HEPATITIS C

Hepatitis C



Hepatitis C virus (HCV) affects 170 mil-lion people worldwide. Around 1.8 per-cent of the U.S. population is positive for HCV antibodies.

For some time, blood transfusion was the primary cause of HCV infection in developed countries. With the introduction of blood-screening measures in the early 1990s, transmission by blood transfusion has decreased considerably. However, new cases continue to emerge, primarily as a result of intravenous drug use and percutaneous or mucous membrane exposure. Nosocomial infection is also a cause of HCV as the rate of transmission is estimated to be 3 percent in needle-stick injuries.



HCV belongs to the family of flavivi-ruses. The structural components include the core and two envelope proteins. One of the envelope proteins, E2, contains the binding site for CD81, which is present on hepatocytes and B lymphocytes and is thought to function as a cellular recep-tor for the virus. The regulatory proteins include helicase, protease, and polymerase. HCV replicates by means of an RNA-dependent RNA polymerase that lacks a “proofreading” function. This process can result in the evolution of genomic varia-tions of the virus within an individual, making immune-mediated control of HCV difficult. In addition, six distinct genotypes and around 100 subtypes of HCV have been identified. Genotypes 1a and 1b are the most prevalent in the United States and western Europe, followed by genotypes 2 and 3. Genotype helps to predict effective-ness of antiviral therapy, with genotypes 2 and 3 demonstrating the best responses.

Study of acute HCV infection has been limited because these individuals are often asymptomatic. It is currently thought that the pathology, which results from HCV infection, is the result of both direct cytopathic effects of the virus and the immune response. The immune response to HCV, as with HBV, is still incompletely understood.



Due to the strict affinity of HCV for human cells, in the past only humans and higher primates such as monkeys could be infected with HCV. However, rodents make for a more appropriate and useful biological model in that their gestational periods are short, they are small, and cost less to maintain. Some models, which are currently being developed, include an immunotolerized rat and a Trimera mouse model. In the immunotolerized rat model, human hepatoma cells (Huh7) are introduced to fetal rats in utero and transplanted with the same cell line after birth. The rat is subsequently infected with HCV using HCV-positive human serum. In the Trimera model, mice are irradi-ated and reconstituted using SCID mouse bone marrow. HCV-infected liver fragments from patients with HCV or ex vivo infected HCV liver fragments are trans-planted into the ear pinna or under the kidney capsule. More research is needed, but these particular models could be help-ful in studying the effects of therapeutic regimens against HCV. In addition, several trans genic mouse models have been stud-ied that have allowed for the analysis of the direct cytopathic effects of HCV protein and its correlation with the pathogenesis of chronic hepatitis C.





In the rare instances in which clinical acute hepatitis has been identified, symp-toms have included jaundice, malaise, and nausea. Although infection becomes chronic in about 75–80 percent of affected individuals, it is often characterized by a prolonged asymptomatic period of any-where from twenty to thirty years. Patients may present with nonspecific symptoms of fatigue (90 percent). Severe complications

and death tend to occur primarily in individuals who progress to cirrhosis, which is around 15–20 percent of infected patients. Extra hepatic manifestations of HCV tend to be associated with autoimmune and lympho proliferative states. These

DIGESTION

Digestion is the process whereby food is broken down into smaller parts,chemically changed, and moved through the gastrointestinal system. The gas-trointestinal (GI) tract consists of the body structures that participate indigestion. Digestion begins in the mouth and ends at the anus. Along the entire GI tract secretions of mucus lubricate and protect the mucosal tissues.

Digestion occurs through two types of action—mechanical and chemical.
 During mechanical digestion,food is broken into smaller pieces by the teeth. It is then moved along the gastrointestinal tract through the esophagus, stomach, and intestines. This movement is caused by a rhythmic contraction of the muscular walls of the tract called peristalsis. Mechanical digestion helps to prepare food for chemical digestion by breaking it into smaller pieces.

During chemical digestion, the composition of carbohydrates, pro-teins, and fats is changed. Chemical changes occur through the addition of water and the resulting splitting, or breaking down, of the food molecules. This process is calledhydrolysis. Food is broken down into nutrients that the tissues can absorb and use. Hydrolysis also involves digestive enzymes that act on food substances, causing them to break down into simple compounds.

Digestion in the Mouth

Digestion begins in the mouth, where the food is broken into smaller pieces by the teeth and mixed with saliva. At this point, each mouthful of food that is ready to be swallowed is called a bolus. Saliva is a secretion of the salivary glands that contains water, salts, and a digestive enzyme called salivary amylase (also called ptyalin), which acts on complex carbohydrates (starch).

The Esophagus

The esophagus is a 10-inch muscular tube through which food travels from the mouth to the stomach. When swallowed, the bolus of food is moved down the esophagus by peristalsis and gravity. At the lower end of the esophagus, the cardiac sphincter opens to allow passage of the bolus into the stomach. The cardiac sphincter prevents the acidic content of the stomach from flowing back into the esophagus.

Digestion in the Stomach

The stomach consists of an upper portion known as the fundus, a middle area known as the body of the stomach, and the end nearest the small intestine called the pylorus.Food enters the fundus and moves to the body of the stomach, where the muscles in the stomach wall gradually knead the food, tear it, and mix it with gastric juices, and with the intrinsic factor necessary for the absorption of vitamin B12, before it can be propelled forward in slow, controlled movements.

Digestion in small intestine

When food reaches the small intestine, the hormone secretin causes the pancreas to release sodium bicarbonate to neutralize the acidity of the chyme. The gallbladder is triggered by the hormone cholecystokinin (CCK), which is produced by intestinal mucosal glands when fat enters, to releasable. Bile is produced in the liver but stored in the gallbladder. Bile emulsifies fat after it is secreted into the small intestine. This action enables the enzymes to digest the fats more easily.
The Large Intestine

The large intestine, or colon,consists of the cecum, colon, and rectum. The cecum is a blind pouchlike beginning of the colon in the right lower quadrant of the abdomen. The appendix is a diverticulum that extends off the cecum. Thececum is separated from the ileum by the ileocecal valve and is considered to be the beginning of the large intestine (colon).


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OBESITY AND ITS TREATMENT (MOST COMMON DIESES)

Definition of obesity



Obesity has traditionally been defined as an excess accumulation of body energy, in the form of fat or adipose tissue. Thus, obesity is a disease of positive energy balance, which arises as a result of dysregulation in the energy balance system – a failure of the regulatory systems to make appropriate adjustments between intake and expenditure. It is now becoming clear that the increased health risks of obesity may be conferred by the distribution of body fat.

The body mass index (BMI) is now the most accepted and most widely used crude index of obesity. This index classifies weight relative to height squared.

The BMI is therefore calculated as weight in kilo-grams divided by height squared in meters, and expressed in the units of kg/m2. Obesity in adults is defined as a BMI above 30.0 kg/m2, while the normal range for BMI in adults is 18.5–24.9 kg/m2. A BMI in the range of 25–30 kg/m2 is considered overweight. In children, it is more difficult to classify obesity by BMI because height varies with age during growth; thus, age-adjusted BMI percentiles must be used.
The more sedentary lifestyle is due to an increased reliance on technology and labor-saving devices, which has reduced the need for physical activ-ity for everyday activities. Examples of energy-saving devices are:

●      increased use of automated transport rather than walking or cycling



●      central heating and the use of automated equipment in the household, e.g., washing machines



●      reduction in physical activity in the workplace due to computers, automated equipment, and elec-tronic mail, which all reduce the requirement for physical activity at work

●increased use of television and computers for entertainment and leisure activities


●use of elevators and escalators rather than using stairs


●increased fear of crime, which has reduced the likelihood of playing outdoors


●poor urban planning, which does not provide adequate cycle lanes or even pavements in some communities.

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What are the BACTERIA

 Bacteria are surrounding us even inside our body. As a representative of Bacteria, the structure and importance of Closteridium IS described here.


Structural features:

1.  It is rod shaped and unicellular.

2.  They live in the intestine of human being, other animal or even in soil. They are without photosynthetic pigments.



3.  They are prokaryotic, i.e. there is no nuclear membrane and nucleolus in their cell .



4.  There are flagella around the cell wall.



5.  They are anaerobic, Gram positive and Spore producing.

Importance of Bacteria :



Structure : Deadly diseases of human being, like - Phthisis (Tuberculosis),Pneumonia, Typhoid, Cholera Diphtheria, Dysentery, Tetanus, H60ping cough, Meningitis etc are caused by different Bacteria. Besides Bacteria is also responsible for various plant diseases.
Food putrification and food poisoning, water pollution and demannuring of soil etc. are also caused by Bacteria. Some antibiotics are prepared from Bacteria.
Vaccines of Cholera, Typhoid, and Phthisis etc are also prepared from Bacteria. Besides Bacteria also perform the important works like; decomposition of rubbish, blending of tea, coffee, tobacco, 'preparation of butter, curd, cheese from milk, extractivn of Jute fibre, extraction of hairs from skin in tannery, preparation of some B-Vitamins, proper management of sewerage lines, and nitrogen fixation etc.



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ENTEROGERMINA -A PROBIOTIC, MEDICINE FOR STOMACH PROBLEM

ENTEROGERMINA - IS AN ORAL SUSPENSION CONTAINING POLYANTIBIOTIC  RESISTENT SPORES OF BACILLUS CLAUSII.

COMPOSITION- IT is  1 mini bottle contains;

 Main element- 2 billions spores of polyantibiotic resistant  bacillus clausii.

what is enterogermina?
It is a probiotic which is useful for the treatment of imbalance of intestinal bacteria flora due to diverse causes.

USES-

IT is use for treating the alterations of the intestinal bacteria flora, enterogermina resore the equilibrium of the intestinal flora changed during diarrhoea, or contributing to correct the consequent dysvitaminosis (that is the imbalance of production and assimilation of the vitamins)

HOW TO USE?

ADULTS - FROM 2 TO 3 MINI BOTTLES A DAY

CHILDERN- FROM 1 TO 2 MINI BOTTLES A DAY

INFANTS- FROM 1 TO 2 BOTTLES A DAY

HOW TO USE - SHAKE THE MINI BOTTLE BEFORE USE

MECHANISM OF ACTION-  The administration of entero. contributes to the recovery of the intestinal  microbial flora altered during the course of intestinal microbial imbalance of diverse origin , due to the action of bacillus clausii 
Adminisstered orally, Bacillus clausii spores, due to their high resistance to the both chemical and physical agents, cross the barrier of the gastric juices reaching, unharmed, the intestianl tract where they are transformed  into metabolically active vegetative cells.

STORAGE- COOL PLACE

MANAGEMENT OF CHRONIC HEART FAILURE💔💔💔💔💔

MANAGEMENT OF CHRONIC HEART FAILURE

The major steps in the management of patients with chronic heart failure are outlined in Table 13–3. The 2009 update to the ACC/ AHA 2005 guidelines suggests that treatment of patients at high risk (stages A and B) should be focused on control of hyperten-sion, hyperlipidemia, and diabetes, if present. Once symptoms and signs of failure are present, stage C has been entered, and active treatment of failure must be initiated.




SODIUM REMOVAL
Sodium removal—by dietary salt restriction and a diuretic—is the mainstay in management of symptomatic heart failure, especially if edema is present. In very mild failure a thiazide diuretic may be tried, but a loop agent such as furosemide is usually required. Sodium loss causes secondary loss of potassium, which is particu-larly hazardous if the patient is to be given digitalis. Hypokalemia can be treated with potassium supplementation or through the addition of an ACE inhibitor or a potassium-sparing diuretic such as spironolactone. Spironolactone or eplerenone should probably be considered in all patients with moderate or severe heart failure, since both appear to reduce both morbidity and mortality.

ACE INHIBITORS & ANGIOTENSIN RECEPTOR BLOCKERS
In patients with left ventricular dysfunction but no edema, an ACE inhibitor should be the first drug used. Several large studies have showed clearly that ACE inhibitors are superior to both pla-cebo and to vasodilators and must be considered, along with

VASODILATORS
Vasodilator drugs can be divided into selective arteriolar dilators, venous dilators, and drugs with nonselective vasodilating effects. The choice of agent should be based on the patient’s signs and symptoms and hemodynamic measurements. Thus, in patients with high filling pressures in whom the principal symptom is dyspnea, venous dilators such as long-acting nitrates will be most helpful in reducing filling pressures and the symptoms of pulmo-nary congestion. In patients in whom fatigue due to low left ven-tricular output is a primary symptom, an arteriolar dilator such as hydralazine may be helpful in increasing forward cardiac output.In most patients with severe chronic failure that responds poorly to other therapy, the problem usually involves both elevated filling pressures and reduced cardiac output. In these circumstances, dila-tion of both arterioles and veins is required. In a trial in African-American patients already receiving ACE inhibitors, addition of hydralazine and isosorbide dinitrate reduced mortality. As a result, a fixed combination of these two agents has been made available as isosorbide dinitrate/hydralazine (BiDil), and this is currently approved for use only in African Americans.

BETA BLOCKERS & ION CHANNEL BLOCKERS
Trials of β-blocker therapy in patients with heart failure are based on the hypothesis that excessive tachycardia and adverse effects of high catecholamine levels on the heart contribute to the down-ward course of heart failure. The results clearly indicate that such therapy is beneficial if initiated cautiously at low doses, even though acutely blocking the supportive effects of catecholamines can worsen heart failure. Several months of therapy may be required before improvement is noted; this usually consists of a slight rise in ejection fraction, slower heart rate, and reduction in symptoms. As noted above, not all β blockers have proved useful, but bisoprolol, carvedilol, metoprolol, and nebivolol have been shown to reduce mortality.

In contrast, the calcium-blocking drugs appear to have no role in the treatment of patients with heart failure. Their depressant effects on the heart may worsen heart failure. On the other hand, slowing of heart rate with ivabradine (an If blocker) appears to be of benefit.

Digitalis
Digoxin is indicated in patients with heart failure and atrial fibril-lation. It is usually given only when diuretics and ACE inhibitors have failed to control symptoms.

THE BREAST ANATOMY

The Breast Anatomy

The female breasts


The female breasts, also known as the mammary glands, are accessory orgns of reproduction.



Situation One breast is situated on each side of the sternumand extends between the levels of the second and sixth rib. The breasts lie in the superficial fascia of the chest wall over the pectoralis major muscle, and are stabilized by suspensory ligaments.



Shape Each breast is a hemispherical swelling and has a tailof tissue extending towards the axilla (the axillary tail of spence).



Size The size varies with each individual and with the stage ofdevelopment as well as with age. It is not uncommon for one breast to be little or larger than the other.



Gross structure


The axillary tail is the breast tissue extending towards theaxilla.



The areoa is a circular area of loose, pigmented skin about2.5 cm in diameter the centre of each breast. It is a pale pink colour in a fair- skinned woman, darker in a brunett, the colour deepening with pregnancy. Within the area of the areola lie approximately 20 sebaceous glands. In pregnancy these enlarge and are known as montgeomery’s tubercles.



The nipple lies in the centre of the areola at the level of thefourth rib. Aprotuberance about 6mm in length, composed of pigmented erectile tissue.The surface of the nipple is perforarted by small orifices which are the openings of the lactiferous ducts. It is covered with epithelium.



Microscopic structure The breast is composed largely ofglandular tissue, but also of some fatty tissue, and is covered with skin. This glandular tissue is divided into about 18 lobes which are completely separated by bands of fibrous tissue. The internal structure is said to be resemble as the segments of a halved grape fruit or orgnge. Each lobe is a self-contained working unit and is composed of the following structures



Alveoli: Containing the milk- secreting cells. Each alveolus islined by millk-secreting cells, the acini, which extract from the mammary blood supply the factors essential for milk formation. Around each alveolus lie myoepithelial cells, sometimes called ‘basket’ or ‘spider’s cells. When these cells are stimulated by oxytocin they contract releasing milk into the lactifierous duct.



Lactifierous tubules:small ducts which connect the alveoli.



Lactifierous duct:a central duct into which the tubules run.



Amplulla:the widened-out portion of the duct where milk isstored. The ampullae lie under the areola.



Blood supply Blood is supplied to the breast by the internalmammary, the external mammary and the upper intercostals arteries.Venous drainage is through corresponding vessles into the internal mammary and axillary veins.





Lymphatic drainage This is largely into the axillary glands, with some dranage in to the portal fissure of the liver and mediastinal glands. The lymphatic vessels of each breast communicate with one another.



Nerve supply The function of the breast is largely controlledby hormone activity but the skin is supplied by breanches of the thoracic nerves. There is also some sympathetic nerve supply, especially around the areola and nipple.