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Digoxin

Digoxin

Digoxin is a cardiac glycoside extracted from the foxglove plant, digitalis. It is widely used in the treatment of various heart conditions, namely atrial fibrillation, atrial flutter and congestive heart failure that cannot be controlled by other medication.

Actions

The main effects of digoxin are on the heart, its extracardiac effects are responsible for most of the side effects, i.e. nausea, vomiting, diarrhea and confusion. Its main cardiac effects are:
- A decrease of conduction of electrical impulses through the AV node, making it a commonly used drug in controlling the heart rate during atrial fibrillation or atrial flutter.
- An increase of force of contraction via inhibition of the Na⁺/K⁺ ATPase pump (see below).

Mechanism of action

Digoxin binds to a site on the extracellular aspect of the α-subunit of the Na⁺/K⁺ ATPase pump in the membranes of heart cells (myocytes). This causes an increase in the level of sodium ions in the myocytes, which then leads to a rise in the level of calcium ions. The proposed mechanism is the following: inhibition of the Na⁺/K⁺ pump leads to increased Na⁺ levels, which in turn slows down the extrusion of Ca²⁺ via the Na⁺/Ca²⁺ exchange pump. Increased amounts of Ca²⁺ are then stored in the sarcoplasmic reticulum and released by each action potential, which is unchanged by digoxin. This is a different mechanism from that of catecholamines. Digoxin also increases vagal activity via its central action on the central nervous system, thus decreasing the conduction of electrical impulses through the AV node. This is important for its clinical use in different arrhythmias (see below).

Clinical use

Today, the most common indications for digoxin are probably atrial fibrillation and atrial flutter with rapid ventricular response. High ventricular rate leads to insufficient diastolic filling time. By slowing down the conduction in the AV node and increasing its refractory period, digoxin can reduce the ventricular rate. The arrhythmia itself is not affected, but the pumping function of the heart improves owing to improved filling. The use of digoxin in congestive heart failure during sinus rhythm is controversial. In theory the increased force of contraction should lead to improved pumping function of the heart, but its effect on prognosis is disputable and digoxin is no longer the first choice for congestive heart failure. However, it can still be useful in patients who remain symptomatic despite proper diuretic and ACE inhibitor treatment. Digoxin is usually given by mouth, but can also be given by IV injection in urgent situations (the IV injection should be slow, heart rhythm should be monitored). The half life is about 36 hours, digoxin is given once daily, usually in 125μg or 250μg dosing. In patients with decreased kidney function the half life is considerably longer, calling for a reduction in dosing or a switch to a different glycoside (digitoxin). Effective plasma levels are fairly well defined, 1-2.6 nmol/l. In suspected toxicity or ineffectiveness, digoxin levels should be monitored. Plasma potassium levels also need to be closely controlled (see side effects below).

Side effects

Owing to its narrow therapeutic index (the margin between effectiveness and toxicity), side effects of digoxin are inevitable. Nausea, vomiting and GIT upset are common, especially in higher doses. Decreased conduction in the AV node can lead to AV blocks, increased intracellular Ca²⁺ causes a type of arrhytmia called bigeminy (coupled beats), eventually ventricular tachycardia or fibrillation. An often described but rarely seen side effect of digoxin is a disturbance of colour vision (mostly yellow and green colour) called xanthopsia. Side effects of digoxin are more common in patients with low potassium levels (hypokalaemia), since digoxin normally competes with K⁺ ions for the same binding site on the Na⁺/K⁺ ATPase pump. However, in patients with acute digoxin toxicity with low potassium levels, potassium supplementation is contraindicated in the presence of an AV block.

Other

Digoxin has potentially dangerous interaction with verapamil and amiodarone. In an overdose, the usual supportive measures are needed. Digoxin cannot be removed by haemodialysis, the antidote is antidigoxin (antibody fragments agains digoxin, trade name Digibind®). Some physical properties of digoxin are water solubility of 64.8mg/L at 25°C and melting point at 249°C.

References

- Rang, Dale, Ritter, Moore. Pharmacology (5th edition), Churchill Livingstone, 2003. ISBN 0443 071454
- Summary of product characteristics, Digoxin 0,125 mg, Zentiva a.s.
- Lüllmann. Pharmakologie und Toxikologie (15th edition), Georg Thieme Verlag, 2003. ISBN 3133 685155 Category:Cardiac glycosides

Cardiac glycoside

Cardiac glycosides are drugs used in the treatment of congestive heart failure and cardiac arrhythmia. These glycosides are found as secondary metabolites in several plants, but also in some animals. Some of these compounds (ouabain and some frog poisons) are used in Africa as arrow-poisons for hunting. Cardiac glycosides work by inhibiting the Na⁺/K⁺ pump. This inhibition increases the amount of Ca⁺⁺ ions available for contraction of the heart muscle, improves cardiac output and reduces distention of the heart. They have an antiarrhythmic effect by prolonging the refractory period of the AV node (Atrioventricular node), reducing the number of impulses reaching the ventricles. Cardiac output is restored but atrial fibrillation or atrial flutter are not abolished. Examples of plants producing cardiac glycosides:
- Strophanthus - ouabain g/k/e-strophanthin
- Digitalis lanata and Digitalis purpurea - digoxin, digitoxin
- Scilla maritima - proscillaridine A
- Adonis vernalis, Adonis aestivalis
- Ammi visnaga
- Crataegus (vitexin, rutin)
- Acokanthera oblongifolia
- Convallaria Some frog-poison contain bufalin, marinobufagenin and bufadienolides, cardiac glycosides. Category:Glycosides

Foxglove

About 20 species, including:
Digitalis ciliata
Digitalis davisiana
Digitalis dubia
Digitalis ferruginea
Digitalis grandiflora
Digitalis laevigata
Digitalis lanata
Digitalis lutea
Digitalis obscura
Digitalis parviflora
Digitalis purpurea
Digitalis thapsi
Digitalis viridiflora Digitalis is a genus of about 20 species of herbaceous biennials, perennials and shrubs that was traditionally placed in the figwort family Scrophulariaceae. Due to new genetic research, it has now been placed in the much enlarged family Plantaginaceae. The term digitalis is also used for preparations containing cardiac glycosides, particularly digoxin, extracted from plants of this genus.

General description

The members of this genus are known in English as foxgloves. They are native to Europe, northwest Africa and west and central Asia. The scientific name means "finger", and refers to the ease which a flower of Digitalis purpurea can be fitted over a human fingertip. "Foxglove" has a similar origin, seen as a suitable glove for a fox paw. The flowers are produced on a tall spike, are tubular, and vary in colour with species, from purple to pink, white and yellow. The best-known species is the Common Foxglove, Digitalis purpurea. It is a biennial, often grown as an ornamental plant due to its violet flowers. The first year of growth produces only the long, basal leaves, while in the second year the erect leafy stem 0.5-2.5 m tall develops. The larvae of the Foxglove Pug feed on the flowers of Digitalis purpurea. Other Lepidoptera species feed on the leaves including Lesser Yellow Underwing.

Medicinal use

The use of Digitalis purpurea extract containing cardiac glycosides for the treatment of heart conditions was first described by William Withering. In contemporary medicine, a purer form of digitalis is used to strengthen cardiac contractility (it is a positive inotrope) and as an antiarrhythmic agent to regulate heart rhythm. It is therefore often prescribed for patients in heart failure. A group of pharmacologically active compounds are extracted mostly from the leaves of the second year's growth, and in pure form are referred to by common chemical names such as digitoxin or digoxin, or by brand names such as Lanoxin, or Purgoxin. Digitalis works by inhibiting sodium-potassium ATPase, which increases intracellular calcium. The increased intracellular calcium gives a positive inotropic effect. It also has a vagal effect on the parasympathetic nervous system, and as such is used in reentrant cardiac arrhythmias and to slow the ventricular rate during atrial fibrillation. The dependence on the vagal effect means that digitalis is not effective when a patient has a high sympathetic nervous system drive, which is the case with acutely ill persons. Digitalis toxicity (Digitalis intoxication) results from an overdose of digitalis and can result in jaundiced (yellow) vision and the appearance of blurred outlines (halos), as well as bradycardia in extreme cases. Because a frequent side effect of digitalis is reduction of appetite, some individuals have abused the drug as a weight loss aid. Digitalis is a classic example of a drug derived from a plant formerly used by folklorists and herbalists: herbalists have largely abandoned its use because of its narrow therapeutic index and the difficulty of determining the amount of active drug in herbal preparations. Once the usefulness of digitalis in regulating pulse was understood, it was employed for a variety of purposes, including the treatment of epilepsy and other seizure disorders, now considered inappropriate.

Media

Image:Digitalis ciliata0.jpg|Digitalis ciliata Image:Wasp_and_her_Yellow_Flower.jpg|Digitalis grandiflora Image:Digitalis_lutea_100705.jpg|Digitalis lutea Image:Digitalis_purpurea_Koehler_drawing.jpg|Digitalis purpurea drawings by Franz Köhler Image:Digitalis_purpurea.jpg|Digitalis purpurea Image:Foxglove2.jpg|Digitalis purpurea Image:Digitalis-stora_hultrum.sweden-22.jpg|Digitalis purpurea Image:Digitalis-stora_hultrum.sweden-21.jpg|Digitalis purpurea var. alba

External link

- [http://www.bris.ac.uk/Depts/Chemistry/MOTM/digitalis/digtalis.htm Molecule of the Month - Digitalis]
- [http://www.emedicine.com/PED/topic590.htm eMedicine link] Category:Plantaginaceae Category:Antiarrhythmic agents Category:Herbal & fungal drugs/medicines ja:ジギタリス

Digitalis

General description

Medicinal use

Media

External link

Atrial fibrillation

Atrial fibrillation (AF or afib) is a cardiac arrhythmia (an abnormality of heart rate or rhythm) originating in the atria. Abnormal electrical impulses in the atria cause the ventricles to contract erratically. AF is the most common cardiac arrhythmia. If rapid, it may compromise blood flow and cause fainting, orthostatic hypotension (low blood pressure on standing up) or low blood pressure. In addition, the erratic wall motion of the atria leads to blood stasis which predisposes to thrombosis and embolism to the brain and other areas, being a prime risk factor for stroke, the most feared complication of atrial fibrillation.

Signs and symptoms

Atrial fibrillation is usually accompanied by symptoms related to either the rapid heart rate or embolization. Rapid and irregular heart rates may be perceived as palpitations, exercise intolerance, and occasionally produce angina and congestive symptoms of shortness of breath or edema. Sometimes the arrhythmia will be identified with the onset of a stroke or a TIA. It is not uncommon to identify atrial fibrillation on a routine physical examination or electrocardiogram. Paroxysmal atrial fibrillation is the episodic occurrence of the arrhythmia and may be difficult to diagnose. Episodes may occur with sleep or with exercise, and their episodic nature may require prolonged ecg monitoring for diagnosis.

Diagnosis

Electrocardiogram

Image:Afib.gif Atrial fibrillation is diagnosed on an electrocardiogram, an investigation performed routinely whenever irregular heart beat is suspected. Characteristic findings are (a "rhythm strip" of lead II is shown):
- absence of P waves
- unorganized electrical activity in their place
- irregularity of R-R interval due to irregular conduction of impulses to the ventricles

Other investigations

While many cases of AF have no definite cause, it may be the result of various other problems (see below). Hence, renal function and electrolytes are routinely determined, as well as thyroid-stimulating hormone (commonly suppressed in hyperthyroidism and of relevance if amiodarone will be administered) and a blood count. A chest X-ray is generally performed. In acute-onset AF associated with chest pain, cardiac troponins or other markers of damage to the heart muscle may be ordered. Coagulation studies (INR/aPTT) are usually performed, as anticoagulant medication may be commenced.

Causes

AF is linked to several cardiac causes, but may occur in otherwise normal hearts. Known associations include:
- Arterial hypertension
- Mitral valve disease (e.g. due to rheumatic heart disease or mitral valve prolapse)
- Heart surgery
- Coronary heart disease
- Excessive alcohol consumption ("binge drinking" or "holiday heart")
- Hyperthyroidism
- Hyperstimulation of the vagus nerve, usually by having large meals ("binge eating") In turn, AF with a rapid rate that goes untreated can cause further damage to the heart muscle. This weakened condition, termed chronotropic cardiomyopathy, is usually a result of a long period of tachycardia(fast heart rate).

Pathophysiology

In atrial fibrillation, the regular impulses produced by the sinus node to provide rhythmic contraction of the heart are overwhelmed by the rapid randomly generated discharges produced by larger areas of atrial tissue. It can be distinguished from atrial flutter, which is a more organized electrical circuit usually in the right atrium that produces characteristic saw toothed waves on the electrocardiogram. Often, the rhythm produced is more rapid than normal, but the difficulty is in obtaining control of the heart rate both at rest and with exercise. Good rate control will usually require two drugs, and can only be checked by observing heart rate response to exercise. An organized electrical impulse in the atrium produces atrial contraction; the lack of such an impulse, as in atrial fibrillation, produces stagnant blood flow, especially in the atrial appendage and predisposes to clotting. The dislodgement of a clot from the atrium results in an embolus, and the damage produced is related to where the circulation takes it. An embolus to the brain produces the most feared complication of atrial fibrillation, stroke, while an embolus may also lodge in the mesenteric circulation (the circulation supplying the abdominal organs) or digit, producing organ-specific damage.

Treatment

Rate and rhythm control

AF can cause disabling and annoying symptoms. Palpitations, angina, lassitude (weariness), and decreased exercise tolerance are related to rapid heart rate and inefficient cardiac output caused by AF. There are two ways to approach these symptoms: rate control and rhythm control. Rate control treatments seek to reduce the heart rate to normal, usually 60 to 100 beats per minute. Rhythm control seeks to restore the normal heart rhythm, called normal sinus rhythm. Studies suggest that rhythm control is mainly a concern in newly diagnosed AF, while rate control is more important in the chronic phase. Rate control with anticoagulation is as effective a treatment as rhythm control in long term mortality studies, the AFFIRM Trial. AF can cause a form of heart failure called tachycardia-induced cardiomyopathy. This can significantly increase mortality and morbidity. The early treatment of AF through either rate-control or rhythm-control can prevent this condition and thereby improve mortality and morbidity.

Rate control

Rate control methods include:
- Beta blockers (e.g. metoprolol)
- Digoxin
- Calcium channel blockers (e.g. verapamil) In refractory cases where none of the above drugs are sufficient, a variety of other antiarrhythmic drugs, most commonly including quinidine, flecainide, propafenone, disopyramide, sotalol, or amiodarone may be used. Of these, only propafenone, sotalol, and amiodarone (which possess some beta blocking activity) control the ventricular rate; the others may maintain sinus rhythm, but may actually increase the ventricular rate. Many of these drugs are less frequently used today than in the past. All (with the possible exception of amiodarone) increase the risk of ventricular tachycardia, which can be fatal. In symptomatic patients with normal heart function, however, the small increase in risk is usually felt to be acceptable. In the presence of heart failure, the only antiarrhythmic drugs thought to be safe are amiodarone and dofetilide. These medications work by slowing the generation of impulses from the atria and the conduction of those impulse from the atria to the ventricles. In patients with AF where rate control drugs are ineffective and it is not possible to restore sinus rhythm using cardioversion, non-pharmacological alternatives are available. For example, to control rate it is possible to destroy the bundle of cells connecting the upper and lower chambers of the heart - the atrioventricular node - which regulates heart rate, and to implant a pacemaker instead. A more complex technique involves ablating groups of cells near the pulmonary arteries where atrial fibrillation is thought to originate, or creating more extensive lesions in an attempt to prevent atrial fibrillation from establishing itself..

Rhythm control

Rhythm control methods include electrical and chemical cardioversion:
- Electrical cardioversion involves the restoration of normal heart rhythm either through the application of a DC electrical shock (electrical cardioversion)
- Chemical cardioversion is performed with drugs, such as amiodarone, propafenone or flecainide. The anti-arrhythmic medications often used in either pharmacological cardioversion or in the prevention of relapse to AF alter the flux of ions in heart tissue, making them less excitable, setting the stage for spontaneous and durable cardioversion. These medications are often used in concert with electrical cardioversion. However, the AFFIRM study showed no difference in risk of stroke in patients who have converted to a normal rhythm with anti-arrhythmic treatment, compared to those who have only rate control.. The main risk of cardioversion is systemic embolization by a bloodclot from the previously fibrillating left atrium. It should not be performed without adequate anticoagulation in patients who have been in atrial fibrillation for more than 48 hours. Whichever method of cardioversion is used, approximately 50% of patient relapse within one year, although the continued daily use of oral antiarrhythmic drugs may extend this period. The key risk factor for relapse is duration of AF, although other risk factors that have been identified include the presence of structural heart disease, and increasing age.

Radiofrequency ablation

Radiofrequency ablation (RFA) uses radiofrequency energy to destroy abnormal electrical pathways in heart tissue. It is used in recurrent AF. The energy emitting probe (electrode) is placed into the heart through a catheter. The practitioner first "maps" an area of the heart to locate the abnormal electrical activity before the responsible tissue is eliminated. Ablation is a newer technique and has shown some promise for cases unresponsive to conventional treatments. New techniques include the use of cryoablation (tissue freezing using a coolant which flows through the catheter), and microwave ablation, where tissue is ablated by the microwave energy "cooking" the adjacent tissue. The abnormal electrophysiology can also be modified in a similar way surgically, and this procedure referred to as the "Cox maze procedure", is commonly performed concomitantly with cardiac surgery. This is an area of active research, especially with respect to the RF ablation technique and emphasis on isolating the pulmonary veins that enter into the left atrium.

Anticoagulation

In confirmed AF, anticoagulant treatment is a crucial way to prevent stroke. Treatment of AF patients over age 60 with warfarin (also known as Coumadin®) results in a significant reduction in the subsequent risk of stroke. Patients under age 65 who have any structural heart disease (ie: valvular heart disease, ejection fraction <= 35%, history of heart attack) also benefit from warfarin. Patients under age 65 who do not have structural heart disease do not require warfarin, and can be treated with aspirin. Other guidelines are also used. The new anticoagulant ximelagatran has been shown to prevent stroke with equal efficacy as warfarin, without the difficult monitoring process associated with warfarin and with possibly fewer adverse haemorrhagic events. Unfortunately, ximegalatran and other similar anticoagulant drugs (commonly referred to as direct thrombin inhibitors), have yet to be widely licensed. License applications made by AstraZeneca, who developed Ximegalatran, have been rejected by both American and European licensing authorities, and its evaluation has been suspended in the UK. This is primarily due to concerns over possible liver toxicity.

References

- Fuster V, Ryden LE, Asinger RW, Cannom DS, Crijns HJ, Frye RL, Halperin JL, Kay GN, Klein WW, Levy S, McNamara RL, Prystowsky EN, Wann LS, Wyse DG, Gibbons RJ, Antman EM, Alpert JS, Faxon DP, Fuster V, Gregoratos G, Hiratzka LF, Jacobs AK, Russell RO, Smith SC, Klein WW, Alonso-Garcia A, Blomstrom-Lundqvist C, De Backer G, Flather M, Hradec J, Oto A, Parkhomenko A, Silber S, Torbicki A; American College of Cardiology/American Heart Association/European Society of Cardiology Board. ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: executive summary. A Report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation): developed in Collaboration With the North American Society of Pacing and Electrophysiology. J Am Coll Cardiol 2001;38:1231-66. [http://www.acc.org/clinical/guidelines/atrial_fib/af_index.htm ACC/AHA/ESC Fulltext]. PMID 11583910.
- Wyse DG, Waldo AL, DiMarco JP, Domanski MJ, Rosenberg Y, Schron EB, Kellen JC, Greene HL, Mickel MC, Dalquist JE, Corley SD; Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med 2002;347:1825-33. PMID 12466506.
- [http://www.cardiologychannel.com/afib/longterm.shtml Long term management of Atrial Fibrillation]

External links

- [http://www.italheartj.org/abstract/I_H_J_2002_3_571-578.htm Hybrid therapy of Atrial Fibrillation] Category:Cardiac electrophysiology

Atrial flutter

Atrial flutter is a rhythmic, fast rhythm that occurs in the atria of the heart. This rhythm occurs most often in individuals with organic heart disease (ie: pericarditis, coronary artery disease, and cardiomyopathy). Atrial flutter is typically not a stable rhythm, and frequently degenerates to atrial fibrillation. However, it may persist for months to years.

Overview

atrial fibrillation

Atrial flutter with 4:1 block. Flutter waves (red triangles) at rate of 240 / minute. QRS complexes (yellow triangles) at rate of 60 / minute.

Atrial flutter is a regular, rhythmic tachycardia originating in the atria. The rate in the atria is over 220 beats/minute, and typically about 300 beats/minute. The morphology on the surface EKG is typically a sawtooth pattern. The ventricles do not beat as fast as the atria in atrial flutter. The AV node acts as a safety valve in the event of any fast rhythm of the heart, including atrial fibrillation and atrial flutter. The AV node slows down conduction of the electrical activity, and if it receives the next action potential before it is ready, the impulse will be blocked at the AV node level, and never reach the ventricles. In the case of atrial flutter, there is a very particular block pattern at the AV node level. In atrial flutter, the AV node typically will block every other electrical impulse, or three out of four impulses. If every other impulse is blocked, known as 2:1 block, while the atrial rate is 300 beats/minute, the ventricular rate will be 150 beats/minute. If three out of four beats are blocked, known as 4:1 block, while the atrial rate is 300 beats/minute, the ventricular rate will be 75 beats/minute. In many individuals, the degree of block is variable - sometimes every other beat is transmitted, sometimes two beats are dropped before the third is transmitted, etc. This is known as varying block. For reasons that are not well understood, a stable 3:1 block is not commonly seen in individuals with atrial flutter. A single individual can have varying degrees of block at different times. The varying degree of block is due to a multitude of factors, including catecholamine release and the use of any drugs that inhibit conduction through the AV node, such as beta blockers, digitalis, and calcium channel blockers. The term 2:1 block comes from the fact that for every two electrical impulses that reach the AV node, only one is transmitted to the ventricle. Similarly, 4:1 block comes from the fact that for every four impulses that reach the AV node, only one is transmitted to the ventricle.

Mechanism of action

Atrial flutter is caused by a reentrant rhythm in either the right or left atrium.

Types of atrial flutter

There are two types of atrial flutter, known as type I and type II.¹ Most individuals with atrial flutter will manifest only one of these types of atrial flutter. Rarely someone may manifest both types of flutter; however, they can only manifest one type at a time.

Type I flutter

reentrant rhythm

Type I atrial flutter, counterclockwise rotation with 4:1 AV nodal block.

Type I atrial flutter, also known as common atrial flutter or typical atrial flutter, has an atrial rate of 240 to 350 beats/minute. However, this rate may be slowed by antiarrhythmic agents. Type I flutter can be entrained by rapid atrial pacing. This means that the re-entrant rhythm of the flutter can be broken if a stimulus enters the re-entrant cycle at just the right point, breaking the cycle and thereby terminating the atrial flutter. While this can be performed with a pacemaker, it is performed almost exclusively in the electrophysiology lab by pacing the atrium at a rate just above the rate of the atrial flutter. While entrainment may break atrial flutter and cause the individual to revert to a normal sinus rhythm, the rapid atrial pacing may cause the individual to go into atrial fibrillation. Type I flutter has two subtypes, known as counterclockwise atrial flutter and clockwise atrial flutter.

Counterclockwise atrial flutter

Couterclockwise atrial flutter (known as cephalad-directed atrial flutter) is more commonly seen than clockwise atrial flutter. The flutter waves in this rhythm are inverted in II, III, and aVF.

Clockwise atrial flutter

Clockwise atrial flutter is less common than counterclockwise atrial flutter. The flutter waves are upright in II, II, and aVF in this rhythm.

Type II flutter

Type II flutter is faster than type I flutter, and usually is 340-430 beats/minute. Unlike type I flutter, the rhythm of type II flutter cannot be entrained by rapid atrial pacing.

Complications

Clot formation

In atrial flutter, as in atrial fibrillation, there is no effective contraction of the atria. In individuals with structural heart disease, this causes stasis of blood in the atria. The stasis of blood leads to formation of thrombus material (clots) within the heart. In the left side of the heart, thrombus is most likely for form in the left atrial appendage. This is important because, since the left side of the heart supplies blood to the entire body, any thrombus material that dislodges from the left side of the heart can potentially embolize to the brain, causing a stroke. Of course, the thrombus material can also embolize to any other portion of the body.

Sudden death

Sudden death is not directly associated with atrial flutter. However, in individuals with a pre-existing accessory conduction pathway, such as the bundle of Kent in Wolff-Parkinson-White syndrome, the accessory pathway may conduct activity from the atria to the ventricles much faster than the AV node. In this case, the atrial rate of 300 beats/minute will lead to a ventricular rate of 300 beats/minute. The ventricles, unable to sustain a ventricular tachycardia at such a high rate, will go into ventricular fibrillation, which will quickly lead to hemodynamic collapse and death.

Treatment

In general, atrial flutter should be treated the same as atrial fibrillation. Both rhythms do not provide effective contraction of the atria. Because of this, there is stasis of blood in the atria. This stasis of blood leads to the potential formation of thrombus material in the atria. Therefore, individuals with atrial flutter require some form of anticoagulation or anti-platelet agent. In addition to the treatments available to individuals in atrial fibrillation, there are a couple of treatment considerations that are particular to individuals with atrial flutter.

Ablation

Because of the reentrant nature of atrial flutter, it is possible to ablate the circuit that causes atrial flutter. This is done in the electrophysiology lab by causing a ridge of scar tissue that crosses the path of the circuit that causes atrial flutter.

Rate control

Control of the ventricular rate in atrial flutter may be more difficult than if the individual was in atrial fibrillation. This is because of properties of the AV node. In atrial fibrillation, the AV node is typically bombarded with signals from the atria at rates in excess of 400 beats/minute. This causes a high degree of block within the AV node, with many signals partially penetrating the node and blocking at the lower levels of the AV node. This phenomenon is known as concealed conduction. In atrial flutter, on the other hand, the AV node receives signals very rhythmically at a rate of about 300/minute. Since the atrial flutter is an organized rhythm of the atria, the block at the AV node will be consistently at the same level, and paradoxically a higher number of impulses will get through per minute. Because of this, it may be easier to control the rate of some individuals if they are converted from atrial flutter to atrial fibrillation. While there are no guidelines for this procedure at this time, this may be attempted in the electrophysiology lab by pacing the atria at rates well over 300 beats/minute.

References

#Chou's Electrocardiography in Clinical Practice, Fifth Edition, Surawicz & Knilans, ISBN 0-7216-8697-4 #Electrophysiologic Testing, Richard N. Fogoros, Blackwell Science, ISBN 0-632-04325-3

Congestive heart failure

Congestive heart failure (CHF) (also called congestive cardiac failure and heart failure) is the inability of the heart to pump a sufficient amount of blood throughout the body, or requiring elevated filling pressures in order to pump effectively. CHF is an abnormal cardiac condition that reflects impaired cardiac pumping and blood flow. The pooling of blood leads to congestion in body tissue. The term heart failure is frequently misused, especially when given as cause of death: it is not synonymous with "cessation of heartbeat" – for which see cardiac arrest. Because not all patients have volume overload at the time of initial or subsequent evaluation, the term "heart failure" is preferred over the older term "congestive heart failure".

Classification

There are many different ways to categorize heart failure, including:
- the side of the heart involved, (left heart failure versus right heart failure)
- whether the abnormality is due to contraction or relaxation of the heart (systolic heart failure vs. diastolic heart failure) The NYHA functional class is a commonly used way to gauge the progression of CHF in a particular patient. This classification is used to determine how much CHF limits their lifestyle, and does not apply to a particular decompensated episode.

Symptoms and signs

Signs of decompensated heart failure include pulmonary edema (fluid accumulation in the lungs), peripheral edema (fluid build-up in dependent portions of the body). Other physical examination findings include rales heard on chest auscultation, an enlarged or pulsatile liver, and jugular venous distension. Symptoms of decompensated heart failure include dyspnea (shortness of breath) on exertion, orthopnea (dyspnea that increases upon lying down), fatigue and paroxysmal nocturnal dyspnea ("cardiac asthma", shortness of breath that occurs hours or minutes after lying down).

Treatment

Individuals with heart failure are sensitive to small shifts in their intravascular volume status (the amount of fluid in their circulatory system). Increasing the volume in their circulatory system can cause symptoms and signs of decompensated heart failure, while decreasing the volume in the circulatory system can cause hypotension. The treatment of CHF focuses on treating the symptoms and signs of CHF and preventing the progression of disease. If there is a reversible cause of the heart failure (e.g. infection, alcohol ingestion, anemia, thyrotoxicosis, arrhythmia, or hypertension), that should be addressed as well.

Medication

Treating the signs and symptoms of CHF involves maintaining a euvolemic state (normal fluid level in the circulatory system). This is done with the judicious use of diuretic agents, vasodilator agents, and positive inotropes. Delaying the progression of heart failure involves the use of ACE inhibitors, beta blockers, and aldosterone inhibitors. These agents have been proven to improve survival in individuals with CHF. While the mechanism of improving is not entirely clear, it appears that these agents prevent remodelling of the heart and therefore prevent progression of dilatation of the left ventricle.

Devices and surgery

Patients with NYHA class III or IV, LVEF of 35% or less and a QRS interval of 120ms or more may benefit from bi-ventricular pacemaker (CRT) placement or surgical remodelling of the heart. These treatment modalities may make the patient symptomatically better, improving quality of life and in some trials have been proven to reduce mortality. In the recently completed COMPANION trial, cardiac resynchronization therapy (pacing the left ventricle as well as the right ventricle) has been shown to improve survival in individuals with NYHA class III or IV heart failure with a widened QRS complex on EKG.² The CARE-HF trial, showed that patients receiving a Medtronic bi-ventricular pacemaker (CRT) and optimal medical therapy benefit from a 36% reduction in all cause mortality, and a reduction in cardiovascular related hospitalization.³ Additionally, patients with NYHA class II, III or IV, LVEF of 35% (without a QRS requirement) may benefit from an Implantable Converter Defibrillator (ICD), a device that is proven to reduce all cause mortality (death) by 23% compared to placebo. This mortality benefit was observed in patients who were already optimally managed on drug therapy.⁴ Another current treatment involves the use of left ventricular assist devices (LVADs). LVADs are battery-operated mechanical pump-type devices that are surgically implanted on the upper part of the abdomen. They take blood from the left ventricle and pump it through the aorta. LVADs are becoming more common and are often used by patients who have to wait for heart transplants. Acorn Cardiovascular, based in St. Paul, Minnesota, recently created the CorCap Cardiac Support Device (CSD), also known as the "heart sock." It is a dacron mesh that is placed around the heart. The elastic CSD works by mechanically restoring the contractility of the expanded heart. The ultimate treatment is cardiac transplant surgery (heart transplant) or implantation of an artificial heart.

References

1. [http://www.acc.org/clinical/guidelines/failure/hf_index.htm ACC / AHA guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult] ([http://www.acc.org/clinical/guidelines/failure/pdfs/hf_fulltext.pdf PDF Copy]) 2. Bristow MR, Saxon LA, Boehmer J, et al for the Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) Investigators. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. [http://content.nejm.org/cgi/content/abstract/350/21/2140 N Engl J Med 2004; 350:2140-2150.] 3. Cleland JGF, Daubert J-C, Erdmann E, et al; the Cardiac Resynchronization -- Heart Failure (CARE-HF) Study Investigators. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med. 2005 March 7 [http://content.nejm.org/cgi/content/short/NEJMoa050496v1 N Engl J Med 2005; 10.1056/NEJMoa050496] 4. Bardy GH, Lee KL, Mark DB, et al for the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) Investigators. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. [http://content.nejm.org/cgi/content/abstract/352/3/225 N Engl J Med 2005; 352:225-237] 5. Donatelle, Rebecca J. Health: The Basics. 6th ed. San Francisco: Pearson Education, Inc. 2005.

Medication

A medication is a licenced drug taken to cure or reduce symptoms of an illness or medical condition. Medications are generally divided into two groups -- over the counter (OTC) medications, which are available in pharmacies and supermarkets without special restrictions, and Prescription only medicines (POM), which must be prescribed by a physician. Most OTC medication is generally considered to be safe enough that most persons will not hurt themselves accidentally by taking it as instructed. Many countries, such as the UK have a third category of pharmacy medicines which can only be sold in registered pharmacies, by or under the supervision of a pharmacist. However, the precise distinction between OTC and prescription depends on the legal jurisdiction. Medications are typically produced by pharmaceutical companies and are often patented. Those that are not patented are called generic drugs.

Some common medications

- Anti-diabetic drugs
- Asthma medication
- Cough medicine
- Diarrhea relief medicine (such as Loperamide)
- Nasal spray (such as Xylometazoline)
- Anti-Inflammatory Medications
- Anti-Pyretic Medications
- Gastrointestinal Medications
- Psychiatric Medications
- Hair Medications

External links

- [http://www.rxlist.com Medication list or vademecum]
- [http://www.theacpa.org/ American Chronic Pain Association (ACPA)]
- [http://www.fda.gov/cder/drug/DrugSafety/DrugIndex.htm Consumer drug information from the FDA]
- [http://www.dmoz.org/Health/Medicine/ Medicinal directory] Category:Pharmacology als:Medikament th:ยา

Nausea

Nausea (Greek Ναυτεία) is the sensation of unease and discomfort in the stomach with an urge to vomit.

Causes

Nausea is a symptom of many conditions. It is also an adverse effect of many drugs. In medicine, nausea is a particular problem during some chemotherapy regimens and following general anaesthesia. Nausea is also a common symptom of pregnancy. Other causes include: altitude sickness, angina, brain tumor, cirrhosis, clinical depression, coeliac disease, colorectal cancer, crohn's disease, decompression sickness, esophagitis, gastroesophageal reflux disease, gastroenteritis, hangover, head injury, hepatitis C, hepatocellular carcinoma, hydrocephalus, hyperthyroidism, hypoglycemia, hyponatremia, hypoxia (medical), intestinal parasite, irritable bowel syndrome, kidney stone, lassa fever, lead poisoning, mastocytosis, ménière’s disease, morning sickness, motion sickness, myocardial infarction, panic attack, peptic ulcer, peritonitis, pneumonia, porphyria, postoperative nausea and vomiting, pseudomembranous colitis, psoriasis, Rocky mountain spotted fever, strep throat, trichinosis, ulcerative colitis, viral infections

Treatment

While short-term nausea and vomiting are generally harmless, they may sometimes indicate a more serious disease. When associated with prolonged vomiting, it may cause dangerous levels of dehydration and/or electrolyte imbalances. Symptomatic treatment for nausea and vomiting may include short-term avoidance of solid food. This is usually easy as nausea is nearly always associated with loss of appetite. Dehydration may require rehydration with oral or intravenous electrolyte solutions. Oral rehydration is safer and simpler in most cases. There are many antiemetics (drugs to treat nausea), although researchers continue to look for more effective treatments. Celiac Disease may also be a symptom if you consume wheat.

Vomiting

Vomiting (or emesis) is the forceful expulsion of the contents of one's stomach through the mouth. Although it probably evolved as a mechanism for expelling ingested poisons, vomiting may result from many causes not related to poisoning, ranging from gastritis to brain tumors, or elevated intracranial pressure (ICP). The feeling that one is about to vomit is called nausea. It usually, but not necessarily, precedes vomiting, but it does not always lead to vomiting. Antiemetics are sometimes necessary to suppress nausea and vomiting. The medical branch investigating vomiting, emetics and antiemetics is called emetology. Antiemetic
Mechanism
Vomiting is co-ordinated in the vomiting center in the lateral medullary reticular formation in the medulla. Receptors on the floor of the fourth ventricle of the brain represent a chemoreceptor trigger zone, stimulation of which can lead to vomiting. The chemoreceptor zone lies outside the blood-brain barrier, and can therefore be stimulated by blood-borne drugs that can stimulate vomiting, or inhibit it. There are various sources of input to the vomiting center:
- As stated earlier, the chemoreceptor trigger zone which lies in the fourth ventricle. This area has numerous dopamine D₂ receptors, serotonin 5-HT₃ receptors, and opoid receptors.
- The vestibular system which sends information to the brain via cranial nerve VIII (vestibulocochlear nerve). It plays a major role in motion sickness and is rich in muscarinic receptors and histamine H₁ receptors.
- Cranial nerve X (vagus nerve), which is activated when the pharynx is irritated, leading to a gag reflex.
- Vagal and enteric nervous system inputs that transmit information regarding the state of the gastrointestinal system. Irritation of the GI mucosa by chemotherapy, radiation, distention or acute infectious gastroenteritis activates the 5-HT₃ receptors of these inputs.
- The CNS mediates vomiting arising from psychiatric disorders and stress. The vomiting act encompasses three types of outputs initiated by the medulla: Motor, Parasympathetic Nervous System (PNS) and Sympathetic Nervous System (SNS). Collectively, they are as follows:
- Increased salivation to protect the enamel of teeth from stomach acids (excessive vomiting does lead to caries). This is part of the PNS output.
- Retroperistalsis, starting from the middle of the small intestine, sweeping up the contents of the digestive tract into the stomach, through the relaxed pyloric sphincter.
- A lowering of intrathoracic pressure (by inspiration against a closed glottis), coupled with an increase in abdominal pressure as the abdominal muscles contract, propels stomach contents into the esophagus without involvement of retroperistalsis. The lower esophageal sphincter relaxes. This is part of the motor output, and it is also important to note that the stomach itself does not contract in the process of vomiting.
- Vomiting is ordinarily preceded by retching. The purpose of retching is to build up the pressure needed to expel the stomach contents from the body. In retching, the body makes movements similar to vomiting. These spasms build up pressure within the chest cavity. When a sufficient amount of pressure has been created, the diaphragm transfers the pressure from the chest to the abdomen, and this pressure then results in actual vomiting.
- Vomiting also initiates a SNS response causing both sweating and increased heart rate. The neurotransmitters that regulate vomiting are poorly understood, but inhibitors of dopamine, histamine and serotonin are all used to suppress vomiting, suggesting that these play a role in the initiation or maintenance of a vomiting cycle. Vasopressin and neurokinin may also participate.
Content
As the stomach secretes acid, vomit contains a high concentration of hydronium ions and is thus strongly acidic. The potential physiological complications associated with excessive vomiting are mainly metabolic alkalosis (increased blood pH), hypokalemia (potassium depletion) and hypochloremia (chlorine depletion). The hypokalemia is an indirect result of the kidney compensating for the loss of acid. The content of the vomitus (vomit) may be of medical interest. Fresh blood in the vomit is termed hematemesis ("blood vomiting"). Old blood bears resemblance to coffee grounds (as the iron in the blood is oxidized), and when this matter is identified the term "coffee ground vomiting" is used. Bile can enter the vomit during subsequent heaves due to duodenal contraction if the vomiting is severe. Fecal vomiting is often a consequence of intestinal obstruction, and is treated as a warning sign of this potentially serious problem ("signum mali ominis"); such vomiting is sometimes called "miserere".
Causes
Vomiting may be due to a large number of causes, and protracted vomiting has a long differential diagnosis.
Digestive tract
Causes in the digestive tract:
- Gastritis (inflammation of the gastric wall, usually by viruses)
- Pyloric stenosis (in babies - this typically causes a very forceful "projectile vomiting" and is an indication for urgent surgery)
- Bowel obstruction
- Acute abdomen and/or peritonitis
- Ileus
- Cholecystitis, pancreatitis, appendicitis and hepatitis
Sensory system and brain
Causes in the sensory system:
- Movement: motion sickness (which is caused by overstimulation of the labyrinthine canals of the ear)
- Meniere's disease Causes in the brain:
- Concussion
- Intoxication with alcohol (being sick whilst being drunk or being sick the next morning suffering from the after-effects, i.e. the hangover).
- Cerebral hemorrhage
- Brain tumors
- Benign intracranial hypertension and hydrocephalus Metabolic disturbances (these may irritate both the stomach and the parts of the brain that coordinate vomiting):
- Hypercalcemia (high calcium levels)
- Uremia (urea accumulation, usually due to renal failure)
- Adrenal insufficiency
- Hypoglycemia Opioids, many chemotherapy drugs and a host of other drugs may cause nausea and vomiting.
Other

- Self-induced
- Eating disorders (anorexia nervosa or bulimia)
- Sexual fetish (emetophilia)
- To remove a poison in case such has been ingested (some poisons should not be vomited as they may be more toxic when inhaled or aspirated; it is generally considered better to ask for help before inducing vomiting)
- After surgery (postoperative nausea and vomiting)
- The sight or smell of decayed food, or others' vomit
- Extreme pain, myocardial infarction (heart attack)
- Pregnancy (morning sickness, hyperemesis gravidarum)
- Violent emotions
- Cyclic vomiting syndrome (a poorly understood condition with attacks of vomiting)
Related medication

Emetics
An emetic, such as Syrup of Ipecac, is a substance that induces vomiting when administered orally or by injection. An emetic is used medically where a substance (typically poison) has been ingested and must be expelled from the body immediately. Inducing vomiting can remove the substance before it is absorbed into the body.
Antiemetics
An antiemetic is a drug that is effective against vomiting and nausea. Antiemetics are typically used to treat motion sickness and the side effects of some opioid analgesics and chemotherapy directed against cancer.
Social implications

Nausea inducement in groups
It is quite common that when one person vomits, others nearby will become nauseated, particularly when smelling the vomit of others, often to the point of vomiting themselves. It is believed that this is an evolved trait among primates. Many primates in the wild will tend to browse for food in small groups. Should one member of the party react adversely to some ingested food it may be advantageous (in a survival sense) for other members of the party to also vomit. This tendency in human populations has been observed at drinking parties, where excessive consumption of alcoholic beverages may result a number of party members vomiting nearly simultaneously, this being triggered by the initial vomiting of a single member of the party.
Context
Most people try to contain their vomit by vomiting into a sink, toilet, or trash can, as both the act and the vomit itself are widely considered embarrassing. On airplanes and boats, special bags are supplied for sick passengers to vomit into. Alternatively, a special disposable bag is available containing absorbent material that solidifies the vomit quickly, making it convenient and safe to keep (leakproof, puncture resistant, odorless) until there is an opportunity to dispose of it conveniently. People who vomit chronically (e.g. as part of an eating disorder such as bulimia nervosa) may devise various ways to hide this abnormality.
In language
As with other physiological processes involving body wastes, vomiting has taboo aspects. This is shown by the large number of colourful euphemisms for vomiting. (see: toilet humour)
In other animals

- Whales vomit regularly (every 7 to 10 days) as a means of the ordinary digestive process, to expel inedible things they have swallowed.
- The domestic cat is well known for its tendency to vomit, particularly when attempting to dislodge hairballs from its throat or upper gastrointestinal tract. Chronic vomiting in cats may indicate underlying liver or kidney dysfunction and should be investigated by a veterinarian. Dogs also vomit often (frequently after eating grass) and are also known for eating their own vomit, a fact even cited in the Bible: KJV Proverbs 26:11 "As a dog returneth to his vomit, so a fool returneth to his folly."
- Owls will expel the undigestible bones and fur of their meals after partial digestion of the nutritious parts rather than passing them through the digestive tract.
- Some adult birds regurgitate food to feed their young, triggered by a feather or a beak of their young. The food can be either incompletely digested or partially predigested, depending on the species. Some bird species may also use regurgitation as a form of defense, vomiting when wounded or molested. When an intruder or a predator comes near a fulmar on its nest, the bird vomits oil up to 3 feet at the enemy.
- When in danger, the sea cucumber may eject its entire digestive tract. The animal is able to re-grow another one.
- Some large mammals, including horses, rarely vomit. Many rodents lack the ability to vomit, which is why mice and rats are easily killed by poisoning.
See also

- emetophobia (fear of vomiting)
- emetophilia (sexual fetish)
- regurgitation
External links

- [http://faq.emetophobia.net/emetophobia.html Emetophobia FAQ]
- [http://www.cvsa.org.uk Cyclical Vomiting Syndrome] Category:Reflexes Category:Symptoms ja:嘔吐 simple:Vomit

Diarrhea

Diarrhea (AmE) or diarrhoea (CwE) is a condition in which the sufferer has frequent and watery, chunky, or loose bowel movements (from the ancient Greek word διαρροή = leakage; lit. "to run through"). In the Third World, diarrhea is the most common cause of death among infants, killing more than 1.5 million per year.

Causes

This condition can be a symptom of injury, disease or foodborne illness and is usually accompanied by abdominal pain, and often nausea and vomiting. There are other conditions which involve some but not all of the symptoms of diarrhea, and so the formal medical definition of diarrhea involves defecation of more than 200 grams per day (though formal weighing of stools to determine a diagnosis is never actually carried out). It occurs when insufficient fluid is absorbed by the colon. As part of the digestion process, or due to fluid intake, food is mixed with large amounts of water. Thus, digested food is essentially liquid prior to reaching the colon. The colon absorbs water, leaving the remaining material as a semisolid stool. If the colon is damaged or inflamed, however, absorption is inhibited, and watery stools result. Diarrhea is most commonly caused by myriad viral infections but is also often the result of bacterial toxins. In sanitary living conditions and with ample food and water available, an otherwise healthy patient typically recovers from the common viral infections in a few days and at most a week. However, for ill or malnourished individuals diarrhea can lead to severe dehydration and can become life-threatening without treatment. It can also be a symptom of more serious diseases, such as dysentery, cholera, or botulism and can also be indicative of a chronic syndrome such as Crohn's disease. Though appendicitis patients don't generally have diarrhea, it is a common symptom of a ruptured appendix. It is also an effect of severe radiation sickness. It can also be caused by excessive alcohol consumption, especially in someone who doesn't eat enough food. Symptomatic treatment for diarrhea involves the patient consuming adequate amounts of water to replace that lost, preferably mixed with electrolytes to provide essential salts and some amount of nutrients. For many people, further treatment and formal medical advice is unnecessary. The following types of diarrhea generally indicate medical supervision is desirable:
- Diarrhea in infants.
- Moderate or severe diarrhea in young children.
- Diarrhea associated with blood.
- Diarrhea that continues for more than 2 weeks.
- Diarrhea that is associated with more general illness such as non-cramping abdominal pain, fever, weight loss, etc.
- Diarrhea in travelers (more likely to have exotic infections such as parasites)
- Diarrhea in food handlers (potential to infect others)
- Diarrhea in institutions (Hospitals, child care, mental health institutes, geriatric and convalescent homes etc). Since most people will ignore very minor diarrhea, a patient who actually presents to a doctor is likely to have diarrhea that is more severe than usual.

Mechanism

To evacuate the contents of the lower digestive tract, the fluidity of the contents of the small and large intestines is increased. Active transport of Na⁺ back into the gut intiates a reverse sodium transport. This causes both Cl^- and HCO₃ to follow passively, as well as water. Now in the intestines, the water dilutes toxins as well as triggers contractions of the intestine due to increase in intestinal distension. These contractions push the contents of the lower GI tract towards and out of the anal canal. Medications such as loperamide are designed to prevent such contractions in response to the distension, and should not be used to prevent diarrhea. Such inhibition actually prolongs the infection or irritation, and can cause a worsening over time because the evacuation of the bowel contents has been delayed.

Acute diarrhea

This may be defined as diarrhea that lasts less than 2 weeks, and is also called gastroenteritis. This can nearly always be presumed to be infective, although only in a minority of cases is this formally proven. It is often reasonable to reassure a patient, ensure adequate fluid intake, and wait and see. In more severe cases, or where it is important to find the cause of the illness, stool cultures are instituted. The most common organisms found are Campylobacter (an organism of animal origin), salmonella (also often of animal origin), Cryptosporidiosis (animal origin), Giardia Lamblia (lives in drinking water). Shigella (dysentery) is less common, and usually human in origin. Cholera is rare in Western countries. It is more common in travelers and is usually related to contaminated water (its ultimate source is probably sea water). Escherichia coli is probably a very common cause of diarrhea, especially in travelers, but it can be difficult to detect using current technology. The types of E. coli vary from area to area and country to country. Viruses, particularly rotavirus, are common in children. (Viral diarrhea is probably over-diagnosed by non-doctors). The Norwalk virus is rare. Toxins and food poisoning can cause diarrhea. These include staphylococcal toxin (often milk products due to an infected wound in workers), and Bacillus cereus (eg rice in Chinese takeaways). Often "food poisoning" is really salmonella infection. Parasites and worms sometime cause diarrhea but often present with weight loss, irritability, rashes or anal itching. The most common is pinworm (mostly of nuisance value rather than a severe medical illness). Other worms, such as hookworm, ascaria, and tapeworm are more medically significant and may cause weight loss, anemia, general unwellness and allergy problems. Amoebic dysentery due to Entamoeba histolytica is an important cause of bloody diarrhea in travelers and also sometimes in western countries which requires appropriate and complete medical treatment.

Chronic diarrhea

Infective diarrhea

It is not uncommon for diarrhea to persist. Diarrhea due to some organisms may persist for years without significant long term illness. More commonly a diarrhea will slowly ameliorate but the patient becomes a carrier (harbors the infection without illness). This is often an indication for treatment, especially in food workers or institution workers. Parasites (worms and amoeba) should always be treated. Salmonella is the most common persistent bacterial organism in humans.

Malabsorption

These tend to be more severe medical illnesses. Malabsorption is the inability to absorb food, mostly in the small bowel but also due to the pancreas. Causes include celiac disease (intolerance to gluten, a wheat product), lactose intolerance (Intolerance to milk sugar, common in non-Europeans), fructose malabsorption, Pernicious anemia (impaired bowel function due to the inability to absorb vitamin B12), loss of pancreatic secretions (may be due to cystic fibrosis or pancreatitis), short bowel syndrome (surgically removed bowel), radiation fibrosis (usually following cancer treatment), other drugs such as chemotherapy, and of course, diarrhea-predominant irritable bowel syndrome.

Inflammatory bowel disease

There are of unknown origin but are likely to be abnormal immune responses to infection. There is some overlap but the two types are ulcerative colitis and Crohn's disease:
- Ulcerative colitis is marked by chronic bloody diarrhea and inflammation mostly affects the distal colon near the rectum.
- Crohn's disease typically affects fairly well demarcated segments of bowel in the colon and often affects the end of the small bowel.

Other important causes

- Ischaemic bowel disease. This usually affects older people and can be due to blocked arteries.
- Bowel cancer: Some (but NOT all) bowel cancers may have associated diarrhea. (Cancer of the large colon is most common)
- Hormone-secreting tumors: some hormones (e.g. serotonin) can cause diarrhea if excreted to excess (usually from a tumor).
- Bile salt diarrhea: excess bile salt entering the colon rather then being absorbed at the end of the small intestine can cause diarrhea, typically shortly after eating. Bile salt diarrhea is a possible side-effect of gallbladder removal. It is usually treated with cholestyramine, a bile acid sequestrant.

Treatment of diarrhea

#Keep hydrated. This is the most appropriate treatment in most cases of minor diarrhea. #Try eating more but smaller portions. Eat regularly. Don't eat or drink too quickly. #Intravenous fluids or a "drip": Sometimes, especially in children, dehydration can be life-theatening and intravenous fluid may be required. #Oral rehydration therapy: Taking a sugar/salt solution, which can be absorbed by the body. #Opioids and their analogs should not be used for infectious diarrhea as they are said to prolong the illness and may increase the risk of a carrier state. Opioids are the most effective antidiarrheals available. Their principal method of action is to inhibit peristalsis. Loperamide, also known as Imodium, is the most commonly used antidiarrheal. Loperamide is chemically related to the drug meperidine or Demerol, but does not cross the blood-brain barrier and does not appear to induce tolerance or dependence. Other opioids used to control diarrhea (in increasing order of strength) are: Lomotil (diphenoxylate with atropine); Lonox (difenoxin with atropine); codeine; opium tincture (laudanum); and morphine. The most potent opioids are generally reserved for chronic diarrhea (e.g., from complications of AIDS). #Antibiotics: antibiotics may be required if a bacterial cause is suspected and the patient is medically ill. They are sometimes also indicated for workers with carrier states in order to clear up an infection so that the person can resume work. Parasite-related diarrhea (e.g. giardiasis) require appropriate antibiotics. Antibiotics are not routinely used, as the cause is rarely bacterial and antibiotics may further upset intestinal flora and worsen rather than improve the diarrhea. Clostridium difficile-associated diarrhea and pseudomembranous colitis is often caused by antibiotic use. #Dietary manipulation: especially avoid wheat products with celiac disease. #Hygiene and isolation: Hygiene is important in limiting spread of the disease. #It is claimed that some fruit, such as bananas, mangoes, papaya and pineapple may have positive effects on this condition. Bananas have the merits of being easily obtainable, and they are unlikely to have any other significant unwanted side effects. Bananas are thought to be "binding," as is mucilage, which you can obtain in capsule form. Mucilage can also be used as cereal for babies, as it is easily digested. The high acid content of pineapple may make this food a bad choice for people suffering from chronic diarrhea.

External links

- [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11100619&dopt=Abstract Reducing deaths from diarrhoea through oral rehydration therapy.] 1: Bull. World Health Organ. 2000;78(10):1246-55.
- [http://rehydrate.org/diarrhoea/index.html Rehydration Project] Category:Gastroenterology Category:Symptoms ja:下痢 simple:Diarrhea

Electrical impulse

Electricity is a general term applied to phenomena involving a fundamental property of matter called an electric charge. This article will introduce and explain some of the basic principles of electricity.

Related concepts

being radiated as light as the air of Earth's atmosphere is shifted from gas to plasma and back. ]] In casual usage, the term electricity is applied to several related concepts that are better identified by more precise terms.
- Electric charge: a fundamental conserved property of some subatomic particles, which determines their electromagnetic interactions. Electrically charged matter is influenced by, and produces, electromagnetic fields.
- Electric field is an effect produced by an electric charge that exerts a force on charged objects in its vicinity.
- Electric potential the potential energy per unit charge associated with a static (time-invariant) electric field.
- Electric current: a movement or flow of electrically charged particles.
- Electrical energy: energy made available by the flow of electric charge through a conductor or from the forces between charged particles.
- Electric power: The rate at which electric energy is converted into another form, such as light, heat, or mechanical energy (or converted from another form into electric energy).

History

Ancient

According to Thales of Miletus, writing circa 600 BCE, a form of electricity was known to the Ancient Greeks who found that rubbing fur on various substances, such as amber, would cause a particular attraction between the two. The Greeks noted that the amber buttons could attract light objects such as hair and that if they rubbed the amber for long enough they could even get a spark to jump. The origin of the word "electricity" is from the Greek word ēlektron, a word the ancient Greeks used for both "amber" and "electrum," and derives from an old root, ēlek- = "shine." The same word was used for both amber and electrum, probably because of the pale yellow color of some varieties of electrum (see electrum). An object found in Iraq in 1938, dated to about 250 BCE and called the Baghdad Battery, resembles a galvanic cell and is believed by some to have been used for electroplating. Additionally, some egyptologists associate the ancient goddess Hathor with artificial light (see Hathor temple). But, remaining unproven are the conjectures that these and other similar ancient artifacts had electrical function and that their associated ancient technology contributed to the development of modern electrical knowledge.

Modern

In 1600 the English scientist William Gilbert returned to the subject in De Magnete, and coined the modern Latin word electricus from ηλεκτρον (elektron), the Greek word for "amber", which soon gave rise to the English words electric and electricity. He was followed in 1660 by Otto von Guericke, who is regarded as having invented an early electrostatic generator. Other European pioneers were Robert Boyle, who in 1675 stated that electric attraction and repulsion can act across a vacuum; Stephen Gray, who in 1729 classified materials as conductors and insulators; and C. F. Du Fay, who first identified the two types of electricity that would later be called positive and negative. The Leyden jar, a type of capacitor for electrical energy in large quantities, was invented at Leiden University by Pieter van Musschenbroek in 1745. William Watson, experimenting with the Leyden jar, discovered in 1747 that a discharge of static electricity was equivalent to an electric current. In June, 1752, Benjamin Franklin promoted his investigations of electricity and theories through the famous, though extremely dangerous, experiment of flying a kite during a thunderstorm. Following these experiments he invented a lightning rod and established the link between lightning and electricity. If Franklin did fly a kite in a storm, he did not do it the way it is often described (as it would have been dramatic but fatal). It was either Franklin (more frequently) or Ebenezer Kinnersley of Philadelphia (less frequently) who created the convention of positive and negative electricity. Franklin's observations aided later scientists such as Michael Faraday, Luigi Galvani, Alessandro Volta, André-Marie Ampère, and Georg Simon Ohm whose work provided the basis for modern electrical technology. The work of Faraday, Volta, Ampere, and Ohm is honored by society, in that fundamental units of electrical measurement are named after them. Volta worked with chemicals and discovered that chemical reactions could be used to create positively charged anodes and negatively charged cathodes. When a conductor was attached between these, the difference in the electrical potential (also known as voltage) drives a current between them through the conductor. The potential difference between two points is measured in units of volts in recognition of Volta's work. The invention of the electric telegraph showed that commercial and practical use could be made of electrical phenomena. By the end of the 19th century electrical engineering became a distinct profession, separate from the physicist or inventor. The late 19th and early 20th century produced such giants of electrical engineering as Nikola Tesla, inventor of the polyphase induction motor; Samuel Morse, inventor of the telegraph; Antonio Meucci, an inventor of the telephone; Thomas Edison inventor of the phonograph and a practical incandescent light bulb; George Westinghouse, inventor of the electric locomotive; Charles Steinmetz, theoretician of alternating current; Alexander Graham Bell, another inventor of the telephone and founder of a sucessful telephone business. The rapid advance of electrical technology in the latter 19th and early 20th centuries lead to commercial rivalry such as the so-called War of the Currents), between Edison's direct-current system or Westinghouse's alternating-current method. Often concurrent research in widely scattered locations lead to multiple claims to the invention of a device or system.

Electric charge

Electric charge is a property of certain subatomic particles (e.g., electrons and protons) which interacts with electromagnetic fields and causes attractive and repulsive forces between them. Electric charge gives rise to one of the four fundamental forces of nature, and is a conserved property of matter that can be quantified. In this sense, the phrase "quantity of electricity" is used interchangeably with the phrases "charge of electricity" and "quantity of charge." There are two types of charge: we call one kind of charge positive and the other negative. Through experimentation, we find that like-charged objects repel and opposite-charged objects attract one another. The magnitude of the force of attraction or repulsion is given by Coulomb's law.

Electric field

The concept of electric field was introduced by Michael Faraday. The electrical field force acts between two charges, in the same way that the gravitational field force acts between two masses. However, electric field is a little bit different. Gravitational force depends on mass, whereas electric force depends on the electric charge on both objects. A positive charge exerts away from the object and a negative charge pulls towards the object equally in all directions; thus it is symetric. The most common experience with electric charge in everyday life is that of static cling - when two particular types of materials are rubbed together, they tend to stick together, at least for a while.

Electric potential

The electric potential difference between two points is defined as the work done per unit charge (against electrical forces) in moving a positive point charge slowly between two points. If one of the points is taken to be a reference point with zero potential, then the electric potential at any point can be defined in terms of the work done per unit charge in moving a positive point charge from that reference point to the point at which the potential is to be determined. For isolated charges, the reference point is usually taken to be infinity. The potential is measured in volts. (1 volt = 1 joule/coulomb) The electric potential is analogous to temperature: there is a different temperature at every point in space, and the temperature gradients indicates the direction of heat flows. Similarly, there is an electric potential at every point in space, and its gradient in the the electric field indicates where charges move.

Electric current

The electric charge which occurs naturally within conductors can be forced to flow, while the charges within insulators are locked in place and cannot be moved. Devices that use charge flow principles in materials are called electronic devices. A flow of electric charge is called an electric current. A direct current (DC) is a unidirectional flow; alternating current (AC) is a flow whose time average is zero, but whose energy capability (RMS level) is not zero. With AC the electric current repeatedly changes direction. Electric current is measured in Amperes Ohm's Law is an important relationship describing the behaviour of electric currents: See also: electrical conduction For historical reasons, electric current is said to flow from the most positive part of a circuit to the most negative part. The electric current thus defined is called conventional current. It is now known that, depending on the conditions, an electric current can consist of a flow of charged particles in either direction, or even in both directions at once. The positive-to-negative convention is widely used to simplify this situation. If another definition is used - for example, "electron current" - it should be explicitly stated.

Electrical energy

Electrical energy, is the flow of electrons or ions. When electrons are flowing through a wire or through hundreds of feet of air in the case of lightning it is because they are being forced to do so by an electrical field. A force is exerted on the electrons and they move. Work is done on the charged particles. A force is pushing them through a distance. More properly, they are moving from outer orbitals of one atom to another, being pushed by the electromotive force. While the electrons are in motion they contain kinetic energy. Consquently, atomic level electricity is a form of kinetic energy.

Electric power

Electric power is the capacity of the circuit for performing work in a particular amount of time. When a charge moves in a conductor, work is done by that charge. Devices can be made which convert this work into heat (Electric arc furnaces), light (light bulbs and Fluorescent lamps), or motion, i.e. kinetic energy (electric motors). The unit for all forms of power is the watt (symbol: W). In practice, however, this is generally reserved for the real power component. Apparent power is conventionally expressed in volt-amperes (VA) since it is the simple multiple of rms voltage and current. The unit for reactive power is given the special name "VAR", which stands for volt-amperes-reactive.

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