Pathophysiology of COPD

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COPD, or chronic obstructive pulmonary disease, is a progressive inflammatory disease connecting the airways, lung parenchyma, and vasculature. It causes the damage and remodeling of the airways and lung tissue. Proper functioning of lungs is rejected continuously by COPD. Over a period of time, these changes result in more severe conditions such as pulmonary hypertension and right heart failure. The precise pathophysiology of COPD is unidentified.

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The inflammatory process is a driving aspect in the pathophysiology of COPD. Recent verification suggests that the inflammatory response results in a number of effects, including an arrival of inflammatory cells such as macrophages, neutrophils and lymphocytes. Thickened airways and structural changes such as increased smooth muscle and fibrosis may also be manifested. Cigarette smoking causes an inflammatory response in the lungs. This response does not cease with the removal of the stimulus, but progresses for an unlimited period of time. COPD is a subset of obstructive lung diseases that includes cystic fibrosis, bronchiectasis and asthma. Degeneration and destruction of the lung and supporting tissue are characteristic of COPD. These processes result in emphysema, chronic bronchitis, or both. Emphysema begins with a small airway disease and progresses to alveolar destruction, with a predominance of small airway narrowing and mucous gland hyperplasia.

The pathophysiology of COPD is not entirely understood. Chronic inflammation of the cells lining the bronchial tree plays a major role. Smoking and, seldom, other inhaled irritants, perpetuates an ongoing inflammatory response that results in airway narrowing and hyperactivity. Airways become edematous, excessive mucus production occurs and cilia function weakly. Patients face increasing difficulty clearing secretions with disease progression. Accordingly, they develop a chronic productive cough, wheezing and dyspnea.

The basic pathophysiologic process in COPD consists of increased resistance to airflow, loss of elastic recoil and decreased expiratory flow rate. The alveolar walls frequently break because of the increased resistance of air flows. The hyper inflated lungs flatten the curvature of the diaphragm and enlarge the rib cage. The altered configuration of the chest cavity places the respiratory muscles, including the diaphragm, at a mechanical disadvantage and impairs their force-generating capacity. Consequently, the metabolic work of breathing increases, and the sensation of dyspnea heightens.

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Acute right ventricular failure—from pathophysiology to new treatments

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We had a good read. For the benefit of yourself. Be sure to read to the end. I want you to get good knowledge from Causes Of Afib . From the Springer article: Acute right ventricular failure—from pathophysiology to new treatments www.springerlink.com by: Mebazaa, Alexandre; Karpati, Peter; Renaud, Estelle; Algotsson, Lars; before levo.avi (970 KB) Journal: Intensive Care Medicine Vol. 30 Issue 2 DOI: 10.1007/s00134-003-2025-3 Published: 2004-02-01

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Hyperthyroidism - Its Pathophysiology

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Atrial Fibrillation - Hyperthyroidism - Its Pathophysiology

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The over stimulation of the thyroid gland leads to hyperplasia of the gland and subsequently this leads to an increase in the secretion of thyroid hormones. The growth in the cells and its multiplication manifest in enlargement of the gland. Noticeable changes occur in all parts of the body as a result of the increased hormone secretion.

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There is elevation in metabolic rate manifesting in elevation in metabolism of protein, fat and carbohydrate. The accelerated protein and fat metabolism lead to weight loss and muscular weakness. The body attempts to remedy the weight loss and so the patient's appetite is increased in the process.

Patient is unable to tolerate hot weather as a result of the increase in the body metabolism. The superficial capillaries dilate leading to increased peripheral blood flow and also an increase in cardiac output as the body tries to eliminate excess heat from the system. This accounts for warm and moist skin and also for the perspiration.

The increase cardiac output in conjunction with hormonal effects on the sympathetic nerves brings about palpitation and tachycardia. There may be ectopic beats or atrial fibrillation in the elderly. There is increase in systolic blood pressure and the pulse pressure. The heart tries to compensate for these increases and may eventually become overwhelmed and fail.

The increase in metabolism also brings about an increase in the absorption of glucose from the intestines. This excessive absorption of glucose triggers off glyconeolysis which in combination with the glucose absorption leads to hyperglycaemia. Excessive glucose in the blood leads to the release of insulin into the blood stream which brings about a rapid fall in blood glucose level. This glyconeolysis and insulin release lead to rapid rise and fall in blood glucose level as well.

Oxygen consumption is increased as a result of the increase in metabolic rate. The increased metabolic rate coupled with increase oxygen consumption leads to changes in perception and co-ordination. Increased sympathetic activity and increase blood flow to the brain lead to nervousness, hyperactivity, hyper-excitability, restlessness, irritability and insomnia.

Increased adrenergic activity results in the retraction of the upper eyelids which presents with increased sclera exposure or exophthalmos. Increased adrenergic activity also causes fine muscle tremors which are noticeable when patient's hands are outstretched.

Excessive thyroid hormones exert some effects on the sympathetic nervous system which lead to increase in peristalsis producing an increase the frequency of bowel motion (diarrhoea).

Noticeable changes occur in the reproductive systems. There is either increase sexual desire or low sex drives in both sexes. In the hyperthyroid males gynaecomastia is sometimes present, whereas there is oligomenorrhoea or amenorrhoea in the females. However, there may be decrease in fertility in severe hyperthyroidism.

The skin becomes thinned and the hair is fine, soft and straight as a result of increased thyroid hormone secretion.

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Etiology and Pathophysiology of Diabetes Mellitus

Causes Chf - Etiology and Pathophysiology of Diabetes Mellitus

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Etiology
Heredity is unquestioned as a prominent factor in the etiology of diabetes mellitus, although the mechanism of inheritance is unknown. Diabetes may be actually a syndrome rather than a specific disease. A variety of genetic mechanisms have been proposed, but most favor a multifactorial inheritance or a recessive gene somehow linked to the tissue-typing antigens, the human lymphocyte-A (HLA) system. However, the inheritance of non-insulin-dependent diabetes and insulin-dependent diabetes appears to be different. Nearly 100% of offspring pf parents who both have non-insulin-dependent diabetes develop that type of diabetes, but only 45% to 60% of the offspring of both parents who have insulin-dependent diabetes will develop the disease. There is also an increase risk of diabetes with obesity. The incidence of the disease doubles with every 20% of excess weight and this figure applies to the young as well as to the older diabetic person. Diabetes is now the sixth leading cause of death by disease in adults and the first leading cause of of new cases of blindness between 20 and 75 years of age. Viruses have been implicated on the etiology of diabetes. The viral theory states that the Beta-cells of some individuals (most specialists believe that the Beta-cells are genetically susceptible because of the defects in the HLA system) are attacked by certain viruses, causing cell damage or death. The body reacts to this damaged or changed tissue in an autoimmune phenomenon, forming antibodies that "attack" the Beta-cells, resulting in cell death. When there are not enough available Beta-cells to supply sufficient insulin to meet the needs of the body, insulin-dependent diabetes results. Tumors of the pancreas, pancreatitis, stress drugs as steroids, stress diseases that involve other endocrine organs such as acromegaly, heredity and viral diseases are now believed to play a part in causing diabetes.

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In non-insulin-dependent, or type II, diabetes disturbed carbohydrate metabolism may be a result of a sluggish or insensitive secretory response in the pancreas or a defect in body tissues that requires unusual amounts of insulin, or the insulin secreted may be rapidly destroyed, inhibited, or in-activated in affected persons. A lack of insulin because of reduction in islet cell mass or destruction of the islets is the hallmark of the person with insulin-dependent, or type I diabetes.

Pathophysiology
Insulin is needed to support the metabolism of carbohydrates, fats and proteins, primarily by facilitating the entry of these substances into the cell. Insulin is needed for the entry of glucose into the muscle and fat cells, for the prevention of mobilization of fats from fat cells, and for storage of glucose as glycogen in the cells of liver and muscle. Insulin is not needed for the entry of glucose into nerve cells or vascular tissue. The chemical composition and molecular structure of insulin are such that it fits into receptor sites on the cell membrane. Here it initiates a sequence of poorly defined chemical reactions that alter the cell membrane to facilitate the entry of glucose into the cell and stimulate enzymatic systems outside the cell that metabolize the glucose for energy production.

With deficiency of insulin, glucose is unable to enter the cell and its concentration in the bloodstream increases, the increased concentration in the bloodstream increases. The increased concentration of glucose (hyperglycemia) produces an osmotic gradient that causes the movement of body fluid from the intracellular space to the extracellular space and into the glomerular filtrate in order to "dilute" the hyperosmolar filtrate. When the glucose concentration in glomerular filtrate exceeds the threshold (180mg/dL), glucose "spills" into the urine along with an osmotic diversion of water (polyuria), a cardinal sign of diabetes. The Urinary fluid losses cause the excessive thirst (polydipsia) observed in diabetes. As might be expected, this water washout results in a depletion of other essential chemicals.

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Pathophysiology of COPD

Atrial Fibrillation - Pathophysiology of COPD

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Do you know - Pathophysiology of COPD

COPD, or chronic obstructive pulmonary disease, is a progressive inflammatory disease connecting the airways, lung parenchyma, and vasculature. It causes the damage and remodeling of the airways and lung tissue. Proper functioning of lungs is rejected continuously by COPD. Over a period of time, these changes result in more severe conditions such as pulmonary hypertension and right heart failure. The precise pathophysiology of COPD is unidentified.

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The inflammatory process is a driving aspect in the pathophysiology of COPD. Recent verification suggests that the inflammatory response results in a number of effects, including an arrival of inflammatory cells such as macrophages, neutrophils and lymphocytes. Thickened airways and structural changes such as increased smooth muscle and fibrosis may also be manifested. Cigarette smoking causes an inflammatory response in the lungs. This response does not cease with the removal of the stimulus, but progresses for an unlimited period of time. COPD is a subset of obstructive lung diseases that includes cystic fibrosis, bronchiectasis and asthma. Degeneration and destruction of the lung and supporting tissue are characteristic of COPD. These processes result in emphysema, chronic bronchitis, or both. Emphysema begins with a small airway disease and progresses to alveolar destruction, with a predominance of small airway narrowing and mucous gland hyperplasia.

The pathophysiology of COPD is not entirely understood. Chronic inflammation of the cells lining the bronchial tree plays a major role. Smoking and, seldom, other inhaled irritants, perpetuates an ongoing inflammatory response that results in airway narrowing and hyperactivity. Airways become edematous, excessive mucus production occurs and cilia function weakly. Patients face increasing difficulty clearing secretions with disease progression. Accordingly, they develop a chronic productive cough, wheezing and dyspnea.

The basic pathophysiologic process in COPD consists of increased resistance to airflow, loss of elastic recoil and decreased expiratory flow rate. The alveolar walls frequently break because of the increased resistance of air flows. The hyper inflated lungs flatten the curvature of the diaphragm and enlarge the rib cage. The altered configuration of the chest cavity places the respiratory muscles, including the diaphragm, at a mechanical disadvantage and impairs their force-generating capacity. Consequently, the metabolic work of breathing increases, and the sensation of dyspnea heightens.

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