EPILEPSY

epilepsy (a disorder of the central nervous system characterized by loss of consciousness and convulsions)

Epilepsy (from the Ancient Greek ἐπιληψία epilēpsía) is a common chronic neurological disorder characterized by recurrent unprovoked seizures. These seizures are transient signs and/or symptoms of abnormal, excessive or synchronous neuronal activity in the brain. About 50 million people worldwide have epilepsy, with almost 90% of these people being in developing countries. Epilepsy is more likely to occur in young children, or people over the age of 65 years, however it can occur at any time. Epilepsy is usually controlled, but not cured, with medication, although surgery may be considered in difficult cases. However, over 30% of people with epilepsy do not have seizure control even with the best available medications. Not all epilepsy syndromes are lifelong – some forms are confined to particular stages of childhood. Epilepsy should not be understood as a single disorder, but rather as syndromic with vastly divergent symptoms but all involving episodic abnormal electrical activity in the brain

Epilepsy Overview

Epilepsy is a condition in which a person has recurrent seizures. A seizure is defined as an abnormal, disorderly discharging of the brain's nerve cells, resulting in a temporary disturbance of motor, sensory, or mental function.
There are many types of seizures, depending primarily on what part of the brain is involved. The term epilepsy says nothing about the type of seizure or cause of the seizure, only that the seizures happen again and again. A stricter definition of the term requires that the seizures have no known underlying cause. This may also be called primary or idiopathic epilepsyEpisodes of abnormal electrical activity within the brain result in seizures. The specific area of the brain affected by the abnormal electrical activity may result in a particular type of seizure.
If all areas of the brain are affected by the abnormal electrical activity, a generalized seizure may result. This means that consciousness is lost or impaired. Often all the person's arms and legs stiffen and then jerk rhythmically.
One seizure type may evolve into another during the course of the seizure. For example, a seizure may start as a partial, or focal, seizure, involving the face or arm. Then the muscular activity spreads to other areas of the body. In this way, the seizure becomes generalized.
Seizures caused by high fevers in children are not considered epilepsy. Also see children's seizures

TYPES OF Epilepsy

When a disorder is defined by a characteristic group of features that usually occur together, it is called a syndrome. These features may include symptoms, which are problems that the patient will notice. They also may include signs, which are things that the doctor will find during the examination or with laboratory tests. Doctors and other health care professionals often use syndromes to describe a patient's epilepsy

The type or types of seizures
The age at which the seizures begin
The causes of the seizures
Whether the seizures are inherited
The part of the brain involved
Factors that provoke seizures
How severe and how frequent the seizures are
A pattern of seizures by time of day
Certain patterns on the EEG, during seizures and between seizures
Other disorders in addition to seizures
The prospects for recovery or worsening

Not every syndrome will be defined by all these features, but most syndromes will be defined by a number of them. Classifying a patient's epilepsy as belonging to a certain syndrome often provides information on what medications or other treatments will be most helpful. It also may help the doctor to predict whether the seizures will go into remission (lessen or disappear).
Partial seizure

Partial seizures (also called focal seizures and localized seizures) are seizures which affect only a part of the brain at onset, and are split into two main categories; simple partial seizures and complex partial seizures
A simple partial seizure will often be a precursor to a larger seizure such as a complex partial seizure, or a tonic-clonic seizure. When this is the case, the simple partial seizure is usually called an aura.
Partial seizures are common in temporal lobe epilepsy

Generalized Seizures

A generalized seizure is a sudden change in consciousness, muscle control or behavior caused by abnormal activity on both sides of the brain. A generalized seizure is different from a partial (focal) seizure, which usually affects a small, localized area of the brain.
Seizures occur when the neurons in the brain suddenly increase activity, causing an electrical storm that can overwhelm the brain. This can result in various symptoms depending on the area of the brain affected. People who have a generalized seizure usually experience symptoms that affect their entire body, such as whole-body muscle contractions or a loss of consciousness.

The most identifiable and traumatic type of generalized seizure is the tonic-clonic seizure, also known as grand mal seizures or convulsions. Many tonic-clonic seizures are isolated events and, although distressing to witness, rarely cause neurological damage.
Generalized seizures may be caused by chronic underlying medical conditions that may require treatment (e.g., epilepsy). Many generalized seizures have no known cause, making them difficult to prevent. In cases where the underlying cause is unknown, seizures can sometimes be controlled with medication.
Generalized seizures can rarely be treated with brain surgery because the abnormal neuron activity occurs in the entire brain. However, people with recurrent generalized seizures that are poorly controlled by medication may be suitable for a type of treatment called vagus nerve stimulation.
There are certain things bystanders can do (and not do) to prevent additional harm to a person having a generalized seizure. For example, nothing should be placed in a person’s mouth during a seizure, and restraint should not be used. It is recommended that bystanders clear the area of furniture and objects that may cause injury to the person having a seizure. Also, the person having the seizure should be gently rolled onto his or her side to prevent choking on vomit or mucus

Mechanisms of Action of Antiepileptic Drugs
Center for Treatment of Epilepsy and Migraine, Kielecka 25, 31-523 Kraków, 2Department of Neurology,
Neuropsychiatric Care Unit, Grunwaldzka 47, 25-736 Kielce, 3Department of Pathophysiology, Skubiszewski Medical
University, Jaczewskiego 8, 20-090 Lublin, 4Isotope Laboratory, Institute of Agricultural Medicine, Jaczewskiego 2,
20-950 Lublin, Poland

Abstract: g-Aminobutyric acid (GABA), one of the main inhibitory neurotransmitters in the brain, interacts with three types of receptors for GABA - GABAA, GABAB and GABAC. GABAA receptors, associated with binding sites for benzodiazepines and barbiturates in the form of a receptor complex, control opening of the chloride channel. When GABA binds to the receptor complex, the channel is opened and chloride anions enter the neuron, which is finally hyperpolarized. GABAB receptors are metabotropic, linked to a cascade of second messengers whilst the physiological meaning of ionotropic GABAC receptors, mainly located in the retina, is generally unknown. Novel antiepileptic drugs acting selectively through the GABA-ergic system are tiagabine and vigabatrin. The former inhibits neuronal and glial uptake of GABA whilst the latter increases the synaptic concentration of GABA by inhibition of GABA-aminotransferase. Gabapentin, designed as a precursor of GABA easily entering the brain, was shown to increase brain synaptic GABA. This antiepileptic drug also decreases influx of calcium ions into neurons
via a specific subunit of voltage-dependent calcium channels. Conventional antiepileptics generally inhibit sodium currents (carbamazepine, phenobarbital, phenytoin, valproate) or enhance GABA-ergic inhibition (benzodiazepines, phenobarbital, valproate). Ethosuximide, mainly controlling absences, reduces calcium currents via T-type calcium channels. Novel antiepileptic drugs, mainly associated with an inhibition of voltage-dependent
sodium channels are lamotrigine and oxcarbazepine. Since glutamate-mediated excitation is involved in the generation of seizure activity, some antiepileptics are targeting glutamatergic receptors – for instance, felbamate, phenobarbital, and topiramate. Besides, they also inhibit sodium currents. Zonisamide, apparently sharing this common mechanism, also reduces the concentration of free radicals. Novel antiepileptic drugs are better tolerated by epileptic patients and practically are devoid of important pharmacokinetic drug interactions.

Key Words: Antiepileptic drugs, GABA, glutamate, ion channels, epilepsy.

RECEPTORS FOR GAMMA-AMINOBUTYRIC ACID

GABA may mediate its synaptic events through two types of receptors - ionotropic and metabotropic. Among ionotropic receptors associated with a chloride channel so
called GABAA and GABAC receptors are distinguished - metabotropic ones linked to the cascade of second intraneuronal messengers are GABAB receptors [4,5].
GABAA receptor complex consists of a number of binding sites for GABA itself, benzodiazepines, barbiturates, ethanol and picrotoxin which is a chloride channel blocker. When GABA binds to its recognition site on the GABAA receptor complex, an opening of the chloride channel occurs with the subsequent influx of chloride anions into a neuron, resulting in its hyperpolarization. Benzodiazepine derivatives (f.e.: diazepam, clonazepam) increase the frequency of the channel
openings whilst barbiturates (f.e.: phenobarbital) prolong the opening time of the channel. Both, benzodiazepines and barbiturates also enhance the affinity of GABAA receptors for
the neurotransmitter [4,5]. In contrast, binding GABA to the GABAB receptors results in the activation of phospholipase A-2 and the following synthesis of arachidonic acid fromphospholipids. Arachidonic acid via regulatory Gi proteins is likely to modulate the activity of adenyl cyclase and cyclic AMP levels. Through the GABAB receptors GABA affects
the release of other important for the neuronal activity neurotransmitters. GABAC receptors are mainly encountered in the retina and their physiological significance is a matter of dispute.

Occurrence of GABA in the central nervous system was demonstrated in 1950 and in the same decade GABA was shown to inhibit seizure activity after its direct cerebralapplication in dogs [7]. Certainly, this gave rise to the assumption that GABA-ergic inhibition may be an important factor in the suppression of seizure activity in epilepticpatients. GABA itself was not a good candidate for an antiepileptic drug since it very poorly entered the brain through the blood- brain barrier. Much attention was paid to a synthesis of GABA-ergic agonists, which would easily penetrate into the central nervous system. Such substances were soon available, for instance agents increasing brain GABA concentration due to the inhibition of GABA
metabolism: aminooxyacetic acid, g -acetylenic-GABA, g - vinyl-GABA or direct agonists, for example - muscimol. Actually, these substances were found to exert anticonvulsant
effects in a variety of experimental models of epilepsy. The initial enthusiasm was, however, not fully justified it soon would come out that muscimol displayed a proconvulsant activity in primates and humans [7]. This was understood in terms of an undesired effects of the diffuse
stimulation of GABAA receptors within the brain. Consequently, the subsequent search for GABA-ergic agents as potential antiepileptic drugs would focus on substances
indirectly enhancing GABA functions - via inhibition of its metabolism or reduction of its neuronal uptake. This strategy led to the discovery of potent anticonvulsant substances -
some of them are nowadays potent antiepileptic drugs

ANTIEPILEPTIC DRUGS AND GABA-MEDIATED
INHIBITION

Valproic acid in the form of sodium salt was introducedto the therapy of epilepsy in the early 60s. One of the most likely mechanisms responsible for its anticonvulsant activitymay be inhibition of its metabolic degradation resulting in the elevation of GABA level in the synaptic cleft [11]. However, there are also data indicating no correlation between the protective action of valproate and GABA increase - in fact, valproate clearly reduced seizure activity produced by the inhibitor of GABA synthesis, izoniazid, but did not restore the reduced GABA level [12]. As already mentioned, benzodiazepines (fe.: diazepam, clonazepam) and barbiturates (fe.: phenobarbital) potentiate GABA-mediated inhibition via the increase in the affinity of this inhibitory neurotransmitter to its recognition sites within the GABAA receptor complex and via the direct influence upon the channel which leads to the enhanced influx ofchloride anions into the neuron and subsequent hyperpolarization. Among novel antiepileptic drugs, tiagabine and
vigabatrin seem to express their anticonvulsant activity mainly through the GABA-ergic system. Other novel antiepileptics associated with GABA-mediated inhibition, which also share additional mechanisms of action, are: felbamate, gabapentin, and topiramate. Tiagabine and vigabatrin, and to a certain degree - gabapentin, may be considered as drugs whose development was associated with so called GABA hypothesis of epilepsy [13]. Vigabatrin is an irreversible inhibitor of GABA transaminase and its administration in animals or humans results in the 3-fold increase in synaptic GABA level [14-16]. Tiagabine inhibits neuronal and glial GABA uptake, leading thus to the enhancement and prolongation of GABA synaptic events [16,17]. The anticonvulsant activity of inhibitors of GABA uptake in various models of experimental epilepsy was shown much earlier but these substances did not cross the blood-brain barrier. This certainly disqualified their possible use as antiepileptic drugs [18]. Probably, as already mentioned, tiagabine and vigabatrin possess mechanisms of action closely related to GABA-mediated events in the synaptic cleft, in contrast to conventional and some novel antiepileptics which may block voltage-dependent sodium and calcium channels and impair glutamate-induced excitation. For instance, sodium channels are blocked by a variety of antiepileptic drugs, including benzodiazepines (at high concentrations), carbamazepine, felbamate, lamotrigine, oxcarbazepine, phenytoin, phenobarbital, topiramate, and valproate. Ethosuximide or zonisamide mainly affect T-type calcium channels, and felbamate, phenobarbital, and topiramate inhibit glutamate excitation [19]. Interestingly, gabapentin, a cyclic analogue of GABA, was designed as a GABA agonist easily passing the blood-brain barrier. However, no receptor activity of gabapentin was detected on the GABAA receptor complex, only increased GABA turnover being found in some rat brain regions [20,21]. Also, gabapentin was documented to increase GABA level in brains of epileptic patients [15]. It is evident now, that this antiepileptic drug binds to the specific unit of voltagedependent calcium channel and inhibits intraneuronal calcium ion flux from the extraneuronal space [22]. Two novel antiepileptic drugs, topiramate and felbamate, although possessing multiple mechanisms of action (see below), affect GABA-mediated inhibition as well. Specifically, the former seems to potentiate effects of endogenous GABA through a novel binding site on the GABAA receptor complex [21,23]. The latter enhanced GABA-dependent chloride currents in rat hippocampal neurons [24]. However, such effect in vitro was no longer evident in the absence of GABA and, moreover, felbamate was not shown to interact directly with the GABAA receptor complex [25]. Among conventional and novel.

ANTI DEPRESSANTS

definition
a mental state characterized by a pessimistic sense of inadequacy and a despondent lack of activity
a long-term economic state characterized by unemployment and low prices and low levels of trade and investment
natural depression: a sunken or depressed geological formation
sad feelings of gloom and inadequacy
a period during the 1930s when there was a worldwide economic depression and mass unemployment
low: an air mass of lower pressure; often brings precipitation; "a low moved in over night bringing sleet and snow"
depressive disorder: a state of depression and anhedonia so severe as to require clinical intervention
a concavity in a surface produced by pressing; "he left the impression of his fingers in the soft mud"
angular distance below the horizon (especially of a celestial object)
pushing down; "depression of the space bar on the typewriter
emotional symptoms
misery,apathy and pessimism
low self-esteem and pessimism
indecisiveness,loss of motivation
biological symptoms
retardation of thought and action
loss of libido
sleep disturbance and loss appetite
another symptoms
Sad, anxious, or "empty" mood that lasts more than 2 weeks.
Trouble sleeping.
Appetite changes - either less appetite and weight loss, or eating more and weight gain.
Loss of interest in doing things you once enjoyed, including sex.
Feeling restless and cranky.
Nagging physical symptoms that don't get better with treatment (like chronic pain).
Trouble paying attention, making decisions, or remembering.
Feeling tired all the time or like you have no energy.
Feeling guilty, hopeless, or worthless.
Thoughts of suicide or death
the monoamine theory
The monoamine hypothesis of depression predicts an impairment in central monoaminergic function. The lesion may comprise deficiencies in the absolute concentrations of norepinephrine and/or serotonin (5-HT). Depletion studies have shown a correlation between such deficiencies and depressive symptoms. Measurement of the concentrations of the neurotransmitters and their metabolites in cerebrospinal fluid, urine, and plasma of patients with depression has yielded equivocal results regarding the possibility of altered metabolism of these neurotransmitters. Other studies have investigated the possibility of altered numbers and/or affinities of the serotonin and norepinephrine receptors and uptake sites. For example, there is evidence for a reduction in the activity of the serotonin reuptake transporter in patients with depression and an increase in the density of 5-HT2 receptors in the brains of suicide victims. Similarly, in the noradrenergic system, up-regulation of beta-adrenoceptors is consistently observed. Most recently, attention has focused on the possibility that a lesion may occur in the postreceptor, subcellular components of the monoamine systems, such as the second messenger processes. Also, experimental evidence has shown "cross-talk" between the noradrenergic and serotonergic systems. There is therefore substantial clinical and experimental evidence that lesions in the serotonergic and noradrenergic systems are responsible for depression and that antidepressant treatment can reverse these alterations
types of anti depressants
Selective serotonin reuptake inhibitors (SSRIs)
Serotonin-norepinephrine reuptake inhibitors (SNRis)
Noradrenergic and specific serotonergic antidepressants (NaSSAs)
Norepinephrine (noradrenaline) reuptake inhibitors (NRIs)
Norepinephrine-dopamine reuptake inhibitors (NDRIs)
Selective serotonin reuptake enhancers (SSREs)
Melatonergic agonists
Tricyclic antidepressants (TCAs)
Monoamine oxidase inhibitor (MAOIs)
Augmenter drugs
mechanisam of action
Bipolar disorder (BPD), the province of mood stabilizers,
has long been considered a recurrent disorder. For more
than 50 years, lithium, the prototypal mood stabilizer, has
been known to be effective not only in acute mania but
also in the prophylaxis of recurrent episodes of mania and
depression. By contrast, the preponderance of past research
in depression has focused on the major depressive episode
and its acute treatment. It is only relatively recently that
investigators have begun to address the recurrent nature of
unipolar disorder (UPD) and the prophylactic use of longterm
antidepressant treatment. Thus, it is timely that we
address in a single chapter the most promising research relevant
to the pharmacodynamics of both mood stabilizers and
antidepressants.
As we have outlined in Fig. 79.1, it is possible to characterize
both the course and treatment of bipolar and unipolar
disorder in a similar manner. Effective treatments exist for
the acute phases of both disorders; maintaining both types
of patients on such drugs on a long-term basis decreases the
likelihood and intensity of recurrences. Further, because the
drugs are given long-term, they produce a cascade of pharmacologic
effects over time that are ‘‘triggered’’ by their
acute effects. Both classes of psychotropic drugs incur a lag
period for therapeutic onset of action, even in the acute
phase; therefore, studies during the past two decades have
focused on the delayed (subchronic) temporal effects of
these drugs over days and weeks. Consequently, it is widely
thought that the delayed pharmacologic effects of these
drugs are relevant for either the initiation of behavioral improvement
or the progression of improvement beyond that
initiated by acute pharmacologic actions. The early realization
that lithium is effective prophylactically in BPD and
the more recent understanding that antidepressants share
this property in UPD have focused research on long-term
events, such as alterations in gene expression and neuroplasticity,
that may play a significant role in stabilizing the clinical
course of an illness. In our view, behavioral improvement
and stabilization stem from the acute pharmacologic effects
of antidepressants and mood stabilizers; thus, both the acute
and longer-term pharmacologic effects of both classes of
drugs are emphasized in this chapter

MOOD STABILIZERS

The term mood stabilizer within the clinical setting is commonly
used to refer to a class of drugs that treat BPD.
However, for the purpose of our discussion, it is important
to differentiate the three clinical phases of BPD—acute
mania, acute depression, and long-term prophylactic treatment
for recurrent affective episodes. Although a variety of
drugs are used to treat BPD (i.e., lithium, anticonvulsants,
antidepressants, benzodiazepines, neuroleptics), we suggest
that only a drug with properties of prophylaxis should be
referred to as a mood stabilizer and included in this chapter.
Significant evidence supports a therapeutic action for lithium,
both in acute mania and prophylactically in a major
subset of patients with BPD 1. However, the data for longterm
prophylaxis with anticonvulsants (i.e., valproate, carbamazepine),
although supported in part in clinical practice,
remains less well established scientifically
In the absence of a suitable animal model, an experimental
approach, used to ascribe therapeutic relevance to any observed
biochemical finding, is the identification of shared
biochemical targets that are modified by drugs belonging
to the same therapeutic class (e.g., antimanic agents) but
possessing distinct chemical structures (e.g., lithium and
valproate). Although unlikely to act via identical mechanisms,
such common targets may provide important clues

Our cleansing cream was developed as an alternative to soaps. It has a fine emulsified texture that can penetrate deeply to remove impurities.
Apply to face and neck with fingertips. Avoid direct eye contact. Rinse with luke warm water and follow with toner.
Due to its mild efficacy, the cleansing cream is appropriate for all skin types

Cleansing Milk

Our cleansing milk gently cleanses, moisturizes and protects your skin due to its dermatologically tested fine emulsion. It acts deeply so that excess sebum, make-up and grime are removed which opens the pores. The milk works like a very mild abrasive mask against dead cells. It restores water balance and acidic pH by nourishing and protecting the skin.
The cleansing milk is formulated with a vitamin compound. Vitamin E neutralizes dangerous free radicals and Vitamin C stimulates collagen.
Use every morning and evening on the face and neck followed by our toner.
The milk is suitable for all skin types and is highly recommended for sensitive skin

FOUNDATION CREAMS

Foundation Cream
Cream makeup foundation dries skin, it clogs pores, creates a “mask” on the face – most of those myths are faulty. Beauty industry is in continuous progress; modern tone creams not only hide skin imperfections, are not visible once applied, but they take care of the skin as well. This article refutes common myths about the foundation product. So, use tone creams freely
Tone Cream Clogs Pores
Modern cream foundations and the creams once used by our grandmothers have absolutely nothing in common. Most of the modern tone creams contain silicon, which does not stick directly to skin but rather creates a tiny web over the skin, protecting it and ensuring sufficient air circulation. The pigmentation particles in the cream are so tiny that they are simply physically unable to clog pores
Cream Foundation Creates a “Mask” on the Face
If you’ve picked a wrong tone colour, it will in fact look like a mask once applied. It is better to choose the tone using trial-and-error method. Come to the store wearing no makeup and apply various foundation tones directly on your skin. You should check how the tone looks in daylight and artificial lightning, as sometimes the shading of the tone depends on the lightning
Foundation is Bad for Skin
If you forget to remove the makeup before going to bed, it is surely not good for your skin. As for the rest of the cases, the modern foundations not only moisturise skin, but also protect it from harmful environment influences. Most of foundation creams contain solar-control factors – it is important to keep in mind, that one should always protect themselves from the sun, in summer as well as in winter. Sun is the main contributor to the skin aging. In winter, when cold wind and frost attack our skin, foundation helps it fight back to those attacks
If I Don’t Have Acne, then I Don’t Need Foundation
Perfect skin can be probably seen only in few children, when they are still infants. Rest of humans, unfortunately, have skin imperfections. Those shortcomings may be small spots, burst vessels, clogged pores, dark circles, bags under eyes and so on. If you prefer natural look, a light base, created using a light foundation and transparent powder, may be enough for you. An evening makeup, on the other hand, requires some tone cream
What Matters Is the Cream, Not How You Apply It
The application technique depends on the type of the cream and the effect you wish to accomplish. Before applying the tone cream, make sure the day cream is completely absorbed, otherwise the tone will spread unevenly. Tomorrow you will learn, how to apply various types of tone creams
how to apply
It seems like no one enjoys dealing with foundation. But how important is foundation? Foundation is probably the most essential cosmetic because it is one of the necessary steps of basic skincare. For healthy skin, you have to protect it. That is where foundation comes in. Foundation protects your skin from the environment-the sun, wind and pollutants
The problem with foundation is that we make common mistakes while applying it. We get the wrong color; it looks "cakey" and sometimes accentuates the flaws we were trying to coverRead
How to choose the perfect color
The key to flawless coverage is not to look like you are wearing a mask. It is NOT possible to pick up a bottle of foundation at a store, hold it up to your face and get the correct color. Honestly, you will need to sit down with a makeup consultant and test the color. It is best to test foundation color with sunlight. The worst lighting is florescent. No one looks good in florescent lighting. Never, never, never test for foundation on your hand or wrist. For ivory/beige women you will need to check your foundation on your neck and jawline. Sometimes the neck is a little different color than the face, usually a little darker and more yellow undertone. Because you will blend your foundation at your jaw line, you will want it to match where it stops at the neck. For bronze women, you will want to match your foundation on your cheek and jaw line. Sometimes there is an unevenness of color and this will help even out your skin tone

Sponge: A sponge is great to give you a light, sheer layer of foundation. It makes the foundation very easy to blend, a necessity for foundation and keeps your fingers clean too! I bounce back and forth between this one and the brush. The downside, a lot of foundation can get absorbed in the sponge so it tends to waste product. You will need to clean your sponge after every use or do what I do, buy a bag full of inexpensive sponges at a department store and trash them after every use.
Brush: I love the brush. The foundation looks perfect when using a brush, I can't really explain why, it just does. Use a foundation brush for a couple of days and it will be hard to go back to what you were using before. The one problem, you have to clean it every time you use it or you will ruin the brush. If you have to reapply your foundation during the day, a brush is the only way to go!
Fingers: Fingers are great because everyone has them, you always know where they are, and they are inexpensive. I personally, don't like the feel of foundation on my fingers so it's not my favorite. But if you don't have issues like me, they work great. Can be hard to blend with so just be careful

SUNSCREEN AND SKIN CARE TIPS

Sunscreen
Most people know that exposure to UV radiation can cause sun damage to the skin, including sunburn, photoaging, and increased risk of skin cancer. But did you know this damage also occurs when you walk from your house to your car or sit next to a window during the day? Even those little bits of exposure add up over the years and can cause wrinkles, dark spots and skin cancer
Sunscreen Decisions
There are several factors to consider when picking out a sunscreen:
How sunscreens work
Everyday sunscreen vs out-in-the-sun sunscreen
Using a sunscreen alone vs sunscreen plus moisturizer
Understanding the UV-index
How to be safe in the sun
Sunscreen Bottom Line
You've worked hard to take care of your skin by cleansing and moisturizing it. Don't undo all those benefits by exposing it to UV radiation. Find a good broad-spectrum sunscreen and make its application a part of your daily routine like brushing your teeth and bathing
Skin Care Tips For Your 30's
When you've reached your 30's, chances are good you've tried your fair share of products in hopes of having perfect skin. Maybe some of them worked for you, of course, some didn't. Then again, maybe you're only now just beginning to think about what the future holds in regards to your skin and you're trying to do all you can now to repair the lack of effort in your past
No matter the reason, today is as good as any day to start taking great care of your skin. And great care starts by knowing what skin type you fall in. Skin types vary by person, and can even vary depending on the seasons or even hormonal change. Once you see what skin type you are today, don't assume it will forever be your skin type. By giving your skin proper attention, you'll be able to see if you're starting to notice your skin getting drier or oilier as time goes on.
Daily Skin Care Basics
Now that you know your skin type, it's time to talk about what yous should be doing each day to properly take care of your skin. Create a skin care regime and make sure you do each step twice a day. I recommend a cleanser, toner and moisturizer. If you have oily or combination skin, stick with a gel based or foaming cleanser. Those of you with normal or dry skin will do best with a cream based cleanser. Toners are optional, but my personal results tell me that it works best for me. You can decide how you feel about toners and go from there.

SKIN CARE

Cleansing
Most of us know that cleansing is an important part of good skin care. The purpose of a cleanser, or soap, is to surround, loosen, and make it easy to remove dirt, debris, germs, excess oils, and left-over products applied to the skin. Unfortunately, there are harmful effects of cleansers on the skin.
Many people have dry skin because of their cleansing routines, not because their skin is normally dry. Often people think that their skin isn't clean unless it feels dry and tight after they wash it. People get used to the way their skin normally feels. They come to expect that they will haYou don't have to feel dry to be clean
You have good options
Use the mildest cleanser possible that still removes dirt, oil and debris ve dry, rough patches on the backs of their hands, itch in winter time, and sometimes have a dull complexion. They don't know that their choice of cleanser could be hurting their skin.
How do you know what type of cleanser to use and where? The first step is to understand your cleanser options:
Bar soaps - The most irritating cleansers but the best to get rid of dirt and grime
Liquid cleansers - A wide variety of tolerability - good for cleaning all but the oiliest skin
Facial cleansers - The mildest cleanser but may not remove oil and dirt as well
Cleansing Bottom Line
You don't have to feel dry to be clean
You have good options
Use the mildest cleanser possible that still removes dirt, oil and debris
Moisturizing
Moisturizing is an essential step in good skin care. A good moisturizer can stop the dry skin cycle from spiraling into cracked, thick, flaky skin. An effective moisturizer will have a combination of ingredients that:
Replenish the skin's natural ingredients that help maintain its structure
Cut down on damage from free-radicals
Help the cells function more normally
Good Moisturizer Ingredients
In the past, moisturizers were essentially water and wax mixtures that worked by trying to hold water in the skin. The only real difference between these moisturizers was how they "felt" to the consumer. Now there is complex science behind the new state-of-the-art moisturizers that are available. Some ingredients that you'll find in a state-of-the-art moisturizer are
Glycerol - Helps water and other moisturizer ingredients penetrate the skin to get where they are needed.
Ceramides - Help replenish the skin's natural oils.
Hydroxy Acids - Help with exfoliation of dead skin cells
Niacinamide - Helps the skin produce more natural oils, and may also help reverse the signs of sun-damaged skin, like brown spots and blotchiness
How to Choose a Moisturizer
Not all skin is the same, and not all moisturizers are the same. Picking out the best moisturizer for your skin depends on what your skin needs. Consider the following skin conditions when choosing a moisturizer:
Moisturizers for dry skin
Moisturizers for oily skin
Moisturizers for normal skin
Moisturizers for acne-prone skin
Moisturizers for red skin
Moisturizers for eczema, atopic dermatitis, or sensitive skin
Moisturizers with sunscreen

GONORRHEA

Gonorrhea (also gonorrhoea) is a common sexually transmitted infection caused by the bacterium Neisseria gonorrhoeae (also called Gonococcus, which is often abbreviated as "GC" by clinicians). In the US, its incidence is second[1] only to chlamydia among bacterial STDs.[2]
The symptoms in males include a yellowish discharge from the penis, which causes painful, frequent urination. Symptoms can develop from two to thirty days after infection. A few percent of infected men have no symptoms. The infection may move into the prostate, seminal vesicles, and epididymis, causing pain and fever. Untreated, gonorrhea can lead to sterility.
Fewer than half the women with gonorrhea show any symptoms, or symptoms mild enough to be ignored. Early symptoms include a discharge from the vagina, some discomfort in the lower abdomen, irritation of the genitals, pain or burning during urination and some abnormal bleeding. Women who leave these symptoms untreated may develop severe complications. The infection will usually spread to the uterus, fallopian tubes, and ovaries, causing Pelvic Inflammatory Disease (PID). It can not be caused by sharing toilets and bathrooms [3].
Some early symptoms of this infection are lower abdomen pain, fever, nausea, and pain during intercourse.
In both men and women if gonorrhea is left untreated, it may spread throughout the body, affecting joints and even heart valves

Symptoms

The incubation period is 2 [1] to 30 days with most symptoms occurring between 4–6 days after being infected. A small number of people may be asymptomatic for a lifetime. Between 30% and 60% of people with gonorrhea are asymptomatic or have subclinical disease.[4] Women may complain of vaginal discharge, difficulty urinating (dysuria), projectile urination, off-cycle menstrual bleeding, or bleeding after sexual intercourse. The cervix may appear anywhere from normal to the extreme of marked cervical inflammation with pus. Possibility of increased production of male hormones is common in many cases. Infection of the urethra (urethritis) causes little dysuria or pus. The combination of urethritis and cervicitis on examination strongly supports a gonorrhea diagnosis, as both sites are infected in most gonorrhea patients. Gonorrhea is caused by the Neisseria gonorrhoeae bacteria. The infection is transmitted from one person to another through vaginal, oral, or anal sexual relations, though transmission occurs rarely with safe sex practices of condom usage with lubrication.
Men have a 20% risk of getting the infection from a single act of vaginal intercourse with a woman infected with gonorrhea. Women have a 60-80% risk of getting the infection from a single act of vaginal intercourse with a man infected with gonorrhea.[5] An infected mother may transmit gonorrhea to her newborn during childbirth, a condition known as ophthalmia neonatorum.[6]
Less advanced symptoms, which may indicate development of pelvic inflammatory disease (PID), include cramps and pain, bleeding between menstrual periods, vomiting, or fever. It is not unusual for men to have asymptomatic gonorrhea. Men may complain of pain on urinating and thick, copious, urethral pus discharge (also known as gleet) is the most common presentation. Examination may show a reddened external urethral meatus. Ascending infection may involve the epididymis, testicles or prostate gland causing symptoms such as scrotal pain or swelling. Instances of blurred vision in one eye may occur in adults

Complications

In men, inflammation of the epididymis (epididymitis); prostate gland (prostatitis) and urethral structure (urethritis) can result from untreated gonorrhea[6].
In women, the most common result of untreated gonorrhea is pelvic inflammatory disease, a serious infection of the uterus that can lead to infertility. Other complications include: perihepatitis,[6] a rare complication associated with Fitz-Hugh-Curtis syndrome; septic arthritis in the fingers, wrists, toes, and ankles; septic abortion; chorioamnionitis during pregnancy; neonatal or adult blindness from conjunctivitis; and infertility. Neonates coming through the birth canal are given erythromycin ointment in eyes to prevent blindness from infection. The underlying gonorrhea should be treated; if this is done then usually a good prognosis will follow

LIVER CIRRHOSIS

Cirrhosis (pronounced /sɪˈroʊsɪs/, si-ROH-sis) is a consequence of chronic liver disease characterized by replacement of liver tissue by fibrous scar tissue as well as regenerative nodules (lumps that occur as a result of a process in which damaged tissue is regenerated),[1][2][3] leading to progressive loss of liver function. Cirrhosis is most commonly caused by alcoholism, hepatitis B and C, and fatty liver disease but has many other possible causes. Some cases are idiopathic, i.e., of unknown cause.
Ascites (fluid retention in the abdominal cavity) is the most common complication of cirrhosis and is associated with a poor quality of life, increased risk of infection, and a poor long-term outcome. Other potentially life-threatening complications are hepatic encephalopathy (confusion and coma) and bleeding from esophageal varices. Cirrhosis is generally irreversible once it occurs, and treatment generally focuses on preventing progression and complications. In advanced stages of cirrhosis the only option is a liver transplant.
The word "cirrhosis" derives from Greek κίρῥος, meaning tawny (the orange-yellow colour of the diseased liver). While the clinical entity was known before, it was René Laennec who gave it the name "cirrhosis" in his 1819 work in which he also describes the stethoscope

Signs and symptoms

Some of the following signs and symptoms may occur in the presence of cirrhosis or as a result of the complications of cirrhosis. Many are nonspecific and may occur in other diseases and do not necessarily point to cirrhosis. Likewise, the absence of any does not rule out the possibility of cirrhosis.
Spider angiomata or spider nevi. Vascular lesions consisting of a central arteriole surrounded by many smaller vessels due to an increase in estradiol. These occur in about 1/3 of cases.[5]
Palmar erythema. Exaggerations of normal speckled mottling of the palm, due to altered sex hormone metabolism.
Nail changes.
Muehrcke's nails - paired horizontal bands separated by normal color due to hypoalbuminemia (inadequate production of albumin).
Terry's nails - proximal two thirds of the nail plate appears white with distal one-third red, also due to hypoalbuminemia
Clubbing - angle between the nail plate and proximal nail fold > 180 degrees
Hypertrophic osteoarthropathy. Chronic proliferative periostitis of the long bones that can cause considerable pain.
Dupuytren's contracture. Thickening and shortening of palmar fascia that leads to flexion deformities of the fingers. Thought to be due to fibroblastic proliferation and disorderly collagen deposition. It is relatively common (33% of patients).
Gynecomastia. Benign proliferation of glandular tissue of male breasts presenting with a rubbery or firm mass extending concentrically from the nipples. This is due to increased estradiol and can occur in up to 66% of patients.
Hypogonadism. Manifested as impotence, infertility, loss of sexual drive, and testicular atrophy due to primary gonadal injury or suppression of hypothalamic or pituitary function.
Liver size. Can be enlarged, normal, or shrunken.
Splenomegaly (increase in size of the spleen). Due to congestion of the red pulp as a result of portal hypertension.
Ascites. Accumulation of fluid in the peritoneal cavity giving rise to flank dullness (needs about 1500 mL to detect flank dullness). It may be associated with hydrocele and penile flomation (swelling of the penile shaft)[citation needed] in men.
Caput medusa. In portal hypertension, the umbilical vein may open. Blood from the portal venous system may be shunted through the periumbilical veins into the umbilical vein and ultimately to the abdominal wall veins, manifesting as caput medusa.
Cruveilhier-Baumgarten murmur. Venous hum heard in epigastric region (on examination by stethoscope) due to collateral connections between portal system and the remnant of the umbilical vein in portal hypertension.
Fetor hepaticus. Musty odor in breath due to increased dimethyl sulfide.
Jaundice. Yellow discoloring of the skin, eye, and mucus membranes due to increased bilirubin (at least 2–3 mg/dL or 30 mmol/L). Urine may also appear dark.
Asterixis. Bilateral asynchronous flapping of outstretched, dorsiflexed hands seen in patients with hepatic encephalopathy.
Other. Weakness, fatigue, anorexia, weight loss.

ASTHMA

Figure A shows the location of the lungs and airways in the body. Figure B shows a cross-section of a normal airway. Figure C shows a cross-section of an airway during asthma symptoms

Asthma (AZ-ma) is a chronic (long-term) lung disease that inflames and narrows the airways. Asthma causes recurring periods of wheezing (a whistling sound when you breathe), chest tightness, shortness of breath, and coughing. The coughing often occurs at night or early in the morning.
Asthma affects people of all ages, but it most often starts in childhood. In the United States, more than 22 million people are known to have asthma. Nearly 6 million of these people are children

description

The airways are tubes that carry air into and out of your lungs. People who have asthma have inflamed airways. This makes the airways swollen and very sensitive. They tend to react strongly to certain substances that are breathed in.
When the airways react, the muscles around them tighten. This causes the airways to narrow, and less air flows to your lungs. The swelling also can worsen, making the airways even narrower. Cells in the airways may make more mucus than normal. Mucus is a sticky, thick liquid that can further narrow your airways.
This chain reaction can result in asthma symptoms. Symptoms can happen each time the airways are irritated.

Sometimes symptoms are mild and go away on their own or after minimal treatment with an asthma medicine. At other times, symptoms continue to get worse. When symptoms get more intense and/or additional symptoms appear, this is an asthma attack. Asthma attacks also are called flareups or exacerbations.
It's important to treat symptoms when you first notice them. This will help prevent the symptoms from worsening and causing a severe asthma attack. Severe asthma attacks may require emergency care, and they can cause death
Asthma can't be cured. Even when you feel fine, you still have the disease and it can flare up at any time.
But with today's knowledge and treatments, most people who have asthma are able to manage the disease. They have few, if any, symptoms. They can live normal, active lives and sleep through the night without interruption from asthma.
For successful, comprehensive, and ongoing treatment, take an active role in managing your disease. Build strong partnerships with your doctor and other clinicians on your health care team.

TONSILS

Tonsils are clumps of tissue on both sides of the throat that trap bacteria and viruses entering through the throat and produce antibodies to help fight infections

Tonsillitis occurs when tonsils become infected and swell. If you look down your child's throat with a flashlight, the tonsils may be red and swollen or have a white or yellow coating on them. Other symptoms of tonsillitis may include

sore throat
pain or discomfort when swallowing
fever
swollen glands (lymph nodes) in the neck

But enlarged or swollen tonsils are a common finding for many kids. Left alone, your child's enlarged tonsils may eventually shrink on their own over the course of several years. Don't rely on your own guesses, though — you might not be able to judge whether your child's tonsils are infected. If you suspect tonsillitis, contact your doctor. Recurrent sore throats and infections should also be evaluated by the doctor, who may order a throat culture to check for strep throat

Warm-water enema and exercises
Daily dry friction and a hip bath, as well as breathing and other exercises, should all form part of the daily health regimen. The bowels should be cleansed daily with a warm-water enema during the period of fasting

Cold pack and Hot Epsom salts bath
A cold pack should be applied to the throat at two-hourly intervals during the day. A hot Epsom salts bath taken everyday or every other day will also be beneficial

AIDS

WHAT IS AIDS?
AIDS stands for: Acquired Immune Deficiency Syndrome

AIDS is a medical condition. A person is diagnosed with AIDS when their immune system is too weak to fight off infections
Since AIDS was first identified in the early 1980s, an unprecedented number of people have been affected by the global AIDS epidemic. Today, there are an estimated 33 million people living with HIV/AIDS.
What causes AIDS

AIDS IS CAUSED BY HIV

HIV is a virus that gradually attacks immune system cells. As HIV progressively damages these cells, the body becomes more vulnerable to infections, which it will have difficulty in fighting off. It is at the point of very advanced HIV infection that a person is said to have AIDS. It can be years before HIV has damaged the immune system enough for AIDS to develop.

WHAT ARE THE SYMPYOMS OF AIDS

A person is diagnosed with AIDS when they have developed an AIDS-related condition or symptom, called an opportunistic infection, or an AIDS-related cancer. The infections are called ‘opportunistic’ because they take advantage of the opportunity offered by a weakened immune system.

It is possible for someone to be diagnosed with AIDS even if they have not developed an opportunistic infection. AIDS can be diagnosed when the number of immune system cells (CD4 cells) in the blood of an HIV positive person drops below a certain level.

Introduction to HIV and AIDS drug treatment

This is the first of a set of treatment pages that give an overview of the issues surrounding HIV and AIDS drug treatment. It is followed by starting HIV & AIDS drug treatment and continuing HIV & AIDS drug treatment

HIV antiretroviral drug treatment

This is the main type of treatment for HIV or AIDS. It is not a cure, but it can stop people from becoming ill for many years. The treatment consists of drugs that have to be taken every day for the rest of a person’s life.
The aim of antiretroviral treatment is to keep the amount of HIV in the body at a low level. This stops any weakening of the immune system and allows it to recover from any damage that HIV might have caused already.

combination therapy

Taking two or more antiretroviral drugs at a time is called combination therapy. Taking a combination of three or more anti-HIV drugs is sometimes referred to as Highly Active Antiretroviral Therapy (HAART

How many HIV and AIDS drugs are there

There are more than 20 approved antiretroviral drugs but not all are licensed or available in every country. See our drugs table for a comprehensive list of antiretroviral drugs approved by the American Food and Drug Administration

Global HIV/AIDS estimates, end of 2007

More than 25 million people have died of AIDS since 1981.
Africa has 11.6 million AIDS orphans.
At the end of 2007, women accounted for 50% of all adults living with HIV worldwide, and for 59% in sub-Saharan Africa.
Young people (under 25 years old) account for half of all new HIV infections worldwide.
In developing and transitional countries, 9.7 million people are in immediate need of life-saving AIDS drugs; of these, only 2.99 million (31%) are receiving the drugs.

TENNIS ELBOW

Doctors first identified Tennis Elbow (or lateral epicondylitis) more than 100 years ago. Today nearly half of all tennis players will suffer from this disorder at some point. Interestingly though, tennis players actually account for less than 5 percent of all reported cases making the term for this condition something of a misnomer

There are 2 additional strain related conditions which are often mistaken for Tennis Elbow. These being Golfer’s Elbow & Bursitis. Before we delve into the details of what Tennis Elbow actually is and options that are available for relieving & preventing the pain...let’s look at the distinguishing characteristics of each of these 3 ailments.

Symptoms Of Tennis Elbow-

Recurring pain on the outside of the upper forearm just below the bend of the elbow; occasionally, pain radiates down the arm toward the wrist.
Pain caused by lifting or bending the arm or grasping even light objects such as a coffee cup.
Difficulty extending the forearm fully (because of inflamed muscles, tendons and ligaments).
Pain that typically lasts for 6 to 12 weeks; the discomfort can continue for as little as 3 weeks or as long as several years

The damage that tennis elbow incurs consists of tiny tears in a part of the tendon and in muscle coverings. After the initial injury heals, these areas often tear again, which leads to hemorrhaging and the formation of rough, granulated tissue and calcium deposits within the surrounding tissues. Collagen, a protein, leaks out from around the injured areas, causing inflammation. The resulting pressure can cut off the blood flow and pinch the radial nerve, one of the major nerves controlling muscles in the arm and hand

Tendons, which attach muscles to bones, do not receive the same amount of oxygen and blood that muscles do, so they heal more slowly. In fact, some cases of tennis elbow can last for years, though the inflammation usually subsides in 6 to 12 weeks

Many medical textbooks treat tennis elbow as a form of tendonitis, which is often the case, but if the muscles and bones of the elbow joint are also involved, then the condition is called epicondylitis. However, if you feel pain directly on the back of your elbow joint, rather than down the outside of your arm, you may have bursitis, which is caused when lubricating sacs in the joint become inflamed. If you see swelling, which is almost never a symptom of tennis elbow, you may want to investigate other possible conditions, such as arthritis, infection, gout or a tumor

prevention-

Lift objects with your palm facing your body.
Try strengthening exercises with hand weights. With your elbow cocked and your palm down, repeatedly bend your wrist. Stop if you feel any pain.
Stretch relevant muscles before beginning a possibly stressful activity by grasping the top part of your fingers and gently but firmly pulling them back toward your body. Keep your arm fully extended and your palm facing outward

HAND INFECTIONS

Most hand infections are bacterial and are the result of minor wounds that have been neglected. Human bite wounds are the second most common cause of hand infections. Hematogenous spread of infection from other sites to the hand is rare but can occur.

A complete history and physical examination is necessary to exclude other associated medical conditions (eg, diabetes, arthritis, immunosuppression1 ) that may compromise therapy. The history should ascertain the mechanism of injury, as this may provide some clues about the organism(s) most likely responsible for the infection. Radiographic evaluation may be indicated if the history and physical examination suggest a possibility of fracture, osteomyelitis, or foreign body

Diagnostic Studies-

In most cases, the diagnosis of infection is made on clinical grounds. Diagnostic studies are frequently necessary to support the diagnosis. If the diagnosis is in doubt, diagnostic studies may be of benefit.The following studies may be performed:
Complete blood count (CBC) may reveal leukocytosis with left shift.
Serum glucose levels may be helpful, particularly in patients with diabetes.
Plain radiographs may be helpful to rule out fractures, foreign bodies, and osteomyelitis. The presence of gas on radiographs suggests the presence of gas-forming organisms, such Clostridium perfringens.
In the presence of obvious purulent drainage, perform wound cultures. In suspected septic arthritis, joint aspiration helps confirm the diagnosis and identify the organisms involved. Use caution in aspiration of joints through infected tissues, as this may result in inoculation of the joint space with organisms.
Ultrasonography may help confirm the clinical suspicion of abscess, septic arthritis, or pyogenic flexor tenosynovitis.
CT scan, MRI, and bone scan may be used to diagnose osteomyelitis.
Tzanck smear is useful when the diagnosis of viral infection is suspected in the presence of a blister that has not resolved spontaneously.

TYPES OF INFECTIONS-

Bite wounds
Bite wounds to the hand may cause cellulitis and abscess. Human bite wounds are particularly virulent because of the gram-positive and anaerobic bacteria present in the mouth. They are frequently the result of punching an opponent in the mouth, with the teeth causing the laceration. Frequently, the tooth penetrates the metacarpophalangeal joint, where the cartilage is particularly sensitive to infection. Every puncture wound near the proximal knuckle must be treated aggressively with exploration, irrigation, antibiotics, and drainage. Human saliva contains more than 109 bacteria per milliliter. The risk of infection is, therefore, great. Because of this risk, human bite wounds to the hand should usually not be closed.3
The infection progresses rapidly, with swelling, tenderness, and erythema presenting within 24 hours of the injury. The cellulitis usually progresses to an abscess if untreated. In the evaluation, wound cultures and radiographs should be obtained to exclude fractures or foreign bodies (eg, teeth).
Bites from cats and dogs are much less likely than human bites to result in infection. Cat bites are less frequent than dog bites but are more likely to cause infection. Animal bite wounds can be closed loosely after debriding the wound edges, provided that they are seen early, thoroughly irrigated, and followed very closely, and that oral antibiotics are administered. Advanced cases require intravenous antibiotics

Midpalmar space infection
The midpalmar space is a potential space between the middle, ring, and small finger flexor tendons and volar interosseous muscles. It extends from the hypothenar muscles ulnarly to the midpalmar septum radially. The accumulation of pus converts this potential space into a true space. The infection usually results from direct open trauma, or it may spread from a pyogenic flexor tenosynovitis. S aureus and streptococci are cultured most frequently.
Radial to the midpalmar septum is the thenar space, which is also a potential space. This space is volar to the adductor pollicis muscle over the second and third metacarpals. It also can be expanded by the accumulation of pus, which is characterized by painful swelling in the thenar space and passive abduction of the thumb. The hypothenar space is a potential space within the fascia of the hypothenar muscles. Infection within this space is rare. It manifests as tenderness and swelling over the hypothenar region

EAR INFECTION AND ITS TREATMENT

The human ear has three main sections, which consist of the outer ear, the middle ear, and the inner ear. Sound waves enter your outer ear and travel through your ear canal to the middle ear. The ear canal channels the waves to your eardrum, a thin, sensitive membrane stretched tightly over the entrance to your middle ear. The waves cause your eardrum to vibrate. It passes these vibrations on to the hammer, one of three tiny bones in your ear. The hammer vibrating causes the anvil, the small bone touching the hammer, to vibrate. The anvil passes these vibrations to the stirrup, another small bone which touches the anvil. From the stirrup, the vibrations pass into the inner ear. The stirrup touches a liquid filled sack and the vibrations travel into the cochlea, which is shaped like a shell. Inside the cochlea, there are hundreds of special cells attached to nerve fibers, which can transmit information to the brain. The brain processes the information from the ear and lets us distinguish between different types of sounds.

What Is a Middle Ear Infection?
Middle ear infections are one of the most common childhood problems. Let's start by talking about infections. An infection (say: in-fek-shun) happens when germs like bacteria and viruses get inside the body and cause trouble. Germs can get into your ears. The ear is divided into three parts: outer, middle, and inner. When the germs bother your outer ear, it's called swimmer's ear.
The middle ear is a small pocket of air behind the eardrum. You have a middle ear infection when germs get into the middle ear and the area fills up with fluid (or pus), which contains germ-fighting cells. When the pus builds up, your ear starts to feel like a balloon that is ready to pop, which can really hurt

How to Prevent Ear Infections
What can kids do to prevent ear infections? You can avoid places where people are smoking, for one. Cigarette smoke can keep your eustachian tubes from working properly.
You also can try not to catch colds. These steps can help:
Stay away from people who have colds, if possible.
Wash your hands regularly.
Try not to touch your nose and eyes.
Good luck staying clear of colds and keeping those pesky germs out of your ears