What is Chronic Bronchitis

Chronic Bronchitis

Chronic Bronchotis is a condition defined clinically as persistent cough with expectoration on most days for at least three monthsof the year for 2 or more consecutive years.The cough is caused by oversecretion of the mucus .Inspite of its name, chronic inflammation of the bronchi is not a prominent feature.

What is Chronic obstructive pulmonary Disease (COPD)

 Chronic obstructive pulmonary Disease

It is Respiratory disrder in which there is chronic, partial or complete obstuction to the airflow at any level from trachea to the smallest airways resulting in functional disability of the lungs.It consists of following 4 entities.

1)Chronic Bronchitis

2)Emphysema

3)Bronchial Asthma

4)Bronchiectasis

Symptoms of tuberculosis

symptoms of tubercuosis include persistent long time cough containing blood mixed sputum,sleeplessness,fever, and chest pain ,loss of apetite, weight loss etc.,

Cause of Ulcer

Cause of Ulcer :

1) Stress  :

Stress can arise from prolonged anxiety, tension and emotion, sever physical discomfort, haemorrhagic and surgical shocks, burns and trauma, thereby resulting in sever gastric ulceration.

Ulcers due to stress condition arising mainly from physiological discomfort and the mechanism of ulceration caused in this case may be different from ulcer caused due to other factors. 

However, mechanism of gastric ulceration is poorly understood.  Recent researches have shown that restraint cold stress causes severe haemorrhoagic ulcer through derangement of the mucosal antioxidant enzymes such as superoxide, dismutase and peroxides.  The stress generate highly reactive OH^– radicals that causes oxidative damage of the gastric mucosa and that the radical is formed by metalcatalysed.  Harber weiss reaction between O₂^– and H₂O₂ following induction of the superoxide dismutase and oxidative damage of gastric peroxidase.

2) Alcohol  :

Alcohol causes secretion of gastric juice and decrease mucosal resistance. Due to of which protein content of gastric juice is significantly increased by ethanol.This could be leakage of plasma proteins in to the gastric juice with weakening of mucosal resistance barrier of gastric mucosa.This lead to peptic ulcer.

3) H. Pylori  :

It is a gram negative bacteria found in gastric and duodenal mucosa of most persons particularly the elderly.  They, while in the mucosa, split urea into ammonia and thus elevates the local pH, damage of local region of the mucosa by high alkalinity.  In this way they strongly help the peptic ulcer development.

Cause of chronic peptic ulcer

Aetiology     or Cause of chronic peptic ulcer:-

1)      Heredity : patients with peptic ulcer often have a family history of the disease.  This is particularly the case with duodenal ulcers, which develop below the age of 20 years.  The relatives of gastric ulcer patients have 3 times the expected number of gastric ulcer but duodenal ulcer occur with the same frequency amongst relatives as in the general population.

2)      Acid-pepsin Vs. Mucosal resistance :- The immediate cause of peptic ulceration is digestion of the mucosa by acid and pepsin of the gastric juice, but the sequence of events leading to this is unknown. Digestion by acid and pepsin can’t be the only factor involved, since the normal stomach in obviously capable of resisting digestion by its own secretion.

The concept of ulcer aetiology may be written as “acid plus pepsin Vs. mucosal resistance”.

3)      Gastric hyper secretion :- Ulcer occur only in the presence of acid and pepsin they are never found in achlorhydric patients such as those with pernicious anaemia.  Acid secretion is more important in the aetiology of duodenal than gastric ulcer.

Peptic ulcer is the most common gastrointestional disorder in clinical practice. However, several classes of agents like H₂ blockers, proton pump inhibitor are being used as effective line of treatment of peptic ulcer. The several side effects associated with the present line of treatment, like Arrythemias, impotence, gynacomastia and hematopoetic changes, of synthetic drugs, etc., limits the usage of there agents for a chronic period is restricted. Comparatively indigenous drugs are possessing fewer side effects. Hence, the search for better alternatives for synthetic drugs is on rise.

Symptoms of peptic ulcer

1 Symptoms:.

Symptoms of a peptic ulcer are

·         Abdominal pain, classically epigastric with severity relating to mealtimes, after around 3 hours of taking a meal.

·         Bloating.

·         Water brash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus)

·         Nausea and copious vomiting.

·         Loss of appetite and weight.

·         Hematemesis (vomiting of blood); this can occur due to bleeding directly from a gastric ulcers or from damage to the esophagus from severe/continuing vomiting.

·         Melena (tarry, foul-smelling feaces due to oxidized iron from hemoglobin).

·         Rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute peritonitis. This is extremely painful and requires immediate surgery.

Prevalence of peptic ulcer

Prevalence of peptic ulcer

Peptic ulcer in India

Peptic ulcer prevalence in India is quite high.  Several field studies from different parts of our country suggest its occurrence in 4 to 10 per thousand population. The areas of high incidence are in the south, up the west coast as far as Bombay all the way up the east coast and inland into Andhra Pradesh, West Bengal, Meghalaya and into plains of assam and Kashmir. The areas of low incidence lie in the north, the Punjab and the adjacent areas of Rajasthan, Haryana, Uttar Pradesh, and Himachal Pradesh.

Peptic Ulcer Disease

Peptic ulcer  :

It is a chronic inflammatory condition involving a group of disorders characterised by ulceration in regions of upper gastrointestinal tract where parietal cells secrete pepsin and hydrochloric acid.

Ulcer is defined as the erosion in the lining of the stomach or duodenum and is caused by the disruptions of the gastric mucosal defense and repair systems. Ulcer in the stomach is called gastric ulcer and in the duodenum is called duodenal ulcer and together peptic ulcer. In clinical practice, peptic ulcer is one of the most prevalent gastrointestinal disorders, commonly occurs in developed countries.Peptic ulcer, also known as PUD or peptic ulcer disease is a break in the lining (mucosa) of the digestive tract produced by digestion of the mucosa by pepsin and acid.

An estimated 15,000 deaths occur each year as a consequence of PUD. In India PUD is common. In Indian pharmaceutical industry, researchers reported that peptic ulcers were been caused by an imbalance between the aggressive factors and a number of known defense mechanisms. Exogenous aggressive factors such as smoke, anti-inflammatory drugs, alcohol, stress, fatty foods and Helicobacter pylori infections triggered tissue necrosis through mucosal ischemia, free radical generation and cessation of nutrient delivery, hydrochloric acid together with pepsin, pancreatic enzymes and bile decreased the defense mechanisms of gastrointestinal mucosa such as the intercellular junctions, local blood flow, mucus/bicarbonate secretion and cellular. Antacids, and antiulcer drugs share 6.2 billion rupees and occupy 4.3% of the market share.

 

Causes of atherosclerosis

Some researchers believe that atherosclerosis may be caused by an
 Infection of the vascular smooth muscle cells; chickens, for example, develop atherosclerosis when infected with the Marek's disease herpesvirus. Herpesvirus infection of arterial smooth muscle cells has been shown to cause cholesteryl ester (CE) accumulation. Cholesteryl ester accumulation is associated with atherosclerosis.

Also, cytomegalovirus (CMV) infection is associated with cardiovascular diseases.
Linus Pauling's and Matthias Rath's extended theory states that deaths from scurvy in humans during the ice age, when vitamin C (an antioxidant) was scarce, selected for individuals who could repair arteries with a layer of cholesterol provided by lipoprotein(a), a lipoprotein found in vitamin C-deficient species (higher primates and guinea pigs). Pauling and Rath theorised that, although eventually harmful, lipoprotein deposition on artery walls was beneficial to the human species and a "surrogate for ascorbate" in that it kept individuals alive until access to vitamin C allowed arterial damage to be repaired. Atherosclerosis is thus a vitamin-C-deficiency disease.

Diagnosis of atherosclerosis

Over the last couple of decades, methods other than angiography and stress-testing have been increasingly developed as ways to better detect atherosclerotic disease before it becomes symptomatic. These have included both (a) anatomic detection methods and (b) physiologic measurement methods.
Examples of anatomic methods include: (1) coronary calcium scoring by CT, (2) carotid IMT (intimal media thickness) measurement by ultrasound, and (3) intravascular ultrasound (IVUS).
Examples of physiologic methods include: (1) lipoprotein subclass analysis, (2) HbA1c, (3) hs-CRP, and (4) homocysteine.

The example of the metabolic syndrome combines both anatomic (abdominal girth) and physiologic (blood pressure, elevated blood glucose) methods.
Advantages of these two approaches: The anatomic methods directly measure some aspect of the actual atherosclerotic disease process itself, thus offer potential for earlier detection, including before symptoms start, disease staging and tracking of disease progression. The physiologic methods are often less expensive and safer and changing them for the better may slow disease progression, in some cases with marked improvement.

Disadvantages of these two approaches: The anatomic methods are generally more expensive and several are invasive, such as IVUS. The physiologic methods do not quantify the current state of the disease or directly track progression. For both, clinicians and third party payers have been slow to accept the usefulness of these newer approaches.

Diagnosis of Atherosclerosis

Diagnosis

Microphotography of arterial wall with calcified (violet colour) atherosclerotic plaque (haematoxillin & eosin stain)

Areas of severe narrowing, stenosis, detectable by angiography, and to a lesser extent "stress testing" have long been the focus of human diagnostic techniques for cardiovascular disease, in general. However, these methods focus on detecting only severe narrowing, not the underlying atherosclerosis disease. As demonstrated by human clinical studies, most severe events occur in locations with heavy plaque, yet little or no lumen narrowing present before debilitating events suddenly occur. Plaque rupture can lead to artery lumen occlusion within seconds to minutes, and potential permanent debility and sometimes sudden death.
Plaques that have ruptured are called complicated plaques.

 The extracellular matrix of the lesion breaks, usually at the shoulder of the fibrous cap that separates the lesion from the arterial lumen, exposing thrombogenic material, mainly collagen, and eventually causing thrombus formation. This thrombus will eventually grow and travel downstream until eventually occluding a narrow artery. Once the area is blocked, blood and oxygen will not be able to supply the vessels and will cause death of cells and lead to necrosis and poisoning. Serious complicated plaques can cause death of organ tissues, causing serious complications to that organ system.

Greater than 75% lumen stenosis used to be considered by cardiologists as the hallmark of clinically significant disease because it is typically only at this severity of narrowing of the larger heart arteries that recurring episodes of angina and detectable abnormalities by stress testing methods are seen. However, clinical trials have shown that only about 14% of clinically debilitating events occur at locations with this, or greater severity of stenosis. The majority of events occur due to atheroma plaque rupture at areas without narrowing sufficient enough to produce any angina or stress test abnormalities. Thus, since the later-1990s, greater attention is being focused on the "vulnerable plaque.
Though any artery in the body can be involved, usually only severe narrowing or obstruction of some arteries, those that supply more critically important organs are recognized. Obstruction of arteries supplying the heart muscle result in a heart attack. Obstruction of arteries supplying the brain result in a stroke. These events are life-changing, and often result in irreversible loss of function because lost heart muscle and brain cells do not grow back to any significant extent, typically less than 2%.