Natural Health Remedies

The prototypic lesion of infective endo carditis, the vegetation is a mass of platelets, fibrin, micro colonies of microorganisms, and scant inflammatory cells.

Infection most commonly involves heart valves (either native or prosthetic) but may also occur on the low-pressure side of the ventricular septum at the site of a defect, on the mural endocardium where it is damaged by aberrant jets of blood or foreign bodies, or on intracardiac devices themselves.

The analogous process involving arteriovenous shunts, arterioarterial shunts (patent ductus arteriosus), or a coarctation of the aorta is called infective endarteritis.

CLASSIFICATION:

Endocarditis may be classified according to the temporal evolution of disease, the site of infection, the cause of infection, or a predisposing risk factor such as injection drug use.

EPIDEMIOLOGY:

While rates of congenital heart diseases remain constant, other predisposing conditions in developed countries have shifted from chronic rheumatic heart disease to illicit IV drug use, degenerative valve disease, intracardiac devices, and health care–associated infection. The incidence of endocarditis is notably increased among the elderly.

Etiology

Although many species of bacteria and fungi cause sporadic episodes of endocarditis, only a few bacterial species cause the majority of cases.

The pathogens vary somewhat with the clinical types of endocarditis, in part because of different portals of entry.

The oral cavity, skin, and upper respiratory tract are the respective primary portals for the viridans streptococci, staphylococci, and Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella causing community-acquired native valve endocarditis.

Streptococcus bovis originates from the gastrointestinal tract, where it is associated with polyps and colonic tumors, and enterococci enter the bloodstream from the genitourinary tract.

Prosthetic valve endocarditis arising within 2 months of valve surgery is generally the result of intraoperative contamination of the prosthesis or a bacteremic postoperative complication.

The nosocomial nature of these infections is reflected in their primary microbial causes: coagulase-negative staphylococci ,S. aureus, facultative gram-negative bacilli, diphtheroids, and fungi.

Transvenous pacemaker lead– and/or implanted defibrillator–associated endocarditis is usually nosocomial.

Endocarditis occurring among injection drug users, especially when infection involves the tricuspid valve, is commonly caused by S. aureus strains.

Number of these cases are caused by Pseudomonas aeruginosa and Candida species, and sporadic cases are due to unusual organisms such as Bacillus, Lactobacillus, and Corynebacterium species.

Tropheryma whipplei causes an indolent, culture-negative, afebrile form of endocarditis.

Pathogenesis

Organisms that cause endocarditis generally enter the bloodstream from mucosal surfaces, the skin, or sites of focal infection. Except for more virulent bacteria e.g., S. aureus that can adhere directly to intact endothelium or exposed subendothelial tissue, microorganisms in the blood adhere to sites at NBTE. If resistant to the bactericidal activity of serum and the microbicidal peptides released locally by platelets, the organisms proliferate and induce a procoagulant state at the site by eliciting tissue factor from adherent monocytes or, in the case of S. aureus, from monocytes and from intact endothelium. Fibrin deposition combines with platelet aggregation, stimulated by tissue factor and independently by proliferating microorganisms, to generate an infected vegetation.

The pathophysiologic consequences and clinical manifestations of endocarditis—other than constitutional symptoms, which probably result from cytokine production—arise from damage to intracardiac structures; embolization of vegetation fragments, leading to infection or infarction of remote tissues; hematogenous infection of sites during bacteremia.

Clinical Manifestations

The clinical syndrome of infective endocarditis is highly variable and spans a continuum between acute and subacute presentations. Native valve endocarditis (whether acquired in the community or in association with health care), prosthetic valve endocarditis, and endocarditis due to injection drug use share clinical and laboratory manifestations.

1. Fever

2. Chills and sweats

3. Anorexia, weight loss, malaise

4. Myalgias, arthralgias

5. Heart murmur

6. New/worsened regurgitant murmur

7. Splenomegaly

8. Clubbing

9. Peripheral manifestations (Osler’s nodes, subungual hemorrhages, Janeway lesions, Roth’s spots)

LABORATORY FINDINGS:

• Anemia

• Leukocytosis

• Microscopic hematuria

• Elevated erythrocyte sedimentation rate

• Elevated C-reactive protein level

• Rheumatoid factor

HOMOEOPATHIC APPROACH:

DIGITALIS

It suits to slow pulse but primarily strong

There is great weakness of cardiac tissue and secondarily pulse becomes weak

Extra exertion increases its rapidity but diminishes its force

This makes the pulse irregular and intermittent

Heart feels as if stood still

There is weakness and numbness of the left arm and often blueness of the surface of the body

The patient fears that heart would stop beating if he does not make a move

CACTUS GRANDIFLORUS:

The characteristic symptom in this remedy is sensation as if heart is grasped with an iron band.

There is soreness and constriction of the chest and it has pains shooting to the left arm.

There is edema and quick throbbing intense and hard pulse which may be intermittent.

There is great irritation of cardiac nerves.

Useful in intense palpitations and fluterring of heart.

Difficult breathing, suffocation, fainting, violent palpitations and inability to lie down are the symptoms.

SPIGELIA:

It is the remedy for painful affections of the heart.

There are sharp shooting pains from the heart to the back and radiating from the heart down the arm ,over the chest and down the spine.

There is palpitation worse from any movement of the arm or body.

There is a purring sensation left in the cardiac region.

The pulse is intermittent and the slightest motion of the arm and hands makes the patient worse.

Irregular and tumultuous action of the heart is also met in this remedy.

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Bleeding from the gastrointestinal (GI) tract may present in five ways. Hematemesis is vomitus of red blood or “coffee-grounds” material.

Melena is black, tarry, foul-smelling stool.

Hematochezia is the passage of bright red or maroon blood from the rectum.

Occult GI bleeding (GIB) may be identified in the absence of overt bleeding by a fecal occult blood test or the presence of iron deficiency.

Finally, patients may present only with symptoms of blood loss or anemia such as lightheadedness, syncope, angina, or dyspnea.

CAUSES OF BLEEDING:

Peptic ulcers are the most common cause of UGIB, accounting for up to 50% of cases; an increasing proportion is due to nonsteroidal anti-inflammatory drugs (NSAIDs), with the prevalence of Helicobacter pylori decreasing.

Mallory-Weiss tears account for 5–10 or 15% of cases. The proportion of patients bleeding from varices varies widely from 5 to 30%, depending on the population. Helicobacter pylori has a clear etiologic role in peptic ulcer disease, but ulcers cause a minority of cases of dyspepsia. Infection with H. pylori is considered to be a minor factor in the genesis of functional dyspepsia.

Hemorrhagic or erosive gastropathy (e.g., due to NSAIDs or alcohol) and erosive esophagitis often cause mild UGIB, but major bleeding is rare.

Esophageal Varices

Patients with variceal hemorrhage have poorer outcomes than patients with other sources of UGIB.

Endoscopic therapy for acute bleeding and repeated sessions of endoscopic therapy to eradicate esophageal varices significantly reduce rebleeding and mortality.

Other Causes

Other, less frequent causes of UGIB include erosive duodenitis, neoplasms, aortoenteric fistulas, vascular lesions [including hereditary hemorrhagic telangiectasias (Osler-Weber-Rendu) and gastric antral vascular ectasia ("watermelon stomach")], Dieulafoy’s lesion (in which an aberrant vessel in the mucosa bleeds from a pinpoint mucosal defect), prolapse gastropathy (prolapse of proximal stomach into esophagus with retching, especially in alcoholics), and hemobilia and hemosuccus pancreaticus (bleeding from the bile duct or pancreatic duct).Acid reflux can result from a variety of physiologic defects. Reduced lower esophageal sphincter (LES) tone is an important cause of reflux in scleroderma and pregnancy.

Many individuals exhibit frequent transient LES relaxations during which acid bathes the esophagus. Overeating and aerophagia can transiently override the barrier function of the LES, whereas impaired esophageal body motility and reduced salivary secretion prolong acid exposure.

Differentiation of Upper from Lower GIB

Hematemesis indicates an upper GI source of bleeding (above the ligament of Treitz). Melena indicates that blood has been present in the GI tract for at least 14 h. Thus, the more proximal the bleeding site, the more likely melena will occur. Hematochezia usually represents a lower GI source of bleeding, although an upper GI lesion may bleed so briskly that blood does not remain in the bowel long enough for melena to develop.

HOMOEOPATHIC APPROACH:

CARBO VEG:

It has continuous passive hemorrhages

The skin is cold and bluish ,pulse is rapid and weak

The patient wants to be fanned ,burning pains across scarum and lower spine

ARSENICUM:

Persistent hemorrhages of low types

Burning pains and irrtitability

CINCHONA:

The blood is dark and clotted and the flow is profuse from mouth.

The bleeding causes fainting and ringing in the ears.

The characteristic symptom is the patient wants to be fanned.

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Jaundice, or icterus, is a yellowish discoloration of tissue resulting from the deposition of bilirubin.

Tissue deposition of bilirubin occurs only in the presence of serum hyperbilirubinemia and is a sign of either liver disease or, less often, a hemolytic disorder.

The degree of serum bilirubin elevation can be estimated by physical examination. Slight increases in serum bilirubin are best detected by examining the sclerae, which have a particular affinity for bilirubin due to their high elastin content.

CLINICAL FEATURES:

As serum bilirubin levels rise, the skin will eventually become yellow in light-skinned patients and even green if the process is long-standing; the green color is produced by oxidation of bilirubin to biliverdin.

Another sensitive indicator of increased serum bilirubin is darkening of the urine, which is due to the renal excretion of conjugated bilirubin. Patients often describe their urine as tea or cola colored. Bilirubinuria indicates an elevation of the direct serum bilirubin fraction and therefore the presence of liver disease.

Increased serum bilirubin levels occur when an imbalance exists between bilirubin production and clearance. A logical evaluation of the patient who is jaundiced requires an understanding of bilirubin production and metabolism.

TYPES:

Unconjugated Hyperbilirubinemia

The critical determination is whether the patient is suffering from a hemolytic process resulting in an overproduction of bilirubin (hemolytic disorders and ineffective erythropoiesis) or from impaired hepatic uptake/conjugation of bilirubin (drug effect or genetic disorders).

Hemolytic disorders that cause excessive heme production may be either inherited or acquired. Inherited disorders include spherocytosis, sickle cell anemia, thalassemia, and deficiency of red cell enzymes.

Conjugated Hyperbilirubinemia

Elevated conjugated hyperbilirubinemia is found in two rare inherited conditions: Dubin-Johnson syndrome and Rotor’s syndrome.

Hepatocellular Conditions

Hepatocellular diseases that can cause jaundice include viral hepatitis, drug or environmental toxicity, alcohol, and end-stage cirrhosis from any cause.

Wilson’s disease, once believed to occur primarily in young adults, should be considered in all adults if no other cause of jaundice is found.

Autoimmune hepatitis is typically seen in young to middle-aged women but may affect men and women of any age.

Alcoholic hepatitis can be differentiated from viral and toxin-related hepatitis by the pattern of the aminotransferases.

Laboratory Tests

These include total and direct serum bilirubin with fractionation,

Aminotransferases

alkaline phosphatase

albumin

prothrombin time tests.

HOMOEOPATHIC APPROACH:

BRYONIA:

Stiching pains in the right hypochondriac region

Liver is swollen and congested and inflamed

Pains in the hypochondriac region are worse from any motion and better by lying on the right side

The patient is chilly and there is bitter taste in the mouth and the stools are hard and dry

MERCURIUS:

Much sensitiveness and dull pain in the region of the liver

Patient cannot lie on the right side

The liver is enlarged and the skin and conjunctiva are jaundiced

Stools are clay colored or yellowish green bilious stools with great deal of tenesmus

PODOPHYLLUM:

Indicated in torpid or chronically congested liver and when diarrhea is present.

The liver is swollen and sensitive, the face and eyes are yellow and there is bad taste in the mouth.

The tongue is coated white or yellow.

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Many people have experienced a yeast infection and almost every women will suffer at least one in their lifetime. Most of these infections are temporary and will heal without any treatment in a week or two. Some people may have to deal with a recurring yeast infection. However, for some, the infection is so frequent that it has become a chronic yeast infection.

Why, for some people, did the yeast infection become chronic? Why is it that nothing seems to be able to get rid of the problem? For many of us with chronic yeast infections, there seem to be no hope and have given up on doing something about it. No amount of medications they have used seem to be of any help at all. The infection has become too strong for the medications.

To understand the problem, we need to know why we get these infections in the first place.

Yeast, a fungus, is always present all around us. They also exist on the skin and in the body too. However, they are normally harmless and will not cause any problems. This is because their population is kept in check by other good bacteria that are co-existing with this fungus in the body.

However, when certain conditions in the environment arise which cause a reduction in the population of the good bacteria, this fungus will be able to grow rather rapidly without much hindrance, resulting eventually in an over-growth which causes a problem. This may be due to taking too much antibiotics or other factors.

What do you think is the first thing some people will do when they get a yeast infection? Yes, they visited the local drugstore and purchased some pharmaceutical products that claim to cure the problem. Big mistake!

What actually happens is that these products take care of the symptoms without addressing the real problem. They do a good job in killing some of the yeast and reduced their population. However, what remains behind are the stronger ones that managed to survive the medication.

Being convinced that these products work, they will use them again in future when they have another occurrence. With each successive use, the accumulation of the stronger yeast on the body grows. Each recurring yeast infection becomes stronger and stronger until it becomes a super yeast infection. When this stage is reached, we are having a chronic yeast infection.

When the yeast infection is chronic, the numerous pharmaceutical products we see in a drug store will no longer be effective. Nothing seem to work anymore as most of the yeast fungus on the body can withstand the medication.

When having chronic yeast infections, you may want to consider using natural remedies to get rid of the problem. These natural remedies will be able to help increase the growth of the good bacteria that will in turn help keep the population of the fungus in check, maintaining a balance. After a while, you will find your chronic yeast infection subsiding until it disappear altogether.

Discover more about natural cures for yeast infections from Sarah’s blog: http://www.yeastinfectionsnaturalcures.com