keratoacanthoma, squamous cell carcinoma, photosensitivity, nausea and diarrhea. 38% of the patients required a dose modification because of its toxic effects. Less than 10% of patients who received vemurafenib experienced problems with high levels of toxicity. The most common of these toxic adverse effects were skin rashes, photosensitivity, and joint pain.

The investigators also reported that 12% of patients who were treated with vemurafenib developed advance forms of cutaneous squamous cell carcinoma, compared with less than 1% of the patients who were treated with dacarbazine.

New Genetic Markers That Can Predict Aggressive Forms Of Prostate Cancer

Prostate cancer, after lung cancer, is the second leading cause of death in men. One of the big problems regarding this disease is the inability to differentiate aggressive forms of prostate tumors from other forms of prostate tumors that might never become clinically significant.

According to a study which was published in August 2011, five variants of genetic markers were identifyed which are associated with aggressive forms of prostate cancer. The researchers said that this is the first study which demonstrates that the genetic markers can provide prognosis information for prostate cancer. The scientists now hope this markers, along with other markers that may be identified in the future, can help prostate cancer patients to be early diagnosed.

Prostate Cancer

This genetic markers which were validated as being associated with aggressive forms  of prostate cancer are single-nucleotide polymorphisms (five of them). This 5 single-nucleotide polymorphisms were located, in the following genes:

1. LEPR, represents the strongest marker which is associated with aggressive forms of prostate cancer. It is a cytokine receptor which can be found in normal and malignant prostate tissue. The binding of leptin to its receptor, leads to the appearance of some effects like stimulation of tissue growth, inflammation, angiogenesis and bone mass regulation, which can affect prostate carcinogenesis. Because of the latter effect, LEPR becomes a interesting marker for prostate cancer progression, because the primary site of metastasis for prostate cancer is the bone and the presence of bone metastases dose not represent a element of good prognosis in patients with prostate cancer;
   
2. CRY1, the cryptochrome 1 gene, it is the marker that regulate the level of androgen hormones, which are known as factors that favor prostate cancer progression. This marker may also function as a tumor suppressors through regulation of cell proliferation, apoptosis, and response to DNA damage;
3. RNASEL is associated with hereditary forms of prostate cancer and is also associated with apoptosis, inflammation, cell proliferation and adhesion;
   
4. IL4 plays a important role in prostate cancer because this marker activate a transcription factor;
   
5. ARVCF is a marker which is member of the p120 catenin family of proteins, which increase expression of cell adhesion and may facilitate the prostate cancer progression.

Patients with 4 to 5 positive genetic markers had a 50% higher risk for aggressive forms of  prostate cancer than patients who had only 2 or fewer positive markers. The researchers noticed that the risk for mortality in patients with prostate cancer, increase with the number of this genetic markers.

Prostate cancer, as all malignant tumors, is a complex disease that results from an interaction between genetic and non-genetic factors. In the past was done a number of studies that have identified some genetic mutations that may be associated with prostate cancer risk. This mutations which are associated with prostate cancer were found on the chromosomes 3, 6, 7, 10, 11, 19, and X.

Gastric Cancer

Gastric cancer represents an important cause of mortality worldwide. Frequency of gastric cancer differs significantly according to geographical areas and is directly related to eating habits, Japan as well as northern Europe have a high incidence of this type of cancer.

Gastric cancer is 2-3 times more common in men than in women and its frequency increases with age, average age of diagnosis is over 60 years. Occcurs rarely under the age of 45 years and gastric cancer rate started to decline in the last decade, with more frequent eradication of Helicobacter pylori infection.

Gastric Cancer

Gastric Cancer Causes

Lately it was more well-established the relationship between infection with Helicobacter pylori and gastric cancer. World Health Organization (WHO) consider that Helicobacter pylori is the main factor in the development of gastric cancer, reason why it was called ” rank I oncogenic factor”. Fact that over a decade has passed to eradicate Helicobacter pylori infection, makes that gastric cancer incidence to be lower.

Gastric Cancer Risk Factors

Risk factors for gastric cancer are represented by:

1. Eating habits. Increased content of nitrosamines in food preserved by salt and smoke are factors favoring the development of gastric cancer, in exchange, diet rich in fruits and vegetables with increased content of vitamin A and vitamin C, protects the stomach.
2. Low socioeconomic status may be a contributing factor, probably through diet and infection with Helicobacter pylori.
3. Genetic factor, proved by the existence of a family predisposition to this type of cancer.
4. Helicobacter pylori infection is increasingly shown to contribute to development of gastric cancer. Helicobacter pylori has been classified by WHO as first order carcinogenic factor, is the first bacterium that is recognized to be involved in developing of a malignancy. Helicobater pylori intervention in gastric cancer development is achieved by inducing an atrophic gastritis with intestinal metaplasia, which has an evolutionary potential to dysplasia and finally to the development of gastric cancer.

Gastric Cancer Causes

Gastric disorders predisposing to gastric cancer are:

1. Chronic atrophic gastritis, with intestinal metaplasia. Most often this type of gastritis is due to an infection with Helicobacter pylori.
2. Gastric adenomatous polyps: is a premalignant condition, particularly those with large size, more than 1cm – 2cm diameter. Endoscopic polypectomy is indicated at the time of their discovery.
3. Gastric resection in history, especially for gastric ulcer, is a risk factor for developing gastric cancer in longer than 15 years after resection. Usually there is an inflammatory gastritis of gastric stump, which can degenerate malignant. This makes the patient with stomach surgery, to be watched endoscopic more than 15 years after the surgery.
4. Gastritis with giant folds, Menetriere gastritis, has a risk of 15% malignant. Fortunately, it is a very rare condition.
5. Gastric ulcer, presents a low risk of malignancy, but often can be confused with an ulcerated gastric cancer, fact that requires biopsy of the lesion.

Symptoms:

Gastric cancer symptoms can be polymorphic, depending on how advanced is the disease. Common symptoms are:

• Epigastric pain;
• Capricious appetite, which can go up to total loss of appetite or complete refusal to eating meat;
• Progressive weight loss, which in advanced forms can reach up to cachexia;
• Iron deficiency anemia;
• Less frequently digestive bleeding may occur, which will allow endoscopy diagnosis of gastric cancer;
• In advanced forms can be palpated  an epigastric mass.

Quite often, gastric cancer can be discovered from an anemic syndrome with or without dyspeptic symptoms.

Early gastric cancer is usually asymptomatic or dyspeptic symptoms may appear subtle. Therefore, his discovery is often accidental, when performing an endoscopy for epigastric symptoms.

Gastric Cancer Morphopathology

Histologically, gastric cancer is a adenocarcinoma, which may appear as protruded, ulcerated or infiltrating cancer. Typical appearance of malignancy is the protruded form of cancer, that bleeds. Ulcerated gastric cancer may be confused endoscopically with gastric ulcer and therefore biopsy is needed to differentiate them.

Extension to nearby organs of gastric cancer (pancreas, transverse colon), appears early in general, as well as lymphatic extension of it. Metastasis is most commonly the liver and lungs  and sometimes may occur carcinomatous peritonitis.

Staging of gastric cancer:

Staging of gastric cancer is made after TNM system (tumor, lymph node, metastasis) and allows the establishment of prognosis and therapeutic approach:

Tumor:

• T1: cancer affects mucosa and submucosa;
• T2: cancer affects muscular of the mucosa;
• T3: cancer affects gastric serosal;
• T4: cancer affects the surrounding organs.

Lymph nodes:

• N0: no lymph node invasion;
• N1: the invasion of neighboring lymph nodes (up to 3 cm of tumor);
• N2: distant lymph nodes invasion.

Metastasis:

• Mo: absence of metastases;
• M1: distant metastases.

Gastric Cancer Diagnosis

Most often the diagnosis start from dyspepsia, epigastric pain, weight loss or an unclear anemic syndrome. The presence of family aggregation of gastric cancer or precancerous lesions, can draw attention to the diagnosis of gastric cancer.

Physical exam is usually poor, but in advanced forms of gastric cancer is allowing the palpation of a epigastric mass or a subclavian adenopathy.

Paraclinical examination:

Laboratory analysis will usually show iron deficiency anemia. There are gastric cancers that may not be accompanied by anemia.

Gastroscopy is the elective diagnostic method. It allows viewing of the lesions, assessing their character and taking multiple biopsies to confirm the histological diagnosis of gastric cancer.

From Histologically point of view, gastric cancer is classified as follows: incipient gastric cancer (superficial, affecting the mucosa and submucosa) and advanced gastric cancer (affecting all layers of stomach). Endoscopic, advanced gastric cancer can be: protruded, infiltrating and ulcerated.

Incipient gastric cancer was classified in terms of endoscopic (Japanese classification of incipient gastric cancer) as follows:

• Type I: protruded type;
• Type IIa: superficial elevated type;
• Type IIb: superficial flat type;
• Type IIc: superficial depressed type;
• Type III: excavated type.

Gastric Cancer Calssification

In incipient gastric cancer, survival at 5 years after surgery is about 95%.

Radiological examination with barium, a method that is outdated in terms of diagnosis, addressing in general to the advanced gastric cancer forms or gastric cancer infiltrating forms.

Abdominal ultrasound, allows highlighting the liver metastases or lymph node metastases.

Echo-endoscopy allows staging T (tumor) from TNM classification by assessing gastric parietal extension and the extension in regional lymph nodes.

Gastric Cancer Prognosis

The prognosis depends on theTNM extension of gastric cancer, histological type and age of the patient. Survival is good only in incipient gastric cancers, approximately 95% at 5 years. Surgery, with intent to eradicate gastric cancer is possible only in one third of cases, and in these survival at 5 years is about 25%.

Gastric Cancer Diagnosis

Gastric Cancer Treatment

Elective treatment of gastric cancer is surgical. Gastric cancers surgically exceeded can be trated endoscopically. Incipient gastric cancer can be treated endoscopically too.

Preoperative and postoperative chemotherapy. Recent studies have suggested that preoperative application of chemotherapy followed by chemo-radiotherapy, cause a major histologic response which can lead to a increased survival rate.

Palliative chemotherapy is used in advanced gastric cancer.

Iron Deficiency Anemia: Definition, Clinical Diagnosis, Complications, Evolution and Treatment

Iron Deficiency Anemia Definition

Iron deficiency anemia is a hypochromic type of anemia caused by a disorder in hemoglobin synthesis due to decreased amount of total body iron. The fundamental disorder is responsible for all the signs and symptoms of this disease. This disease is affecting both sexes and occurs at all ages but predominantly in women. It is the most common form of anemia encountered in clinical practice.

Iron Deficiency Anemia Symptoms

It should be mentioned right at the beginning that anemia occurs most often secondary to other diseases. So patients history is very important to elucidate the diagnosis. Signs of central nervous system and sense organs:

• Asthenia
• Morning headache
• Fatigue
• Tinnitus
• Balance disorders
• Vertigo

The onset is insidious and the progression of signs is gradual.

Examination of skin and mucous membranes:

• Skin is pale, dry, nails are brittle, break easily, have longitudinal grooves, platonichie type changes (flattened nails) or koilonichie (concave shape or cracks). The hair grows grey faster, may fall more easily and is brittle. Mucous membranes ar pale as well.

Anemia

Cardiovascular system signs: Appear parallel with the degree of anemia and patient age:

• Palpitations
• Effort dyspnoea
• Extrasystoles
• Angina-type chest pain, to heart attacks and leg edema.

Signs of the digestive system:

• Angular stomatitis (cheliosis) may appear or small, very painful, cracks at the mouth corners. Tongueburns appear spontaneous or stimulated by acidic foods or drinks due to atrophy of the lingual papillae. Atrophy of the pharyngeal mucosa leads to dysphagia especially for solid food, sign called Winson Plummer syndrome. These inflammatory changes continue into the esophagus and especially the gastric mucosa where hypertrophic gastritis installes. Gastritis has no clinical manifestations, but is sometimes associated with marked reduction of gastric secretion.

Splenomegaly:

• It is present in 10% of patients, it is moderate in size and returns to normal after correction of iron deficiencys.

Genito-urinary disorders:

• The most common is the menstrual disorder in women, menorrhagia (an abnormally heavy and prolonged menstrual period at regular intervals), which is relieved after specific treatment.

Other signs and symptoms:

• Ozaena (nasal mucosal atrophy) occurs in patients with severe iron deficiency
• Pica: representing appetite for inedible but nontoxic substances (earth, lime) and occurs in iron deficiency anemia with severe mental disorders.
• Immune deficiencies favoring repeated infections.

Anemia Symptoms

Iron Deficiency Anemia Complications

Cardiovascular: mostly occur in elderly with known coronary heart disease, vary from unstable angina to myocardial infarction and heart failure.
Severe mental disorders: dizziness, dementia, anemic coma. Digestive: gastiric cancer, gastric mucosal atrophy, intestinal disorders like nonspecific enterocolitis.

Iron Deficiency Anemia Evolution

Evolution of patients with iron deficiency anemia is closely correlated with the degree of anemia and the time of its diagnosis. Once the diagnosis and cause of iron deficiency anemia has been detected, after a well managed treatment, the evolution is favorable. Prognosis is good, ad integrum restitutio in most cases.

Iron Deficiency Anemia Treatment

Etiologic treatment: targets detection and removing the causes of iron deficiency anemia.

Pathogenic therapy (the cause): targeting the correction of iron deficiency. Iron preparations are used orally, bivalent compounds (glutamate, aspartate or iron sulfates), the minimum dose of 100-200 mg / day of elemental iron. The main preparations used are Glubifer 3×2 dg/ day, Ferro-Gradumet 2 dg / day, Sorbifer 1 dg / day, preferably taken in the morning. Because of gastrointestinal side effects (nausea, burns), preparations can be administered after a light diet. Duration of treatment varies from 4-6 months to a year, depending on the severity of anemia. The treatment will continue for 4-6 months after correction of hemoglobin values for recovery of iron deposits. Parenteral preparations are administrated only in case of absolute digestive intolerance, severe enteropathy, severe anemia.

Anemia Treatment

The dose used is 100 mg / day intramuscular, to be mentioned is the risk of anaphylactic shock from injectable iron preparations, and therefore treatment should be started in a hospital under strict medical supervision and prior to testing. Among the injectable iron preparations , the most common used are : Iron polymaltose 1 vial / day intramuscular, Ferrum Haussmann 1 vial / day intramuscular. Emergency transfusions to patients with severe anemia (Hb less than 6 g%) associated with ischemic heart disease.

Atrioventricular Block (AV Block) – Symptoms And Treatment

A disturbance in conduction between the sinus impulse (atrial impulse) and its associated ventricular response is called atrioventricular block. (AV block) .The conduction may be abnormally slowed or completely blocked. The AV block results from a functional or pathologic defect in the AV node, bundle of His or bundle branches. Cardiac ischemia and infarction are frequently associated with conduction blocks and delays.

Three categories of AV blocks have been traditionally described

• First-degree block
• Second-degree block(which includes types I and II)
• Third-degree block( complete)

First-degree block . It is generally identified on the ECG by a prolonged PR interval(more than 0,20 second). The rhythm remains regular and each P wave is associated with a QRS complex.

First-degree block is a common finding and may occur in the absence of organic heart disease.Drugs and organic heart disorders(myocardial ischemia, congenital heard defects) may be at the root of first-degree block. First-degree block is generally monitored but is not actively managed except to alleviate the underlying cause if possible.

Second -degree block

It is diagnosed when some of the atrial impulses are not conducted to the ventricles.

Two types os second-degree block are identified by the pattern of non-conducted impulses:

• Type I(also known as – Mobitz type I, Wenckenbach)

It is associated with progressive lengthening PR intervals until one P wave is not conducted(dropped beat).The pattern repeats, causing the QRS complexes to occur in groups. This means: the PP intervals are constant, whereas the RR intervals vary.

Type I second-degree  block is usually due to reversible ischemia of the AV node, often associated with acute MI. The ischemic node is slow to recover after each depolarisation, resulting, thus, in a longer and and longer nodal delay until one impulse is not conducted. This phenomenon( Wenkenbach phenomenon) gives the AV node time to recover, and the next atrial impulse is conducted more quickly with a nearly normal PR interval, beginning the cycle again.Treatment is rarely required.If the block progresses to type II block, a pacemaker may be required.

• Type II

Is identified by the presence of non-conducted P waves(dropped beats) with a consistent PR interval.The QRS complex is usually but not always, wide( 0.12 second or greater)

PR Interval

Type 2nd Degree Block

Type II block is usually associated with pathologic lesion of the bundle of His, the right bundle branch or both.It is the bundle branch block that causes abnormally enlarged QRS complexes. Type II is less common than type I but it is more serious. The pathology associated with this type of block is usually anterior septal MI or fibrosis of the conduction system. The evolution of this block might be complete heart block with slow ventricular escape rhythm and poor cardiac output. Type II block may also result in severe bradycardia (SLOW HEART BEAT RATE) due to the number of dropped beats. Symptomatic type II block may require implantation of a pacemaker.

Third- degree block

This block may occur as a result of pathological lesion of the AV  node, bundle of His, or bundle branches.

No impulses are conducted from the atria to the ventricles and a jonctional or an escape rhythm is evident.

The ECG shows regularly occurring P waves that are totally independent of the ventricular rhythm.

If the QRS is narrow, the block is most likely in the AV node, proximal to the bundle of His

Third Degree Block

A prolonged QRS interval(more than 0,12 second) indicates pathology distal to the bundle of His within the bundle branches.

Prolonged QRS Interval

The severity of symptoms is determined primarily by the heart rate, with slower rhythms being more serious.Apacemaker is usually required.

Symptoms:

First-degree AV block has no symptoms

Second-degree AV block of type I– is characterised by the temporary absence of a heart beat described by the patient as a break.

Second-degree AV block of type II-the patient might have bradycardia, a decrease in the ability to adapt to exertion, rarely syncope.

Third-degree AV block -can have one of the following clinical manifestations:

• Severe bradycardia
• Syncope
• Cardiac failure symptoms
• Rare, regular arterial pulse

Treatment:

• Medication – alters the properties of ion movement across cardiac membranes and affect automaticity as well as the rate and duration of depolarisation and repolarisation.

Class I ( blocks the ions of sodium)

• Procainamide, Quinidine
• Lidocaine, Tocainide
• Flecainide, Propafenone

Class II (indirectly blocks the ions of calcium)

• Atenolol, Metoprolol,Propanolol

Class III ( blocks the ions of potassium)

• Amiodarone, Sotalol, Ibutilide

Class IV ( blocks the ions of calcium)

• Diltiazem, Verapamil

Other:

• Digitalis (enhances vagal tone, slows heart rate and AV conduction

• Pacemaker implantation – should be performed in any patient with symptomatic bradycardia and irreversible second  or third degree  AV block regardless of the cause or level of block in the conducting system.
• Implantable defibrillators – that detect  lethal rhythms and apply electric shocks to convert to normal sinusal rhythm( for those at high risk)

Treatment for this tpe of dysrhithmias ( AV blocks) centers on maintaining adequate cardiac output, providing antiarhytmic drugs when needed and managing the underlying pathological process.

Insomnia or Sleeplessness Causes And Treatment

Insomnia is mainly the incapability to sleep. Insomnia can also be considered a symptom that can accompany several medical, emotional and psychological disorders. There are several types of insomnia:

• Transient insomnia – it usually lasts less than a week. It is caused by several factors such as change of sleep environment, depression and other stress factors. It results in daytime drowsiness and poor psychomotor performance;
• Acute insomnia – it lasts less than a month. It actually represents an exaggerated form of transient insomnia. It presents with the same results;
• Chronic insomnia – it lasts for more than a month. When insomnia reaches this level, it rarely is a secondary disorder. It is the primary disorder. The results are: muscle fatigue, hallucinations and mental fatigue (even double vision);

Insomnia

Causes of insomnia:

• Inadequate sleep hygiene: Consumption of caffeine or other stimulant drugs should be avoided before going to bed, or even in the afternoon, for some patients are highly sensitive. It is not recommended for patients to compensate loss of sleep by sleeping late or by napping. It only damages nocturnal sleep more.

Insomnia patients are strongly advised to keep to a regular sleep schedule and avoid naps regardless of the amount of nocturnal sleep.

• Adjustment insomnia: Acute emotional stress factors can also cause insomnia;

• Psychophysiologic insomnia: Insomnia can persist  beyond duration of stress factors, because patients  anticipatory anxiety about the prospect of another sleepless night followed by another day of fatigue. Typically, patients spend hours in bed focusing on and brooding about their sleeplessness.

• Physical sleep disorders: Physical disorders can interfere with sleep and cause insomnia. There should be mentioned several disorders that cause mainly pain and discomfort, such as: arthritis, cancer, herniated disk. Nocturnal seizures will also interfere with sleep.

• Mental sleep disorders: Most mental disorders cause insomnia and EDS. Most patients with major depression report these symptoms.

• Sleep deprivation: Patients experiencing this syndrome get a poor sleep during night time thus resulting insomnia. Possible causes are various social or personal commitments. It is the most common cause of EDS, which disappears when sleep time is increased.

• Drug-related sleep disorders: Insomnia can result from intense use of stimulants such as amphetamines, caffeine, other sedatives, antimetabolite chemotherapy, anticonvulsants, oral contraceptives, methyldopa, propranolol, alcohol, and thyroid hormone preparations. Many psychoactive drugs can induce abnormal movements during sleep.

Treatment:

• Cognitive-behavioral strategies and hypnotics – suitable for patients who need rapid relief and whose insomnia has had daytime effects such as EDS and fatigue ;
• Relaxation training;
• Stimulus Control;
• Cognitive Therapy

Insomnia Treatment

If depression is accompanied by insomnia, antidepressants that provide strong sedation may as well be recommended by the patient’s physician, such as: amitriptyline, doxepin, mirtazapine, paroxetin, trazodone. There is a small chance that these drugs can cause EDS and other side effects, such as weight gain.

Narcolepsy Symptoms And Treatment

Narcolepsy is a neurological disorder which causes excessive drowsiness and sleeping episodes, all of the sudden and of short period. Narcolepsy appears even if the patient is well rested at night, thus the inability of the patient to lead a normal life. Sleeping while the patient is involved in certain activities, while driving or at work can cause disasters. REM sleep intrudes into wakefulness and into the transition from wakefulness to sleep. Many symptoms of narcolepsy result from postural muscle paralysis and vivid dreaming, which characterize REM.

Narcolepsy

Symptoms:

• Uncontrollable sleep attacks during daytime – Sleep episodes vary from few to many per day.  Sleep tends to occur during easy activities (eg, reading, watching television, attending meetings) but may also occur during complex tasks (e.g., driving, speaking, writing, eating). Patients may also experience sleep attacks”episodes of sleep that strike without warning. Patients may feel refreshed when they awaken yet fall asleep again in a few minutes;
• Excessive drowsiness ;
• Sudden loss of muscular control – cataplexy – Temporary muscular weakness without loss of consciousness; it is provoked by sudden emotions: anger, fear, joy or surprise. Weakness is confined to the limbs. These attacks resemble the loss of muscle tone that occurs during REM sleep;
• Hallucinations – Vivid auditory or visual hallucinations may occur when just falling asleep (hypnagogic) or immediately after awakening (hypnopompic). They are difficult to distinguish and are somewhat similar to vivid dreams, which are normal in REM sleep;
• Hypersomnia during nocturnal sleep.

These symptoms first appear between 10-25 years although it is not uncommon for narcolepsy to strike at any age. But rarely does it strike after 50. There are some reported cases where 3 – year olds were diagnosed with narcolepsy.

Treatment:

Modafinil, stimulants, Na oxybate, Antidepressants

Narcolepsy does not have a current cure. Sleep episodes and cataplexy, can be controlled in most patients with drug treatment. It is easier, in some cases,to treat the symptoms and not the disease as a whole. Two classes of antidepressant drugs have proved effective in controlling cataplexy in many patients: tricyclics (including imipramine, desipramine, clomipramine, and protriptyline) and selective serotonin reuptake inhibitors (including fluoxetine and sertraline). In general, antidepressants produce fewer adverse effects than do amphetamines. But troublesome side effects still occur in some patients, including impotence, high blood pressure, and heart rhythm irregularities.

Nocturnal Myoclonus or Sleep Movement

Nocturnal myoclonus is a disorder that unleashes the tendency of moving the legs, or sometimes arms. It appears whenever the person in cause is resting or sleeping. This type of sleep movement also unleashes involuntary movement of the legs when the patient is not sleeping. Sleep movement can also be associated to other medical diseases, such as anemia, renal dysfunctions, disorders of the thyroid gland, the Parkinson’s disease or even alcoholism.

Nocturnal Myoclonus

Symptoms of Nocturnal myoclonus

• Intense desire of leg movement;
• Uncomfortable sensation at the legs level;
• Sleeping disorders and problems falling asleep;
• Spasmodic, involuntary moves of the legs which appear during the night;
• Stress;

Causes of Nocturnal myoclonus

It is believed that a possible cause of  nocturnal myoclonus would be the perturbation of a chemical substance released in the cerebral level, called dopamine. It has the role of movement coordination. The level of dopamine decreases at night, thus the explanation of the sleep movement.

Another cause of nocturnal myoclonus can be the iron deficiency, which also contributes to the release of dopamine. Sleep movement syndrome has been divided in two types:

1. The first type of nocturnal myoclonus is considered to appear at any certain age. It frequently appears when the patient is still young, but it can also appear after approaching the age of 50.
2. The second type of nocturnal myoclonus appears as a complication of several diseases:

• Anemia;
• Chronic renal insufficiency;
• Pregnancy;
• Chronic alcoholism.

There are also some pills which can contribute to complicate the symptoms such as: antidepressants, anti-psychotics, anti-hypertension or those prescribed for heart conditions, allergy treatment and tranquilizers.

Treatment of nocturnal myoclonus – there is a series of measures which can be taken in order to overcome sleep movement disorder (nocturnal myoclonus):

Changing the lifestyle :

• Avoiding substances like alcohol, nicotine, coffee;
• No smoking;
• Following a regular exercising program during the day, not before you go to bed;
• Following a sleeping pattern, respecting the sleeping hours daily, no naps during the day, avoiding stimulating substances such as caffeine;
• Avoiding drugs which can trigger sleep movement symptoms or even worsen them.
• Massaging the legs;
• Taking a hot bath in the evening;
• Reading or watching TV in order to distract one’s attention
• Assuring a quiet and calm place to sleep;
• Avoiding big meals before going to bed.

Striae Distensae or Stretch Marks

• Massaging the affected area with a brush in order to intensify blood flow;
• Applying emollient creams on the affected areas so that the skin stays thin;
• Dietary rich in vitamins C and E, zinc and silicate and minerals which contribute to maintaining health;
• Drink plenty of liquids and exercise a lot in order to maintain a good  blood flow in the subcutaneous tissues.

Other means of treatment:

• Applying topical retinoids – Retinoids are derived from vitamin A. They are usually used in skin lesions;
• Laser therapy  – it consists of 6 sessions and does not remove the stretch marks completely;
• Chemical peeling – it has the role of removing the superficial layers of the skin. It also has the role of collagen synthesis.

Carbohydrate Intolerance

Carbohydrate intolerance is a disease that causes inability to digest certain carbohydrates due to a lack of intestinal enzymes. Carbohydrates are the primary source of energy and one of the most important nutrients in the human diet. Enzyme deficiencies can be congenital or acquired. Congenital deficiencies are rare; acquired lactase deficiency seems to be the most common form of carbohydrate intolerance.

Carbohydrate Rich Foods

Symptoms and signs of carbohydrate intolerance :

• Watery diarrhea;
• Bloating;
• Excessive flatus;
• Nausea;
• Abdominal cramps after ingesting lactose.

The patient should recognize his carbohydrate intolerance early in life and avoid eating dairy products. Diarrhea can get severe enough even to purge other nutrients before they are absorbed. Symptoms of carbohydrate intolerance are also similar to irritable bowel syndrome, therefore a visit to the physician is highly recommended. Diagnosing carbohydrate intolerance is considered an easy procedure. It can be diagnosed on patient history and supported diet. Patients usually have a history of intolerance to milk and dairy foods. The carbohydrate intolerance diagnosis is also suggested with the help of a H₂ breath or a lactose tolerance test.

Lactose Tolerance

Lactose tolerance test is less specific. Oral lactose is administrated. Lactose-intolerant patients develop diarrhea, abdominal bloating, and discomfort within 20 to 30 min. Low lactase activity in a jejunal biopsy specimen is diagnostic, but endoscopy is needed to obtain a specimen and is not routine.

Treatment of carbohydrate intolerance:

There is no specific cure, to improve the body’s ability to produce more enzymes, but symptoms can be controlled through diet. Commercial digestive enzymes  are the only resort to treat those who do not wish to diet or cannot help avoiding carbohydrate foods.  Carbohydrate intolerance disappears when the condition is successfully treated. Carbohydrate treatment should be specific for each patient. Young children with lactose intolerance should avoid milk products and perhaps switch to soy-based formula, or drink milk treated with lactase enzymes. Small amounts of foods containing lactose ingested throughout the day are better tolerated than a large amount consumed all at once. For those who find themselves unable to ingest any form of lactose, there are some pills available on the market, but they should be taken only at the physician’s recommendation, even though they can be purchased without prescription. There is no specific way to prevent this carbohydrate intolerance. A proper dietary management and regular visits to your physician should help lead a normal life.