ANTI ARRHYTHMIC DRUGS

ARRHYTHMIA-TREATMENTS

 ARRHYTHMIA the irregular rhythmical beats of heart may result many times fatal if unattended

The Anatomy of Electrical Conduction Of the Heart Beats

As in the above diagram the electrical conduction of the heart muscle is clitched to start at the Sinu-Atrial (SA) node the most auto generated electrically depolarizable tissue in our body.

The atrium contracts and the conduction spreads down wards like waves to reach Atrio-Ventricular (AV) node as in the above figure.

The AV node is situated in between the Right Atrium (RA) and the Right Ventricle and this AV node is acting as protective shield to filter of any unwanted excessive impulses from above to pass further down to this shield.Also AV node acts as a Gate to pass needed impulses from the SA node sufficient for ventricular contraction.

Ventricular contraction not begins immediately when the impulses reaches AV node as the node is situated more towards the right as in the figure above,and because both right and left ventricle needed equal impulses to contract.To disperse the impulse equally from AV node  to both the sectors nature has provided a special tissue which is a portion of AV node.This special tissue is known as Bundle of His as you can note in the figure.This tissue is branched equally to right and left.AV node send impulses to Bundle of His which sends the impulses to both right and left down to the bottoms of both the ventricles known as Purkinje Fibers and the ventricles contracts.
This can be easily illustrated by an ECG as followsl;-

P-wave represent the Atrial depolarization and contraction
PR-interval represents the conduction of the impulse from the Atria to Purkinje fibers
QRS curve the rapid repolarize and depolorization of Ventricles
The ST segment represent the resting period or plateu period of the myocardium. 
There are two types of impulse defects may occur during a rhythm. 
1.Defects in the formation of the impulses as during stresses,straining to expell the feces in constipation,weight lifting,hard excercise.These impulses are non pathalogic and need no medical interventions.It can get corrected by taking rest and relax.
2.Defects in the conduction of formed impulses due to some underlying causes such as HT,Cardiac Failure,MI,Drugs,Infections,Anginas,Valvular defects and cardiac muscle damages may be pathologic and is known as Pathologic Arrhythmias and may be fatal.This condition needs medical intervensions.Also arrythmias can be pathologic if impulses originates from other parts of the myocardium especially from the fast acting cells instead of the pace maker tissues such as SA node and AV node.
Treatments 
 Class-IA-.Sodium channel blockers
Quinidine
Procainimide 
Disopyramide

Quinidine

Uses-Ventricular tachycardia and supraventricular arrhythmias,Atrial fibrillation and Atrial flutter
Quinidine prolongs the QT intervals and thereby calm down the rapid depolarization of fast acting muscles like Purkinje fibers and inturn calm down ventricular fibrillation.
Quinidine is administered orally
It is metabolised in the liver and half life is 6 to 8 hrs.
Toxicity 1.GI disturbances like Diarrhea,Nausea,Vomiting.
               2.Cinchonism such as blurred vision,dizziness,head ache,and tinnitus
               3.Syncope with light headedness and possible faint.
               4.Thrombocytopenia
               5.Excess prolongation of QT intervals result in a brady arrhythmia known as Torsade de Points causes immediate death.
               6.AV block
Drug Interactions 1.Increases plasma levels of digoxin and oral anti coagulants
                                2.Quinidine plasma levels are rapidly depleted by Phenytoin and Phenobarbital

Procainamide

Uses 

1.Venricular and supraventricular arrhythmias

2.Premature ventricular contractions

Procainamide is taken by oral,i.v.;or i.m.

Toxicity 1.Lupus like rashes or arthralgia.Renal involvement is unusual

               2.Pericarditis,

               3.Hellucination,and psycoses

               4.Torsade de Points.

Disopyramide

Action is very similar to the other two above mentioned drugs but produce prolonged negative inotropic (decreasing frequency of contractility) and stronger anticholinergic effect.
This medicine can be taken by I.V. or by Oral
Uses Both ventricular and supra ventricular arrhythmias
Kinetics Largely excreted by kidneys unchanged
Toxicity 1.Dry mouth, Blurred vision,Urinary retention,Constipation and Glacoma
               2.Torsade de Points
               3.Contra indicated in left ventricle dysfunction as it may leads to Heart Failure
               4.Because of the anticholinergic effects protate gland would be affected. 
Class - IB   
1.Lidocaine
2.Tocainide
3.Mexiletine
4.Phenytoin

Lidocaine (Xylocaine)

Lidocaine a local anethetic exert blocking effect on sodium channels

Use Lidocaine is the drug of choice for ventricular arrhythmias

Route I.V. only

Kinetics Lidocaine is metabolised in liver and care should be taken while using in liver dysfuntion

Toxicity CNS effects like Drowsiness,numbness,slurred speach,and convulsions

Nystagmus a condition at which rapid and involuntary movements of eyeballs occur

Tocainamide(Tonocard)

Usesd in ventricular arrhythmias

Taken orally

Toxicities 1.Bradycardia;2.Tachycardia;3.AV block;4.Hypotension

                  5.Nausea;6.Tremor;7.Lung fibrosis(Rare) ;8.Aplastic anemia(Rare)

Mexiletine (Mexitil)

Used in ventricular arrhythmias

Can be taken orally

Toxicity Dizziness;Nausea,& Vomiting;Erythrocytopenia;Thrombocytopenia;Leucopenia;Agranulocytosi s and Nystagmus

Phenytoin (Dilantin)

This drug block the inactivated sodium channel and keep it blocked for a long time and there by it is useful for convulsions and atrial and ventricular arrhythmias.

Can be taken orally or by I.V.

Side effects are similar as above.

Class-IC 

 1.Flecainide

2.Propafenone

3.Morizicine

Used in supraventricular and ventricular arrhythmias in patients with normal heart structure

Toxicity 1.This medicine should be used only if other medicines are ineffective because the Cardiac Arrhythmia Suppressor Trial (CAST) studies proved that this medicine is fatal to those who suffered recent heart attacks,and who suffer asymptomatic ventricular arrhythmias.

               2.CNS effects like blurred vision,and headaches

               3.Heart Arrest in patients who have defective conduction system.

Propafenone (Rhythmol)

Used in supraventricular and ventricular arrhythmias

Blocks sodium channels upto Purkinje fiber level and thereby correcting the ventricular contraction similar to flecainide but also have some beta adrenergic blocking effects.

Toxicity is having a proarrhythmogenic effect and beta blockade effects like Bronchospasm,bradycardia.

Class-II Antiarrhythmic Drugs-The Beta Adrenergic Blockers

In this class the most commonly used medicines as antiarrhythmics are as follows:-

1.Propranolol

2.Sotalol

3.Esmolol

Sotolol can be included in Class-III too.

The mechanism of these drugs are generally depressing the automaticity of the myocardium other than the pacemakers like SA and AV nodes and make the pacemakers to little calm by slowing their contractions and elongating their refractory periods and thereby preventing the arrhythmic excitations of the heart.

Sotolal is used clinically ventricular fibrillation

Esmolol is short acting and can be used safely during emergencies such as surgery.

Class-III -Potassium Channel Blockers

1.Bretylium 2.Amiodarone 3.Sotolol 4.Procainamide

The mechanism of action is by blocking the potassium channels so that there is no sodium influx and potassium efflux and there by prolong the ventricular excitations

These drugs can be used to treat venricular fibrillations

Postural hypotention can be an adverse effect of these medicines

Amiodarone is the drug of choice used in the name of Cardarone.

This drug also exhibits Class-I and Class-II properties also.

Amiodarone is used in Arterial flutter and ventricular arrhythmias 

Amiodarone can be taken orally as well as by I.V.route.

Toxicities 1.Lung fibrosis;2.Tremor ;3.Live damage;4.Photosensiivity;5.Corneal micro deposits;6.Thyroid defects leads to iodine accumulation and thereby bluish body skin discolouration;

Class-IV-Calcium channel Blockers

1.Verapamil

2. Diltiazem

3.Nifedipine

The mechanism of action is blocking the L-type calcium channels and thereby calm down the SA and AV nodes.The actions are mostly supra ventricular and hence can be used in atrial flutters

 

 

 

 

 

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4.http://surefile.org/file/057686B  -- CONTACT DERMATITIS BEST TREATMENT OPTIONS

5http://surefile.org/file/057eM8   --TREATMENT OPTIONS FOR VIRAL INFECTIONS

CONGESTIVE HEART FAILURE (CHF)-TREATMENTS

CONGESTIVE HEART FAILURE

It is a pathological condition with multiple etiologies in which the left ventricle fails to contract sufficiently to deliver the blood through the aorta to our body tissues for their metabolic needs.The inability of the left ventricle to function properly the result is collection of waste fluids into its muscles and make it more congestive.Hence the name Congestive Heart Failure

CHF is commonly occuring in elderly patients of above 40 yrs.But it may occur at any age as a result of any one of the underlying heart and vascular diseases such as Angina,MI, Hypertension and Coronary Artery Disease etc.etc.

Myocardial stress such as heavy stress on the wall of left ventricle due to the absence of the interventricular wall (septal wall) or its dysfunctioning (Congenial Heart Failure),traumas,diseases like Rheumatic fever,pulmonary embolism, infections, anemia,pregnancy,drugs,fluid overload,arrhythmias and valve defects may all become the etiological factors.

Types of HFs

1.Low output vs High out put HF

If the metabolic demands are normal but the heart cannot meet the requirements is known as Low output Heart Failure (The most common type)

In case of high metabolic demand conditions due o hypertension or anemia and if the heart is unable to meet he requirements then it is known as High output Heart Failure.

2.Left side vs. Right side Failure

The sighns and symptoms are result from blood backing up in the failing ventricle except in the HF due to increased body demand in which blood will not be much backed up but there is left ventricle failure occurs.

Initially the symptoms tends to be specific to one sided failure but later eventually both side involvement is seen.
Leftside failure can be attributed by when the blood cannot be properly pumped by the inability of the left ventricle into the aorta through the aortic valve,leads to he accumulation of blood in it.
Because of this the left ventricle cannot receive further blood flow from the left atrium through the Miral valve (the valve between the left atrium and left venricle),and inturn because of the blood accumulation in the left atrium it itself cannot accept further blood flow from the pulmonary(lungs) vein and hence the fluid portion of the blood will be pumped back to the lungs leads to Pulmonary Edema.
Right side failure can be atributed by the inability of right ventricle to pump the blood into the pulmonary artery through the pulmonic valve.The blood get accumulated inside the ventricle and is known as Right side failure.
Because of this accumulation the fluid portion of the blood backs up throughout the body (in the veins,liver,legs and bowels) leads to Systemic Edema
Treatment Options is composed of avoiding drugs which can exacerbate the cause as follows.
The followings are the substances which should not be taken in CHF:-
1.Androgens
2.Corticosteroids
3.Estrogens
4.Licorice
5.Guanethidine
6.Lithium carbonate
7.Methyldopa (a centrally acting antihypertensive drug)
8.Salicylates and other NSAIDs
Because all the above drugs causes sodium and water retensions
Second options are releiving the symptoms and improve pump functions by,
a)Reducing metabolic congestion and needs by relaxations,rest,and medications.
b)Reducing fluid intakes
c)Taking digitalis and other inotropic(improving heart contractions)
  drugs
d)Patient educations
Pathophysiology God has given to our body every aspects of self defence and self corrections to some extend inorder to minimise the inconveniences caused by the disorders.Similarly in case of CHF if we left uncare at first our body trys to care it by some compensative activities as follows:-
Sympathetic Responses by which the norepinephrine outflow will act on the heart to increase the contractility,heart rate and the bloodflow which with no otherway redisributed to ensure perfusion of the heart.
Hormonal Stimulation The redistribution of bloodflow to the heart will result in renal insult which decreases glomerular filteration rate (GFR),leads to sodium retension,water retension,activation of the renin-angiotensin-aldosteron system to add to more sodium and water retension.
Cardiac Hypertrophy, The above process of fluid retension will lead to thickening and enlargement of cardiac wall.This will make larger contractile cells and diminishing the capacity of the cavity in an attempt to precipitate expulsion of blood at lower volumes.
Frank-Sterling Mechanism is that increase fiber dilation hightens the contractile force which then increase the energy released.
as a result,1)the heart pumps all the blood it receives.2)as blood volume increases the various cardiac chambers dilate by stretch and enlarge in attempt to accommodate excess fluid.c)as these stretched muscles contract and the contractile force increase proportionally to their dilation.Then the stretched fibers snap back like a rubber band expelling the extra fluid into the arteries.
The above compensation processes may or may not result in a permenant solution as it depending upon the severity of the condition.If the condition is mild the above compensation process may be successful with the Grace of Almighty.If not the tragic events of decompensation process follows as below:-
Overtime the body gets exhausted of its all compensation mechanism and become self defeated.
As the strain continues,total peripheral resistance and afterload pressure further increase and thereby making the ventricular muscle further weaker to expell the blood.
After load is the amount of contractile force required to overcome the interventricular forces and the pressure in aorta (in case of left ventricle) to eject the blood.
Afterload is defined as the pressure in ventricular muscles during contraction.It is the interventricular systolic pressure.
Preload is the force exerted on the ventricular muscle at the end of diastole.
As the fluid volume expands proportionally  the demand also expands on the already exhausted pump,allowing increased volume remain in the ventricle.
The resulting fluid backup produces signs of CHF 
Physical Symptoms
1.Tiredness and fatigue
2.Coughing
3.Shortness of breath or difficult to breath (Due to Left Ventricle failure)
4.Swelling of abdomen and systemic edima(Due to right sided CHF)
Mostly the symptoms are very similar to that of Heart Attack
The following image will illustrate the symptoms diagrammatically

MEDICATIONS
The pharmaceutical therapeutics is based on three approaches as follows:-
1.Improving heart muscle contractions
2.Reduce preload (The filling of ventricles)
3.Reduce afterload(The resistance pressure against which the heart must pump)
The Drugs Options are as follows:-
1.Cardiac Glycosides (e.g)Digoxin(Lanoxin);Digitoxin
2.Bipyridinederivatives(e.g)Amrinone(Inocor);Milrinone(Primacore)
3.Beta-Adrenergic Agonists (e.g) Dolbutamine (e.g) and Dopamine
4.Vasodilators (e.g) Nitrates (Nitroglycerine,Isordil,Amylnitrate);Hydralazine and ACE Inhibitors (Enalapril and other ...prils)
5.Diuretics (No monotherapy,as an adjunct only)
 

 

 

   

MYOCARDIAL INFARCTION-HEART ATTACK

HEART ATTACK(M.I.)

When the heart muscle cells dies with necrosis there is complete blockade of coronary blood supply to heart with prolonged ischemia,and complete occlution of the coronary artery the ultimate result is Myocardial Infarction or Heart Attack.During and after the attack the left ventricle become enlarged and hypertrophied due to the outside pressure.

Etiology:The most common cause is acute thrombus (clot) formation following fissuring and rupture of the lipid rich atherosclerosis plaque and platelet aggregation in the already congested coronary artery. Rare association of the coronary arterial spasm may also contribute to the cause.
Heart Attack is one of the morbid result of prolonged ischemia followed by angina pectoris.
The long time Ischemic Heart Desease caused by decreased blood flow to the heart muscle due to obstruction of the blood flow by the clots,the diffused plaque from the atherosclerosis,followed by platlet aggregation,would certainly leads to MI if left untreated.
Because these condion may kill the heart muscle cells by depriving of oxygen which leads to necrosis and ischemia which will eventually lead to MI.

Sudden death is caused by MI which can trigger the abrupt onset of ventricular fibrillation,the most disorganized and lethal arrhythmia,which can suddenly stop the cardiac output.If this emergency situation is not medically intervened immediately by cordial thump,or defibrillation by counter shock the result is death. 
Generally if there is uncontrolled ventricular fibrillation followed by recusciation occur the situaion is emergency and is known as Sudden Death Syndrom 
In MI a portion of the of the heart muscle suffer prolonged severe supply block of oxygenated blood because of a clot formation,leading to blood vessel damage to form atherosclerosis and platelet aggregations.

Symptoms: 

1.Severe pain radiating from the lower left side to the shoulder.back and neck

2.Shortness of breath

3.Nausea with vomiting or without vomiting;some times stomach pain

4.Hypertention or hypotention

5.Dizziness with headpain,and Fatigue

6.Throat or jawpain

7. Unusual loud snoring with cjocking voice may indicate the presence of sleep apnea,a warning signal to heart attack

8.Sweating

9.Non stopable coughing

10.Diaphoresis (Excretion or oozing of moisture through sweating)

11.Heart murmurs,with tachyarrythmias or bradyarrythmias

25% of the heart attacks are not showing the above symptoms and are silent in eldely patiens,patients with Diabetes and Hypertension

MI can be cassified as 1.Anterior;2.Lateral and 3. Inferior.

But more conveniently and medically classified by ECG as 1.Q-wave MI

2.Non Q-wave MI

What is a Q-wave:-

A Q-wave in an ECG represent any down ward left to right depolarization of the interventricular septum during which ventricles dilates to get filled by blood.See the figure down

In the above ECG look at small downward graphic dip indicated by the arrows and circle.

If there is a problem in the normal depolarizing effects of inter ventricular muscle the Q-wave will be elongated

If this is the condition then there is much chances to get an Q-wave mediated MI.But a problem in Q-wave may not always result to an MI.The presence and elongated  Q-wave indicates there are necrosis.This can be corrected by Coronory bypass surgery if done within a few hours of the post MI.
Generally Q-wave syndroms accounts for 40 to 70% of MI events when compared with non Q-wave MIs.In Q-wave mediated MI there is usually an elevated ST segment.In non Q-wave MIs there is depression in ST-segments.
The most serious warning is a sudden ventricular arrythmia with fibrillation occur without any warnings.

Therapy

 Goals:1.Elimination of clot formations by using Thrombolytics

            2.Releiving Pain

            3.To Prevent arrhythmias

            4.To reduce cardiac workload and stabilize rhythm.

            5.Limiting the affected area and preserving the pump function.

            6.Solving the other complications like nausea,vomiting,stomach aches,arrythmias,blood pressure variations etc.etc.

If not contra indicated four groups of medications can be used in MIs

1.Thrombolytics

2.Beta blockers

3.Nitrates

4.Aspirin

Apart from these Morphine,Lidocaine,Heparine and Warfarine can also be used at times.

The first choice is using thrombolytics such as streptokinase,Urokinase,and Alteplase.as thrombus and embols are the major causes of coronary atherosclerosis plaque apart from LDL and Triglycerides.ACE inhibitors and Calcium channel blockers can also be tried but their efficacy is yet to be proved.

If in case thrombolytics are contraindicated then Percutaneous Transluminal Coronory Angioplasty(PTCA) is proved efficaceous.

Thrombolytic agents were used in patients with suspected MI with prolonged chest pain.

But any benifits that attained by Thrombolytic may seen not immediate but occur as late as 12 hrs.after the pain starts.

Administration of streptokinase IV should be started within 12 hrs and optimally 6 hrs of the pain starts.

Aspirin can be used along with a thrombolytic agent to regulate the circulation in the dosage of 160 mg to 325 mg.for life after the first attack.Get a physicians advice for dosage.

Heparin can be used along with a thrombolytic agent to prevent reocclusion of the coronary artery even heparin is proved in reducing mortality even if it is used without a thrombolytic agent after the first attack.

An IV bolus of 5000 units followed by a continous infusion of 1000 units/hr is its usual dosage.The goal is to maintain the Activated Partial Thromboplastin Time (APTT) between 1 & 1/2 or 2 & 1/2 times normal.

Warfarin can be used in patients with mural thrombus.

Beta Adrenergic blockers propranolo,metoprolol,atenolol,and timolol are commonly used with success.

Nitrates Nitroglycerin is in the most common usage.It should be administered sublingually at the onset of the pain.

 

ACNE TREATMENTS

ACNE VULGARIS

Acne is a big problem experienced especially at the time of puberty by some adolescents.Male children when they attained puberty the matured male sex organs starts to produce the acne cause male sex hormone known as Testosterone in various amounts depending on their genetic nature.However there are so many other factors can cause acne to get at any age. 

Acne vulgaris is defined as a disorder of the pilosebaceous units mainly of the neck,back, and face.The pilosebaceous glands are the hair producing glands located in the skin throught our body except the palms of the hands and the soles of the feet.There are non hair producing sebaceous glands are also exits along side and equally distributed throughout our body similar to the pilosebaceous glands.

Due to some conditions such as excess production of testosteron or blocks at the sebum secretions these pilosebaceous units produce lesions,which starts open or closed comedones and evolve into inflammatory popules.These popules either resolve into macules or develop into pyoderma.

Fortunately acne vulgaris is self limiting and need no physician to treat and can be controlled by self medications available at OTC with some pharmacy councillings.But exceptions are there if the acne becomes a tumor by some mismedications like over use of benzoyl peroxides at high concentration.

Pathology

A.The incidence of acne involves three sequences

a.Excess sebum secretions due to some reasons like over stimulation of the glands by androgens at puberty in both male and female adolescents.

b. When testosterone is converted to dihydrotesterone which stimulates the sebum secretions.

c.Development and stimulation of sebum glands by DHT.

Normally the keratinized horney cells are sloughed off from the epithelial linings of the pilosebaceous duct in the hair follicle and are carried out to the surface of the skin as sebum.

But in case of over stimulation the horney cells fails to sloughed of and block the passage which leads to the formation of bumps at the surface of the skin.

Causative Bacterium: The presence Propionibacterium acne is  significant in the sebum of those who are having acne which is not present in normal people.The reason is unknown as still it is hard to conclude that acne is from purely infectious origin as mostly it is not contageous.Yet the micro organism is contributing to the formation of acne by digesting sebum triglycerides and produces various irritating fatty acids which causes comedones and inflammations.

Stages of Acne

1.Blockade of the pilosebaceous duct by the horney epithelial keratinised cells to form comedon as white head either closed or opened

2.The closed comedon develops into either a popule as black head.The black colour is attributed either by melanin or oxidized lipid.

3.The lesion may enlarge and filled with pus and is know as a pustule.

4.In bad pathological conditions the papule may develop into more painfull cysts or nodules,with unknown causes.

5.The term pimple can be refered to whiteheads,blackheads,papules and pustules.

Clinically acnes are either symptomatic or asymptomatic.Cysts and nodules are usually painfull and can form scars and to be refered to a skin specialist.

Asymptomatic acnes can be treated on OTC with pharmacist's advices 
Complicating Factors There are many drugs which are comedogenic and may make the acne to get worsen.They are,
1.Topical and systemic Bromides and Iodides
2.Topical coal tar products
3.Topical and systemic Androgens and Progestins
4.Phenytoin
5.Lithium
6.Topical and systemic corticosteroids
7.Stress
8.Oily and fatty diets and chocholates are not acne producing.
9.Physical trauma and irritations,this includes agressive scrubbing of face,wearing headphones,cradling the chin with the hand,and picking the pimples can contribute to worst sequences.Gentle face wash with mild soap is better
10.Some cosmetics are comedogenic such as lanolin,petrolatum jelly,cocoa butter and avoid them.
11.Some women can experience acne at premenstural cycle.
12.High humidity and sweating can contribute to the formation of acne.

Treatments

Generally most patients can be treated successfully with either topical or systemic medications or both.Acne often improves when the patients reaches early twenties.

Acne can be Mild to Moderate to Severe

In mild cases there are a few papules and pustules without any single cysts or nodules.Daily a gentle face wash with a mild soap is beneficial.Fatty and oily diets should be avoided.High humidity and sweating also to be avoided.Keep the stress at the bay.Chocholate and nuts can be used without any harm.

In moderate cases there are many papules and pustules with a few cysts and nodules.Treatment options include salicylic acid,sulphur and resorcinol approved by FDA.There are scruffs such as Clearacil Adultcare,Clearasil Clearstick and Benzoyl peroxide 5 and 10 can be used.But while using Benzoylperoxide take an advice from a doctor and be carefull that high usage of this madicine may cause skin cancer,but not yet to be concluded. Before apply the product should be tested for allergy as follows
Wash the area with a mild soap and dry it.apply a small quantity and leave it for 20 minutes.
1.Benzoyl peroxide is available as alcoholic gel,cream and lotion.The gel preparation is more effective
There is no much difference in clinical effect between the preparations 2.5 %,5 % and 10%
This product discolour hair and cloth.Beware of that.
Benzoyl peroxide is thrown from first to third category by the FDA on safety concerns
 2.Salicylic acid The first category medicines available in 0.5% to 2%.This is an irritant keratolytic agent increase epithelial cell turnover and safer than B.P.
3.Sulphur The first category medicine available in strength as 3 % to 8 %.It is keratolytic and antibacterial.But sulphur on prolonged use may be acnegenic.
4.Resorcinol This medicine comes under second category as a single agent but jump into the first category when combined with sulphur in a proper proportion as the effect and safety are increased.
In severe cases there are numerous number of papules and pustules with many cysts and nodules.These cases should avoid self treatments and to be refered to a skin specialist as there is a need for antibiotic therapies.

CONTACT DERMATITIS-SOLUTIONS

CONTACT DERMATITIS

Contact Dermatitis is one of the most common dermatological problems with irritating and annoying consequences in social life.While at office,at home and at social events with friends these consequences are the most disturbing one and produce uneasiness to scratch the irritating area in front of others.
Usually a foreign body touches your skin and enter into our body may produce antibodies to fight the invader.Mast cells are triggered to release various inflammatory chemical such as histamine and ecosanoids to express the body its inconvenience by its own languages such as itching edema infammations etcetc.

There are wo type of contact dermatitis as follows:-
A.Irritant Contact Dermatitis is caused by direct contact with a primary irritant and the primary irritants are of the types as follows:-
1.Absolute Primary Irritants These are corrosively skin damaging substances such as strong acids,alkalis and similar industrial chemicals
2.Relative Primary Irritants These are the most common cases of contact dermatitisseen in clinical practices.These irritants are less toxic than absolute primary irritants and they require repeated frequent contacts to establish a dermatitis.(e.g)soaps,detergents benzoylperoxide and some plants

B.Allergic Contact Dermatitis These are the worst annoying and irritating skin conditions.Almost most of the things which are allergic to the skin can produce this dermatitis.Some plants,many chemicals,can cause allergic contact dermatitis.The best example is the contact dermatitis produced by poison ivy plant.The plant produces on contact with our skin a peculiar type of reaction mediated by T-Cells(T-lymphocytes) a type of WBC circulating in our blood through the lymphatic system and need the following sequence of events must occur to provoke it.

a)The skin epidermis must come in contact with the allergen (the hapten)
b)Thereby a hapten-epidermal protein complex must form as the antigen
c) The antigen must enter into the lymphatic system
d)Immunologically competent lymphatic cells must be formed which are selectively active against the invading antigen
e) In this condition if a second contact between the skin epidermis and a hapten occurs then the incidence of contact dermatitis starts. 
f)The duration between the first contact and the second contact is known as the induction period and it may last for 4 to several weeks.Once the induction period completed a minute second contact will produce a severe eczema with an onset of 12 hrs and attain the peak at 48 hrs to 72 hrs after exposure.
Once the sensitivity is fully developed it will last for life
Most contact allergens produce sensitization only to a small populations except the poison ivy which produces sensitization to almost 99% of the populations,who come in contact with it.
PHASES OF CONTACT DERMATITIS

1.Acute Stage Wet lesions such as leaking blisters,weaping skin,erythema,edema, vesicles and oozing.

2.Sub Acute Stage Crusts and scabs form over the already wet lesions.Allergic contact dermatitis and irritant contact dermatitis caused by absolute primary irritants such as strong chemical can produce both acute and sub acute stages.

3.In this stage initially the lesions become dry and thickend to form fissures.Later erythema,lichenification,and excoriations appear.This stage occurs mostly with irritant contact dermatitis caused by relative primary irritants.

Allergen Producing Plants 1.Poison ivy;2.Poison oak 3.Poison sumac
In all the above plants a previous contact must be necessary to produce swensitization to form dermatitis by the second one.
In most of these poisonous plants the main sensitizing agent is an oleo resin known as urushiol oil 
The plants must be bruised or crushed inorder to contact with the oleoresin which is presen in the roots,stems,leaves and fruits.
The oleoresin can remain in tools, toys, cloths,pets and fingernails for longer time if these items comes in contact with the bruised poison plants.
urushiol oil is not volatile if a person sits simply nearby the plant without touching it will not get contact dermatitis
But in a burning plant the oleoresin droplets may be carried by the smokes and get deposited in our skin to produce the dermatitis.
 
For further detailed study of treatments please click here and download it

SUN PROTECTION

OTC TREATMENTS FOR SUN RADIATION PROBLEMS-1

The scotching summer is ahead.In tropical countries like Middle East the summer would roast the sands continously for eight months.In other parts of the world like Europe,Eastern Asia,Central Australia,and the Americas there are frequent attacks of heat waves with the raises in mercurily level as high as 45 Degree Celcius.
Our skin is more vulnerable to the attacks of heat waves especially by the Ultra Violet region of the EMR radiating from the SUN.Generally over exposure to the scotching sunlight will damage our skin
SUNTAN  is a skin response to injury by sunlight.Only UV over exposure of the skin would produce SUNTAN and SUNBURN

THE ULTRA VIOLET SPECTRUM:-

UV-B in mild exposure by evening sunlight is responsible for the preparation of Vitamin-D3 by our body from skin cholesterol
UV-B radiation is erythrogenic and long time exposure to it at peak hours like 10 a.m to 2 p.m it can cause severe erythema and skin cancers.

The sunburn is more likely to occur in high altitudes as UV-B intensity increases by every 4 % with an increased altitude height by every 250 meters. Our solar radiation contains electrical (vertical) and as well as corrospondig magnetic (horizontal) oscillating waves.Hence this is generally known as Electro-Magnetic Radiations or simply by the term EMR.
This EMR contains three portions as Ultra-viotet,Visible and Infra-red regions.Out of these three regions the Ultra-Violet or the UV region is having the heat waves with more frequent and congestive waves with shortest lenghths with the highest skin penetrating power.
The UV spectrum ranges from 200 to 400 nanometers(nm).A nanometer is one thousandth of a millimeter.Imagine the shortest lenghth of one UV wave to another.Therefore the waves are highly frequent with high penetrating power and the most dangerous.
Further the UV radiation is devided into A,B,and C. and each differ from the other by the wavelengths with corrosponding frequencies as follows:-
UV-A :-The smallest sizes of photon radiation with shortest wavelenghths ranges from 320-400 nm.UVA is having more penetrating power and can pass the ozone layer to reach the earth 10 to 100 times more than UV-B.As these are very small photons hence they are less likely causes erythema but these UV-A deeply penetrating into the dermis and make the skin more vulnarable to the effect of UV-B which is carcinogenic.Also UV-A can produce photoaging and photodermatoses on prolonged exposure.
Becareful when you go for a walking when the season is cloudy and pleasant,and on a fullmoon out walk as these seasons are the one with maximum UV-A radiations.
Further UV-A can be divided into two as 1,and 2.UV-A-1 is less likely erythrogenic and melanogenic than UV-A-2 and the UV-A-2 is more likely to UV-B.
UV-A is often tanning boths and is often entertained in the psoralen plus UV-A(PUVA) treatment of psoriasis.
UV-B they are radiations of little bit bigger photonic particles than UV-A particles with the wave lengths of 290nm to 320nm.As these are bigger particles and having less penerating power than the UV-A particles but still they can pass the ozone layer and reaches the earth,and produces more serious effects to the skin like skin erythemas,and skin cancers.
These radiations causes sunburn and suntan more effectively.A proper exposure to this radiation during sunbath with a fixed and calculated time by your skin doctor,you can get a good protective suntan at your skin.
SUNTAN is natural way of tanning or blackening your skin by calculative exposure to the sulight to protect your skin from further damages by the sun.UV-B radiation is good skin tanner because it is melonogenic.But a doctor should advice.Also a small exposure to this radiati
UV-C:-It is bigger particles than the other two radiation the least penetrating power because they have long wavelength with less frequencies and hence most of them are retained by the ozone layer from not reacing the earth.

OTHER SKIN REACTIONS TO SUNLIGHT

1.Actinic keratosis it is a precancerous condition may happen after long time sun exposure.It is typically araising at the middle or later age,with the manifestations of sharp demarcated,roughened hardened growth,which may be fltened or raise leads to squamous cell carcinoma.
2.Skin cancers
A.Squamous cell carcinoma Leasions apperaed mostly as thickened rough particles which can bleed.Among the skin cancers it accounts for 15%
B.Basel cell carcinoma It appears as pearly transluscent bumps and originates in the basal cell.It accounts for 80% of the skin cancers.
C.Malignant melanoma originates from the melanocytes and is the most dangerous form of skin cancers.It is charectorised by the changes in the appearances of moles such as colour fading,dissappearing,shape and borders of the mole becomes irregular,asymmetrical,and diameter over 6 m.m.
3.Drugs Induced Skinreactions
A.Photo-Allergic Reactions occur when light makes a drug into an antigen or a photoallergen (Hapten) if the drug is repeatedly used as skin creams.For example some creams or ointments if repeatedly uses may suddenly produce skin rashes as they become allergents due to light.
B.Phototoxic reactions occurs when light transfer a drug into a toxic form,which result into a tissue damage.
C.Implicated Drugs Many drugs are implicated in causing photo allergy or photo toxic reactions.(e.g)1.thiazides;2.tetracyclines;3.Phenothiazines;4.Sulphonamides;and sunscreens.Some drugs are producing both photo toxic and photo allergic reactions.
4.Photodermatoses They are photo reactions caused by light of specific wavelenghths.(e.g)1.Polymorphous light erruptions;2.Lupus erythematous;and solar urticaria.
5.Photoaging It is the aged appearence of skin by sun exposure and not by real aging.Dry,scaly,yellow skin with deep wrinkles,thin and more fragile.
SUNSCREEN AGENTS
People can protect their skin from violent UV radiations by avoiding exposure,by wearing protective clothings and by applying sunscreen agents.
The sunscreens should be applied evenly throughout all the exposed parts of our skin,30 minutes to 2 hrs (for PABA and PABA esters),before sun exposure to allow proper penetration,and binding to the skin.
Persipiration,swimming,bathing,clothing,sand baths,towel bath may remove the sunscreen and needed to be reapplied.
Hence we must by the products after seeing the labels for the how for the products substand inspite of persipiration and swimming.
If a product is labelled as water proof that means it can adhere on the skin upto a maximum period of 80 minutes swimming
If a product is labelled as water resistant means it can withstand with our skin upto a maximum period of 40 minutes swimming.
Sunscreens should be noted in the label for their Sun Protection Factor (SPF).Baby oils,mineral oil,olive oil,and cocoa butter are not sunscreens but can be used to produce a Tan.
SPF of 30 is enough to give 97% protection from the UV radiation.The American FDA is recommending the upper limitation of SPF is 30 only any benifits getting by increasing this limit is interestingly negligible.An SPF of 15% is the upper limitation set by Skin Cancer Foundation.Hence products with SPF mor than 30 as SPF 50 ,SPF 100 etc.etc on the labels are merely for business attractions and of no use.
SPF can be calculated by Minimal Erythema Dose (MED) of the protected skin devided by that of the unprotected skin
MED is defined as the amount of sun radiation needed to produce minimal skin redness.
For example a man who gets minimal skin redness by the exposure of his skin 20minutes to the sun and want to stay in the sun for 120 minutes can use a sunscreen with the SPF of 6 as (120/20=6).When he use the sun screen of SPF-6 should its substantivity so that it must not be femoved by swimming or clothing.
An SPF of 15 can give 93% protection from the UV-B radiation.
Some people may get allergic reactions to some sunscreen cream beware of that.

TYPES OF SUNSCREENS

Physical sun blocks are opaque preparations that can block from UV to visible portions (290 nm to 700 nm) of the sunlight.These products often contains concenterated Titanium Di Oxide,and Zinc Oxide.These products are not attractive for greater area use but can be used in smaller areas like upper nose.Newer products with diluted titanium dioxides are available and are more cosmetic and attractive.Red Petrolatum covers a spectrum of 290 nm to 365 nm.
Chemical sun screens acts by absorbing a specific portion of the UV radiation inorder to prevent to reach the skin.These are of 5 groups as followsl:-
1.PARA AMINO BENZOIC ACID (PABA) and its esters primarily absorbs UV-B radiations (e,g) p-amino benzoic acid,glyceryl PABA,padimate-O.
Cinnamates primarily absorb UV-B rays.(e.g) cinoxate,octyl methoxycinnate.
Salicylate primarily absorb UV-B rays.(e.g) ethyl hexyl salicylate and homosalate.
Benzophenones absorb UV-B and a portion of UV-A rays.(e.g) oxybenzone,dioxybenzone.Because of their extensive coverage these can be used for photosensitivity reactions.
Miscellaneous the newer product butylmethoxydibenzoylmethane prvides full coverage UV-A and UV-B .This product with the combination of oxybenzone,and octyl methoxycinnamate offers the greatest protection in both UV-A and UV-B
Special agents of interests
Dihydroxyacetone (DHA) it offer an artificial suntan by reacting with keratin in the stratum corneum
It is not offering protection from UV rays and it is not producing natural looking tan.It's can withstand for a limited period and would peel off automatically.Also it will discolour hair and clothing.
Beta carotene a vitamin-A precursor can produce discolouration when taken orally.It is protective against some forms of abnormal photosensitivity like erythropoietic protoporphyria.But it is not protective against sunburn in normal individuals.
Tyrosine As tyrosine is a precursor in the synthesis of tan producing pigment melanin it is also used as an tanning agent but it is not a proved agent.