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PubMed2003

[Pathophysiology and treatment of postoperative acute respiratory disturbance].

One major concern after surgery is postoperative pulmonary complications such as atelectasis, aspiration, pneumonia, and respiratory failure. Progress in preoperative and postoperative rehabilitation, in systemic management including respiratory management, and progress in understanding the pathophysiology of acute respiratory failure have improved prevention and the outcome of treatment. However, some conditions remain very difficult to treat, like respiratory failure accompanied by infection or multiple organ failure. In the 1960s, the concept of acute respiratory distress syndrome or adult respiratory distress syndrome was postulated. Tremendous amounts of basic and clinical research have been done to clarify the pathophysiology of and to establish treatment modalities for acute respiratory failure. Our understanding of acute respiratory failure has progressed from the role of microembolism syndrome to cellular components such as neutrophils and platelets and then to humoral factors such as endotoxins, complement factors, and numerous cytokines. In this article, the pathophysiology of acute lung injury and its diagnostic criteria, treatment modalities such as respirator management to protect lung tissue from barotrama and volutrauma by yielding hypercapnea (permissive hypercapnea), drug therapy with neutrophil elastase inhibitor, mechanical support using extracorporeal membrane oxygenation, liquid ventilation, continuous hemodiafiltration, and endotoxin elimination columns are discussed. Early diagnosis and early treatment are mandatory to improve survival in patients with acute respiratory failure, although we have not yet fully understood the pathophysiology of this disease entity sufficiently.

Acute Disease↗

PubMed2004

[Current controversies in pathophysiology of cervical spondylotic myelopathy].

Cervical spondylotic myelopathy is the most severe consequence of degenerative disease of cervical spine. In this article we perform a bibliographic review, addressing current controversies in its pathophysiology. Present work lines of most groups dedicated to the study of this condition are focused on improving surgical techniques designed for the treatment of this disease. Pathophysiological studies are scarce, and most of our pathophysiological knowledge of cervical spondylotic myelopathy is based in works done in 60s and 70s. Literature of the last decade lacks neurochemichal studies parallel to those existing for acute spinal injury. In the same way, only three prospective clinical trials comparing conservative and surgical treatment have been done, and none of them has demonstrated clear superiority of surgery. Given the high prevalence of this disease, the need for deep knowledge of its pathophysiologic, neurochemichal and molecular basis, and the optimization of surgical treatment is justified. This probably implies the need for prospective randomized trials to determine which patients are going to benefit from surgery.

Cervical Vertebrae↗

PubMed1992

[Pathological and pathophysiological studies on central nervous system in experimental cerebral ischemia of the rat].

The present study was undertaken to elucidate the pathological and pathophysiological characteristics of experimental cerebral ischemia in rats. The purpose of this study was also to clarify whether this animal model is useful for the research of multiple cerebral infarction. In order to create a cerebral ischemia model, arterioles were embolized by injecting 2000 carbon-microspheres (50 microns in diameter) into the right internal carotid artery of ketamine anesthetized rats. Pathological studies and pathophysiological evaluations were performed by electrocorticography (ECoG) and by measuring regional cortical blood flow (CBF) in embolized rats. An attempt was also made to examine learning ability: embolized rats were subjected to the passive avoidance test. Pathophysiological studies revealed most microspheres to be located in the ipsilateral hemisphere with a few in the contralateral hemisphere. Most foci of cerebral infarction were distributed in the area fed by the ipsilateral middle cerebral artery and the anterior cerebral artery, while a few of them were found in the area fed by the contralateral anterior cerebral artery. Regions of cerebral infarction consisted of microcerebral infarctions, some of which were fused to each other. The pathological characteristics of this experimentally induced cerebral ischemia were those of multifocal cerebral infarction. Both ECoG and CBF decreased after injection of carbon-microspheres, and these two parameters did not recover for more than 60 min in both hemispheres. Seven days after cerebral embolization, the shortened response latency in the passive avoidance test, possibly indicating memory impairment, was observed. Our findings suggest that cerebral ischemia of the rat produced by carbon-microspheres (50 microns in diameter) is useful in the pathophysiological investigation of multiple cerebral infarction.

Acute Disease↗

PubMedDate not supplied

The role of gastric accommodation in the pathophysiology of functional dyspepsia.

BACKGROUND AND OBJECTIVES: The pathophysiology of functional dyspepsia is not yet completely known. Several mechanisms have been suggested as having a role in symptom onset and impaired gastric accommodation to meal is one of the most frequent. This review will focus on the pathophysiological and clinical aspects of this abnormality. EVIDENCE AND INFORMATION SOURCES: Medical peer-reviewed literature was considered to elucidate the role of gastric accommodation in the pathophysiology of functional dyspepsia. STATE OF THE ART: Impaired gastric accommodation to meal is present in around 40% of patients with functional dyspepsia and it was shown to be associated with the presence of early satiety. Unfortunately, a definitive treatment of this abnormality with fundus-relaxing drugs is not yet available. PERSPECTIVES: Further studies are needed to better clarify the role of each single pathophysiological mechanism on clinical manifestations of functional dyspepsia. Research is still ongoing to offer a valid therapeutic approach.

Dyspepsia↗

PubMed2006

[The pathophysiology of irritable bowel syndrome: inflammation and motor disorder].

Irritable bowel syndrome (IBS) is one of the most common disorders and a heterogeneous condition in view of symptoms and underlying mechanisms. Though underlying causes of pathophysiologic changes remain unclear, low grade mucosal inflammation and abnormal intestinal motility are accepted mechanisms which alter gut function and generate symptoms of IBS. First, before 1980s, abnormal colonic and rectal motor functions were regarded as the main pathophysiology of IBS, but only 25-75% of IBS patients have apparent motor abnormalities which differ from the motor functions in normal controls. So, various gastrointestinal motility tests were not indicated for the diagnosis of IBS. The high-amplitude propagating contractions of colon in IBS patients may be related to the visceral pain perception. Second, the low grade mucosal inflammation may be involved in the pathophysiology of visceral hypersensitivity. Post infectious IBS (PI-IBS) occupied 6-17% of the total IBS and some previous prospective studies reported that 7-33% of acute bacterial enteritis patients developed IBS after 6-12 months of infection. The relative risk of IBS in the gastroenteritis cohort was 11.9 and the strongest risk factor is the duration of diarrhea. After enteritis event, the increased number of immunocytes, mast cells and large amount of lymphocytes infiltration were revealed in mucosa and enteric nervous system of the gut. Beside the inflammatory cells, enterochromaffin cells, cytokines and inducible nitric oxide may be related to the pathophysiologic mechanism of PI-IBS. Lastly, the abnormalities in the gastrointestinal autonomic nervous system can induce constipation or motor disorders, but further research should elucidate it.

Gastrointestinal Motility↗

PubMed2006

Esophageal impedance monitoring and pathophysiology of gastroesophageal reflux disease.

Up until now, most pathophysiological concepts about gastroesophageal reflux derived from measurement of esophageal pH. However, pH monitoring does not detect all gastroesophageal reflux events, particularly when little or no acid is present in the refluxate. Esophageal impedance measurements made possible to detect and quantify all types of reflux i.e. acid, weakly acidic and non-acid reflux and to characterize the air-liquid composition of the refluxate. This new tool stimulated us to re-examine different aspects of the pathophysiology of GERD, but considering all gastroesophageal reflux events rather than only acid reflux. In this text we first analyzed gastric factors and the impact of gastric emptying on the characteristics of the refluxate. We then foccussed on the antirreflux barrier at the gastro-esophageal junction and we analysed the patterns of air and liquid reflux during transient lower esophageal sphincter relaxations (TLESRs), the most frequent mechanism for reflux in patients with GERD. With failure of the antireflux barrier, reflux occurs and we discussed in detail the air-liquid patterns, composition and proximal extent of the refluxate in normal subjects and patients with GERD both in resting and ambulatory conditions. The volume and chemical clearance mechanisms triggered after acid and non-acid reflux were characterized. The effect of esophagitis or Barrett's mucosa on electrical conductivity and impedance was analyzed as an expression of mucosal damage and increased ionic permeability. We discussed the role of non acid and gas reflux in esophageal and extraesophageal symptoms in patients with GERD. We believe that better understanding of the pathophysiology of GERD can help to characterize the relationship between gastroesophageal reflux and symptoms; the factors that determine esophageal and extraesophageal mucosal damage and/or eventual carcinogenesis related to reflux and to provide a tailored treatment to each patient targeting the individual pathophysiological defect.

Electric Impedance↗

PubMed1990

Hemodynamic and neurohumoral evidence of multifaceted pathophysiology in human hypertension.

As hypertension advances, secondary pathophysiologic changes are induced in multiple organs. Consequently, we investigated the pathophysiology of the earliest forms of hypertension--e.g., borderline hypertension. Borderline hypertension is associated with abnormal autonomic control of the circulation; sympathetic drive to the heart, blood vessels, and kidney is increased, cardiac parasympathetic inhibition is decreased, and plasma norepinephrine is increased. The hemodynamic picture is one of increased cardiac output not met by adequate vasodilation. The condition of "hyperkinetic" borderline hypertension is a precursor of more severe hypertension. In due course, a transition from high cardiac output to high vascular resistance occurs, while the enhanced sympathetic tone recedes toward normal values. The mechanism of hemodynamic transition is easily understood: cardiac output decreases due to structural changes and receptor downregulation, whereas ensuing vascular hypertrophy increases vascular resistance. The apparent regression of plasma norepinephrine values is explained in the framework of our hypothesis of the "blood pressure-seeking properties of the central nervous system." Large body mass and overweight are a consistent feature of borderline hypertension. A recent study in Tecumseh, Michigan shows that weight, plasma norepinephrine, a hyperkinetic state, and plasma insulin values are correlated in the general population. The explanation of this interrelationship will greatly advance our understanding of hypertension. From the pathophysiological viewpoint, the paradoxical outcome of clinical trials involving older antihypertensive medication is not surprising. The complexity of pathophysiologic interrelationships and the fact that risk factors for atherosclerosis are increased in hypertension suggest that reduction of blood pressure cannot be expected to ameliorate all consequences of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamics↗

PubMedDate not supplied

[The role and achievements in clinical pathophysiology in the Novi Sad region].

Nowadays, clinical pathophysiology in our conditions is a firmly founded branch of medicine which has had an important role in the improvement of diagnostics, scientific and researching work and all forms and levels of education at the Medical Faculty in Novi Sad. The value and usefulness of clinical pathophysiology has been particularly important in the team work within the Clinical center in Novi Sad in the time it was organized as an unique health care institution. Pathological physiology was ready to take over all its tasks foreseen within this type of organization, and through further constructional and equipment improvements it could soon achieve European standards in its work. Professionally unjustified decision for abandoning the concept of Clinical center in Novi Sad has greatly affected health care service in general. Twenty years of work on the improvement of pathophysiology have been thrown away and its important role in the first-class treatment of the patients has been certainly discredited but not denied. If health care service happens to be reorganized following the model of developed countries there will be a chance for the revitalization of clinical pathophysiology and finalization of its development to fulfill the interests of patients for obtaining the high quality treatment in our conditions.

Health Services↗

PubMed1998

Advanced systolic heart failure: emerging pathophysiology and current management.

Systolic heart failure leads to progressive left ventricular impairment, has a poor prognosis and negatively affects the patient's quality of life, especially when the disease advances to the point where it causes refractory symptoms. Ventricular remodeling, one of the consequences of advanced systolic heart failure, results from complex pathophysiologic mechanisms and leads to hemodynamic compromise, clinical deterioration and death. The nursing literature on heart failure has focused on neuroendocrine changes and the pharmacologic management in response to these changes. Little emphasis has been placed on other pathophysiologic mechanisms that lead to a worsening of ventricular function or on advances in clinical research that may influence current and future nursing management of the patient throughout the continuum of care. For therapy to be individualized, it is necessary for nurses to understand the pathophysiology of systolic heart failure and the importance that nursing actions have on augmenting medical management to alleviate symptoms and to deter the progression of the pathophysiologic state. Such an understanding should ultimately reduce morbidity and mortality and optimize quality of life.

Cardiovascular Agents↗

PubMed1983

The cardiomyopathies. A pathophysiologic approach to therapeutic management.

"Cardiomyopathies" are a disparate group of myocardial disorders, usually of unknown or obscure origin, characterized by systolic or diastolic myocardial dysfunction but involving conditions of widely divergent pathophysiology. For purposes of devising appropriate clinical management, a useful classification scheme can be created with reference to the type of pathophysiologic abnormality exhibited. On this basis, three major types can be identified: (1) congestive (poor systolic function, normal diastolic function, left ventricular dilatation without the expected degree of compensatory hypertrophy), (2) hypertrophic (supernormal systolic function, subnormal diastolic function, and pronounced left ventricular hypertrophy, usually asymmetric, without dilatation), and (3) restrictive (normal or near-normal systolic function and subnormal diastolic function, usually mild symmetrical left ventricular, without dilatation). Noninvasive identification of these pathophysiologic features can be useful in optimizing management programs.

Cardiomyopathy, Dilated↗

PubMedDate not supplied

Malignant ascites: new concepts in pathophysiology, diagnosis, and management.

Malignant ascites is a manifestation of advanced malignant disease that is associated with significant morbidity. Mainstays of treatment include diuretics and recurrent large volume paracentesis. Although lymphatic obstruction has been considered the major pathophysiologic mechanism behind its formation, recent evidence suggests that immune modulators, vascular permeability factors, and metalloproteinases are contributing significantly to the process. These new observations offer the opportunity for development of new, more targeted therapies for the treatment of malignant ascites. This article uses a clinical case to highlight the problem, then reviews these new concepts in the pathophysiology of malignant ascites formation. The diagnosis and management of this challenging medical problem are subsequently discussed, with emphasis on how these new pathophysiologic insights are being applied to the development of novel therapies that may soon change how we manage this troubling clinical condition.

Ascites↗

PubMed2002

Pathophysiological characterization of isolated diastolic heart failure in comparison to systolic heart failure.

CONTEXT: Many older patients with symptoms of congestive heart failure have a preserved left ventricular ejection fraction (LVEF). However, the pathophysiology of this disorder, presumptively termed diastolic heart failure (DHF), is not well characterized and it is unknown whether it represents true heart failure. OBJECTIVE: To assess the 4 key pathophysiological domains that characterize classic heart failure by systematically performing measurements in older patients with presumed DHF and comparing these results with those from age-matched healthy volunteers and patients with classic systolic heart failure (SHF). DESIGN AND SETTING: Observational clinical investigation conducted in 1998 in a general community and teaching hospital in Winston-Salem, NC. PARTICIPANTS: A total of 147 subjects aged at least 60 years. Fifty-nine had isolated DHF defined as clinically presumed heart failure, LVEF of at least 50%, and no evidence of significant coronary, valvular, or pulmonary disease. Sixty had typical SHF (LVEF < or =35%). Twenty-eight were age-matched healthy volunteer controls. MAIN OUTCOME MEASURES: Left ventricular structure and function, exercise capacity, neuroendocrine function, and quality of life. RESULTS: By echocardiography, mean (SE) LVEF was 60% (2%) in patients with DHF vs 31% (2%) in those with SHF and 54% (2%) in controls. Mean (SE) LV mass-volume ratio was markedly increased in patients with DHF (2.12 [0.14] g/mL) vs those with SHF (1.22 [0.14] g/mL) (P<.001) and vs controls (1.49 [0.17] g/mL) (P =.002). Peak oxygen consumption by expired gas analysis during cycle ergometry was similar in the DHF and SHF groups (14.2 [0.5] and 13.1 [0.5] mL/kg per minute, respectively; P =.40) and in both was markedly reduced compared with healthy controls (19.9 [0.7] mL/kg per minute) (P =.001 for both). Ventilatory anaerobic threshold was similar in the DHF and SHF groups (9.1 [0.3] and 8.7 [0.3] mL/kg per minute, respectively; P<.001) and in both was reduced compared with healthy controls (11.5 [0.4] mL/kg per minute) (P<.001). Norepinephrine levels were similar in the DHF (306 [64] pg/mL) and SHF (287 [62] pg/mL) groups (P =.56) and in both were markedly increased vs healthy controls (169 [80] pg/mL) (P =.007 and.03, respectively). Brain natriuretic peptide was substantially increased in both the DHF (56 [30] pg/mL) and the SHF (154 [28] pg/mL) groups compared with healthy controls (3 [38] pg/mL) (P =.02 and.001, respectively). Quality-of-life decrement score as assessed by the Minnesota Living with Heart Failure Questionnaire was substantially increased from the benchmark score of 10 in both groups (SHF: 43.8 [3.9]; DHF: 24.8 [4.4]). CONCLUSION: Patients with isolated DHF have similar though not as severe pathophysiologic characteristics compared with patients with typical SHF, including severely reduced exercise capacity, neuroendocrine activation, and impaired quality of life.

Aged↗

PubMed2000

The yin and yang of nitric oxide: reflections on the physiology and pathophysiology of NO.

Nitric oxide (NO.) is an arginine-derived nitrogen-based radical that is rapidly becoming one of the most important molecular species to be discovered. Over the past decade, an explosion of evidence has revealed the extreme complexity of function of this seemingly simple inorganic molecule. It is now evident that NO. demonstrates a functional dualism, playing a pivotal role in numerous physiologic and pathophysiologic processes. Whether this molecule is beneficial or detrimental is dependent upon the tissue of generation, the level of production, the oxidative/reductive (redox) environment in which this radical is generated, and the presence or absence of NO. transduction elements. Nitric oxide is generated by three independent isoenzymes that resemble the p-450 enzyme superfamily in both form and function. It ultimately alters enzymatic function through covalent modification, redox interactions, and interactions with metallic functional centers. This radical is a key figure in a number of pathophysiologic processes by means of similar yet uncoordinated interactions. In consideration of the already broad spectrum of roles attributed to NO., it seems highly likely that this molecule will be implicated in an ever widening variety of functions relative to the practice of otolaryngology-head and neck surgery. This article reviews the enzymology, signal transduction mechanisms, physiology, and pathophysiology of NO. as it pertains to head and neck cancer.

Animals↗

PubMed1978

Disseminated intravascular coagulation and related syndromes: etiology, pathophysiology, diagnosis, and management.

Disseminated intravascular coagulation (DIC) is being recognized with increased frequency and not only are newer diagnostic modalities becoming available for this syndrome, but newer, some controversial, methods of management are also being recognized and may prove to increase survival in DIC. In addition, several syndromes classically considered separate, definitive disease entities, may actually share similar or identical pathophysiology to DIC. This review summarized current, as well as controversial aspects of etiology, pathophysiology, clinical and laboratory diagnosis, and management of DIC. In addition, a brief discussion of syndromes which may share similar or identical pathophysiology to DIC is included.

Anemia, Hemolytic↗

PubMed1996

Pathophysiologic significance of left ventricular hypertrophy in dilated cardiomyopathy.

BACKGROUND AND HYPOTHESIS: Patients with dilated cardiomyopathy (DCM) with left ventricular hypertrophy (LVH) have been found to have a better prognosis than patients without LVH. However, the pathophysiologic mechanism for that has not been investigated. We sought to clarify the pathophysiologic significance of LVH in DCM. METHODS: We performed isoproterenol infusion echocardiography (0.02 micrograms/kg/min) in 17 patients with DCM, and measured plasma epinephrine and norepinephrine levels at rest and at the end of ergometer exercise in 14 of the 17 patients. Patients were classified into groups according to the presence (9 patients) (LVH+) or absence (8 patients) (LVH-) of LVH. Left ventricular hypertrophy was defined as an inter-ventricular thickness or posterior wall thickness > or = 13 mm. RESULTS: Although there was no significant difference between groups in fractional shortening at rest during isoproterenol infusion, fractional shortening was significantly higher in the LVH(+) group than in the LVH(-) group (29 +/- 9 vs. 17 +/- 8%; p < 0.025). Although there was no significant difference in plasma norepinephrine level, it was significantly lower in the LVH(+) group than in the LVH(-) group (233 +/- 169 vs. 519 +/- 258 pg/ml; p < 0.05) at the end point of the exercise. CONCLUSION: Systolic reserve, represented by the response to isoproterenol, is greater in patients with DCM with LVH than in those without LVH, and a lower plasma level of norepinephrine is needed to activate the myocardium during exercise in patients with DCM with LVH. This pathophysiologic characteristic could be one of the mechanisms which explain a better prognosis in patients with DCM with LVH.

Adult↗

PubMed2002

Pathophysiology of Parkinson's disease: from clinical neurology to basic neuroscience and back.

Parkinson's disease (PD) is characterized by motor and nonmotor (cognitive and limbic) deficits. The motor signs of PD include hypokinetic signs such as akinesia/bradykinesia, rigidity and loss of normal postural reflexes, and hyperkinetic signs such as tremor. Dopamine depletion in the striatum is the hallmark of PD and of its animal models, still the pathophysiology of the parkinsonian symptoms and especially of parkinsonian tremor are under debate. The most extreme hypotheses argue about peripheral versus central nervous system origin, intrinsic cellular oscillator versus network oscillators, and basal ganglia-based pathophysiology versus cerebellar-thalamic based pathophysiology. Recent studies support the view that parkinsonian symptoms are most likely due to abnormal synchronous oscillating neuronal activity within the basal ganglia. Peripheral factors do only play a minor role for the generation, maintenance, and modulation of PD tremor and other signs. The most likely candidates producing these neuronal oscillations are the weakly coupled neural networks of the basal ganglia-thalamo-cortical loops. However, the present evidence supports the view that the basal ganglia loops are influenced by other neuronal structures and systems and that the tuning of these loops by cerebello-thalamic mechanisms and by other modulator neurotransmitter systems entrain the abnormal synchronized oscillations. Neurosurgical procedures, such as lesions or high-frequency stimulation of different parts of the loop, might resume the normal unsynchronized activity of the basal ganglia circuitry, and, therefore, ameliorate the clinical symptoms of Parkinson's disease.

Animals↗

PubMed2002

Pathophysiology of nonparkinsonian tremors.

Patients with nonparkinsonian tremors are the second largest group treated with functional neurosurgery. We summarize the present pathophysiological knowledge of these conditions. Essential tremor (ET) may be due to oscillations within the olivocerebellar circuit. There is experimental evidence from animal models for such a mechanism, and clinical data indicate an abnormal function of the cerebellum in ET. Cerebellar tremor may be closely related to the tremor seen in advanced ET. The malfunction of the cerebellum causes a pathological feed-forward control. Additionally an oscillator within the cerebellum or its input/output pathways may cause cerebellar tremor. Almost nothing is known about the pathophysiology of dystonic tremor. Holmes tremor is based on a nigral and a cerebellar malfunction and presents clinically as the combination of tremor in Parkinson's disease and cerebellar tremor. Neuropathic tremor can be extremely disabling and is thought to be due to an abnormal interaction of the disturbances within the periphery and abnormal cerebellar feedback. Unlike the case of Parkinson's disease, functional neurosurgery of nonparkinsonian tremors is not yet based on a solid pathophysiological background.

Brain↗

PubMed1993

CNS signal transduction in the pathophysiology and pharmacotherapy of affective disorders and schizophrenia.

Until recently, research on the neurochemical basis of affective disorders (AD) and schizophrenia (SCZ) focused on detecting postulated disturbances in presynaptic neurotransmitter release and metabolism, or postsynaptic receptor function. New insights into the molecular mechanisms involved in the propagation of neurotransmitter signals across biological membranes and in the regulation of neuronal responses have allowed the development of novel hypotheses, which may explain the altered postsynaptic neuroreceptor responsivity thought to be integral to the pathophysiology of these disorders. In this review we evaluate evidence from both basic science and clinical research implicating disturbances in postreceptor signal transduction in the pathophysiology and pharmacotherapy of AD and SCZ. Specific findings regarding potential postreceptor sites of pathophysiology are highlighted in each of these disorders, together with the growing body of data on the possible postreceptor loci of psychotropic drug action, especially lithium and antidepressants.

Animals↗