Do I have Fibrosis?
More information about symptoms of Fibrosis and related conditions:
Medical Books Excerpts Excerpts of published medical book chapters related to Fibrosis are available from published medical books for more detailed information about Fibrosis.
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the symptoms of Fibrosis.
The clinical effects of cystic fibrosis may become apparent soon after birth or may take years to develop. They include major aberrations in sweat gland, respiratory, and GI function. Sweat gland dysfunction is the most consistent abnormality. Increased concentrations of sodium and chloride in the sweat lead to hyponatremia and hypochloremia and can eventually induce fatal shock and arrhythmias, especially in hot weather.
Respiratory symptoms reflect obstructive changes in the lungs: wheezy respirations; a dry, nonproductive paroxysmal cough; dyspnea; and tachypnea. These changes stem from thick, tenacious secretions in the bronchioles and alveoli and eventually lead to severe atelectasis and emphysema. Children with cystic fibrosis display a barrel chest, cyanosis, and clubbing of the fingers and toes. They suffer recurring bronchitis and pneumonia as well as associated nasal polyps and sinusitis. Death typically results from pneumonia, emphysema, or atelectasis.
The GI effects of cystic fibrosis occur mainly in the intestines, pancreas, and liver. One early symptom is meconium ileus; the neonate with cystic fibrosis doesn't excrete meconium, a dark green mucilaginous material found in the intestine at birth. He develops symptoms of intestinal obstruction, such as abdominal distention, vomiting, constipation, dehydration, and electrolyte imbalance. As the child gets older, obstruction of the pancreatic ducts and resulting deficiency of trypsin, amylase, and lipase prevent the conversion and absorption of fat and protein in the GI tract. The undigested food is then excreted in frequent, bulky, foul-smelling, pale stools with a high fat content. This malabsorption induces poor weight gain, poor growth, ravenous appetite, distended abdomen, thin extremities, and sallow skin with poor turgor. The inability to absorb fats results in a deficiency of fat-soluble vitamins (A, D, E, and K), leading to clotting problems, retarded bone growth, and delayed sexual development. Males may experience azoospermia and sterility; females may experience secondary amenorrhea but can reproduce. A common complication in infants and children is rectal prolapse secondary to malnutrition and wasting of perirectal supporting tissues.
In the pancreas, fibrotic tissue, multiple cysts, thick mucus, and eventually fat replace the acini (small, saclike swellings normally found in this gland), producing symptoms of pancreatic insufficiency: insufficient insulin production, abnormal glucose tolerance, and glycosuria. About 15% of patients have adequate pancreatic exocrine function for normal digestion and, therefore, have a better prognosis. Biliary obstruction and fibrosis may prolong neonatal jaundice. In some patients, cirrhosis and portal hypertension may lead to esophageal varices, episodes of hematemesis and, occasionally, hepatomegaly.
Source: Professional Guide to Diseases (Eighth Edition), 2005
Clinical manifestations of cirrhosis and fibrosis are similar for all types, regardless of the cause. Early indications are vague, but usually include GI signs and symptoms (anorexia, indigestion, nausea, vomiting, constipation, or diarrhea) and a dull abdominal ache. Major and late signs and symptoms develop as a result of hepatic insufficiency and portal hypertension:
❑ Respiratory — pleural effusion and limited thoracic expansion due to abdominal ascites, interfering with efficient gas exchange and leading to hypoxia
❑ Central nervous system — progressive signs or symptoms of hepatic encephalopathy — lethargy, mental changes, slurred speech, asterixis (flapping tremor), peripheral neuritis, paranoia, hallucinations, extreme obtundation, and coma
❑ Hematologic — bleeding tendencies (nosebleeds, easy bruising, and bleeding gums) and anemia
❑ Endocrine — testicular atrophy, menstrual irregularities, gynecomastia, and loss of chest and axillary hair
❑ Skin — severe pruritus, extreme dryness, poor tissue turgor, abnormal pigmentation, spider angiomas, palmar erythema, and possibly jaundice
❑ Hepatic — jaundice, hepatomegaly, ascites, edema of the legs, hepatic encephalopathy, and hepatorenal syndrome comprise the other major effects of full-fledged cirrhosis
❑ Miscellaneous — musty breath, enlarged superficial abdominal veins, muscle atrophy, pain in the right upper abdominal quadrant that worsens when the patient sits up or leans forward, palpable liver or spleen, and temperature of 101° to 103° F (38.3° to 39.4° C). Bleeding from esophageal varices results from portal hypertension.
Source: Professional Guide to Diseases (Eighth Edition), 2005
The usual presenting symptoms of IPF are dyspnea and a dry, hacking, and typically paroxysmal cough. Most patients have had these symptoms for several months to 2 years before seeking medical help. End-expiratory crackles, especially in the bases of the lungs, are usually heard early in the disease. Bronchial breath sounds appear later, when airway consolidation develops. Rapid, shallow breathing occurs, especially with exertion, and clubbing has been noted in more than 40% of patients. Late in the disease, cyanosis and evidence of pulmonary hypertension (augmented S 2 and S3 gallop) commonly occur. As the disease progresses, profound hypoxemia and severe, debilitating dyspnea are the hallmark signs.
Source: Professional Guide to Diseases (Eighth Edition), 2005
The clinical effects of cystic fibrosis may become apparent soon after birth or may take years to develop. They include major aberrations in sweat gland, respiratory, and GI functions.
In cystic fibrosis, sweat gland dysfunction is the most consistent abnormality. Increased concentrations of sodium and chloride in the sweat lead to hyponatremia and hypochloremia and can eventually induce fatal shock and arrhythmias, especially in hot weather.
Such symptoms reflect obstructive changes in the lungs: wheezy respirations; a dry, nonproductive, paroxysmal cough; dyspnea; and tachypnea. These changes stem from thick, tenacious secretions in the bronchioles and alveoli and eventually lead to severe atelectasis and emphysema.
Children with cystic fibrosis display a barrel chest, cyanosis, and clubbing of the fingers and toes. They suffer recurring bronchitis and pneumonia and associated nasal polyps and sinusitis. Death typically results from pneumonia, emphysema, or atelectasis.
The GI effects of cystic fibrosis occur mainly in the intestines, pancreas, and liver. One early symptom is meconium ileus; the newborn with cystic fibrosis doesn’t excrete meconium, a dark green mucilaginous material found in the intestine at birth. He develops symptoms of intestinal obstruction, such as abdominal distention, vomiting, constipation, dehydration, and electrolyte imbalance.
Eventually, obstruction of the pancreatic ducts and resulting deficiency of trypsin, amylase, and lipase prevent the conversion and absorption of fat and protein in the intestinal tract. The undigested food is then excreted in frequent, bulky, foul-smelling, and pale stool with a high fat content.
This malabsorption induces poor weight gain, poor growth, ravenous appetite, distended abdomen, thin extremities, and sallow skin with poor turgor. The inability to absorb fats produces deficiency of fat-soluble vitamins (A, D, E, and K), leading to clotting problems, retarded bone growth, and delayed sexual development. Males have been found to have congenital bilateral absence of the vas deferens, causing sterility; females may experience secondary amenorrhea but can reproduce.
A common complication in infants and children is rectal prolapse. This stems from malnutrition and wasting of perirectal supporting tissues.
In the pancreas, fibrotic tissue, multiple cysts, thick mucus and, eventually, fat replace the acini (small saclike swellings normally found in this gland). This results in signs of pancreatic insufficiency: insufficient insulin production, abnormal glucose tolerance, and glycosuria.
About 15% of patients are pancreatic sufficient, having adequate pancreatic exocrine function for normal digestion. These patients have a better prognosis.
Biliary obstruction and fibrosis may prolong neonatal jaundice. In some patients, cirrhosis and portal hypertension may lead to esophageal varices, episodes of hematemesis and, occasionally, hepatomegaly.
Source: Handbook of Diseases, 2003
These general reference articles may be of interest in relation to medical signs and symptoms of disease in general:
Full list of premium articles on symptoms and diagnosis
The symptom information on this page attempts to provide a list of some possible signs and symptoms of Fibrosis. This signs and symptoms information for Fibrosis has been gathered from various sources, may not be fully accurate, and may not be the full list of Fibrosis signs or Fibrosis symptoms. Furthermore, signs and symptoms of Fibrosis may vary on an individual basis for each patient. Only your doctor can provide adequate diagnosis of any signs or symptoms and whether they are indeed Fibrosis symptoms.
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