Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “pathophysiology”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 613 records · Page 34Linked to original sources
PubMed2000

The pathophysiologic and prognostic significance of acidosis in severe adult malaria.

OBJECTIVE: To investigate the pathophysiology and prognostic significance of acidosis in severe adult malaria. DESIGN: Cohort study. SETTING: The intensive care unit of an infectious diseases hospital in southern Vietnam. PATIENTS: Three hundred forty-six consecutive adult patients with severe falciparum malaria. INTERVENTIONS: Measurements of baseline venous lactate and pyruvate concentrations and an extensive range of clinical and laboratory variables were made, and patients were followed up carefully until death or discharge from the hospital. Admission arterial blood pH and gas tensions were recorded in 296 patients, and hepatic venous sampling was done in 12 patients. MEASUREMENTS AND MAIN RESULTS: Overall, 198 (67%) patients were acidotic (standard base deficit [SBD], >3.3 mmol/L [n = 196], or arterial Pco2, >45 torr [6 kPa] [n = 3]). Hyperlactatemia (plasma lactate, >4 mmol/L) occurred in 120 (35%) of the 346 patients and was associated significantly with acidosis (p < .0001). The hepatosplanchnic lactate extraction ratio was negatively correlated with mixed venous plasma lactate (r2 = .50; p = .006). Hyperlactatemia, metabolic acidosis (SBD, >3.3), and acidemia (pH <7.35) were strongly positively associated with a fatal outcome (relative risks [95% confidence interval], 4.3 [range, 1.8-10.6], 5.0 [range, 3.0-8.1], and 2.7 [range, 1.8-4.1], respectively). The SBD was the single best clinical or laboratory predictor of fatal outcome. The overall median lactate/pyruvate ratio was raised at 30.6 (range, 20.6-62.3; normal range, <15), suggesting hypoxia and anaerobic glycolysis, and was significantly higher in fatal cases (p < .0001). In an additive multivariate model, the two main independent contributors to metabolic acidosis were plasma creatinine, as a measure of renal dysfunction, and venous plasma lactate, together accounting for 63% of the variance in SBD. In univariate analyses, they contributed 29% and 38%, respectively. CONCLUSIONS: These results confirm the importance of acidosis in the pathophysiology of severe adult malaria and suggest a multifactorial origin involving tissue hypoxia, liver dysfunction, and impaired renal handling of bicarbonate.

Acidosis↗
PubMed2002

Marked difference in pathophysiology between tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats.

OBJECTIVE: Tissue factor and lipopolysaccharide frequently have been used to induce disseminated intravascular coagulation in experimental animal models. Although the pathophysiology of disseminated intravascular coagulation may differ according to the agents used to induce it, these previous models have not distinguished between the use of different disseminated intravascular coagulation-inducing agents. In this study, we attempted to evaluate the characteristic features of these agents in two types of disseminated intravascular coagulation models, with special reference to selected hemostatic parameters and pathologic findings in the kidney. DESIGN: Prospective, comparative, experimental study. SETTING: Laboratory at a university hospital. SUBJECTS: Twenty-seven male Wistar rats, age 6-7 wks, weighing 160-170 g. INTERVENTIONS: Three groups of animals were studied: a control group (n = 8) receiving physiologic saline, a tissue factor-treated group (n = 11) receiving tissue factor 3.75 units/kg, and a lipopolysaccharide-treated group (n = 8) receiving lipopolysaccharide 30 mg/kg; each group sustained infusion for 4 hrs via the tail vein. MEASUREMENTS AND MAIN RESULTS: The degree of hemostatic activation in both types of experimental disseminated intravascular coagulation was identical, based on the results of thrombin-antithrombin III complex levels. Markedly elevated D-dimer concentrations were observed without organ dysfunction or fibrin deposition in the kidney on administration of tissue factor, whereas markedly elevated plasminogen activator inhibitor activity, decreased antithrombin III activity, severe organ failure, and marked fibrin deposition in the kidney were observed for lipopolysaccharide administration. CONCLUSION: Because pathophysiology differed remarkably between the tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats, we recommend that they be assessed carefully as distinct entities to determine implications of their experimental and clinical use.

Animals↗
PubMed2002

Aquaporins in brain: distribution, physiology, and pathophysiology.

Water homeostasis in the brain is of central physiologic and clinical importance. Neuronal activity and ion water homeostasis are inextricably coupled. For example, the clearance of K+ from areas of high neuronal activity is associated with a concomitant water flux. Furthermore, cerebral edema, a final common pathway of numerous neurologic diseases, including stroke, may rapidly become life threatening because of the rigid encasement of the brain. A water channel family, the aquaporins, facilitates water flux through the plasma membrane of many cell types. In rodent brain, several recent studies have demonstrated the presence of different types of aquaporins. Aquaporin 1 (AQP1) was detected on epithelial cells in the choroid plexus whereas AQP4, AQP5 and AQP9 were localized on astrocytes and ependymal cells. In rodent brain, AQP4 is present on astrocytic end-feet in contact with brain vessels, and AQP9 is found on astrocytic processes and cell bodies. In basal physiologic conditions, AQP4 and AQP9 appear to be implicated in brain homeostasis and in central plasma osmolarity regulation. Aquaporin 4 may also play a role in pathophysiologic conditions, as shown by the reduced edema formation observed after water intoxication and focal cerebral ischemia in AQP4-knockout mice. Furthermore, pathophysiologic conditions may modulate AQP4 and AQP9 expression. For example, AQP4 and AQP9 were shown to be upregulated after ischemia or after traumatic injuries. Taken together, these recent reports suggest that water homeostasis in the brain is maintained by regulatory processes that, by control of aquaporin expression and distribution, induce and organize water movements. Facilitation of these movements may contribute to the development of edema formation after acute cerebral insults such as ischemia or traumatic injury.

Animals↗
PubMed1999

Beneficial interactions between pharmacological, pathophysiological and hypertension research.

The treatment of essential hypertension continues to be carried out by drugs, combined with the adaptation of life style. The development of various types of antihypertensive drugs has not only greatly improved the management of hypertension, but also offered significant methodological sophistication of the pharmacological and pathophysiological sciences. Antihypertensive drugs and related experimental agents have been widely used in pharmaco-logical and pathophysiological research. The beneficial effects of such agents will be illustrated by means of several examples, emphasizing the sympathetic nervous system, the renin-angiotensin-aldosterone system, and calcium homeostasis as major targets. As pharmacological tools, which are also antihypertensives, we discuss various types of centrally acting antihypertensives, ganglionic and peripheral neuronal blocking agents, alpha- and beta-adrenoceptor antagonists, angiotensin converting enzyme (ACE)-inhibitors, renin-inhibitors, angiotensin II-receptor antagonists (AT1-blockers) and calcium antagonists. Finally, a few remarks will be made concerning the beneficial therapeutic effects of classic and newer antihypertensive drugs, such as beta-blockers, diuretics, calcium antagonists, ACE-inhibitors and AT1-blockers.

Aldosterone↗
PubMed2002

Mineralocorticoid receptors and pathophysiological roles for aldosterone in the cardiovascular system.

For almost 40 years since its discovery in 1953, the mineralocorticoid hormone, aldosterone, was considered to affect blood volume, and thus blood pressure, by its action to retain sodium at epithelial tissues. Over the past decade, direct effects of aldosterone on the heart and blood vessels, and on the cerebral control of blood pressure, have been established in experimental animals. Simultaneously, the incidence of primary aldosteronism in essential hypertension is now acknowledged to be 10-20%, rather than <or= 1%, underscoring a previously unrecognized role for aldosterone in hypertension. The 30% improvement in mortality (and 35% in morbidity) seen in the RALES trial with the addition of low-dose spironolactone to best practice therapy in moderate to severe heart failure, similarly points to an unrecognized role for aldosterone in the pathophysiology of heart failure. Currently, both experimental and clinical studies are directed towards establishing the mechanisms involved in these pathophysiological effects of aldosterone in the cardiovascular system, and of the role of mineralocorticoid receptor antagonists in offsetting or blocking such effects. A brief account of the current state of these mechanisms in at a cellular and tissue level forms the basis of this review.

Aldosterone↗
PubMed1992

Acute MI: a review of pathophysiology, treatment, and complications.

Few areas of clinical medicine have undergone advancements in the last decade as dramatic as those in the management of acute myocardial infarction (AMI). Nursing care of the AMI patient should be based on a comprehensive knowledge of the pathophysiology involved in order to intervene appropriately, understand medical therapies utilized, and anticipate complications. This article offers an in-depth review and update of the pathophysiology of AMI, current recommendations regarding management of the patient with acute infarction, and an overview of complications that still pose a threat to recovery in some patients.

Cardiovascular Agents↗
PubMed1988

Circadian patterns of myocardial ischemia: pathophysiologic and therapeutic considerations.

Recent evidence suggests that acute myocardial infarctions tend to occur most frequently in the early morning hours after awakening. In addition, the peak time of occurrence of out-of-hospital sudden death is during the same morning period, which suggests that the pathophysiologic factors influencing these acute ischemic and arrhythmic events may be similar. Although it is clear that arising from sleep is associated with an increased heart rate and blood pressure, two important determinants of myocardial oxygen demands, other factors may be responsible for a paradoxical decrease of coronary blood flow at the same time. It is possible that vascular receptor sensitivity may vary or that the early morning hours may be associated with a hyperaggregability of platelets; this would provide an additional pathophysiologic explanation for ischemic events related to platelet aggregation and coronary thrombosis, which are known to play a central role in the initiation of unstable angina, acute infarction, and sudden death. An understanding of the circadian pattern of ischemic events may be a guide for future therapeutic interventions during this period. Studies suggest that use of medications that provide continuous antiischemic activity throughout the 24-h day should be considered.

Circadian Rhythm↗
PubMed1990

Pathophysiologic events related to thermal injury of skin.

Acute thermal injury of skin equivalent to second-degree injury and involving approximately 25% of total body surface results in a series of pathophysiologic events which lead to both local and distant tissue/organ injury. The distant effects involve intravascular hemolysis and acute lung injury, both of which can be attributed to complement activation and intravascular stimulation of neutrophils, resulting in oxygen radical production, which results in injury of red cells and pulmonary vascular endothelial cells. At the local site of thermal injury, the progressive increase in vascular permeability is linked to complement activation and histamine release, the outcome of which is interaction of histamine with xanthine oxidase, resulting in enhanced catalytic activity of the enzyme. Toxic oxygen products of xanthine oxidase, including H2O2 and its conversion product, the hydroxyl radical, appear to be linked to the damage of dermal vascular endothelial cells, resulting in progressive vascular permeability. The increased vascular permeability can be greatly attenuated by the use of inhibitors of xanthine oxidase, the inhibitor of histamine release (cromolyn), catalase, an iron chelator (deferoxamine), or scavengers of the hydroxyl radical. Interestingly, neutrophils appear to play little if any role in dermal vascular injury in this animal model of thermal trauma. Those studies suggest that pathophysiologic events following local thermal trauma are complex and involve a variety of mediator pathways.

Animals↗
PubMed1991

Tourette syndrome and other tic disorders. Diagnosis, pathophysiology, and treatment.

In this report, we discuss the definition, characteristics, pathophysiology, and treatment of tic disorders with a major emphasis on Tourette syndrome. Although the diagnosis of a tic disorder depends on the presence of motor and/or phonic tic(s), patients with these problems also have a variety of co-morbid features including obsessive-compulsive symptoms, attention-deficit hyperactivity disorder, behavioral difficulties, and learning disabilities. Conservative estimates for Tourette syndrome suggest a prevalence rate of 0.1-1.0 per 1000. This syndrome is inherited in a sex-influenced autosomal dominant pattern with either chronic multiple tic disorder or obsessive-compulsive disorder as alternative phenotypes of the putative gene. Current evidence continues to support a pathophysiologic mechanism involving synaptic neurotransmission, with the dopaminergic system as a primary candidate. Therapeutically, it is essential to clarify whether a patient's problems are related to tics or associated behavioral difficulties. Pharmacotherapy for motor and phonic tics is strictly symptomatic and should be reserved for those with functionally disabling symptoms. A comprehensive individualized treatment program is often required in the care of individuals with tic disorders.

Behavior↗
PubMed2000

Severe hypophosphatemia. Pathophysiologic implications, clinical presentations, and treatment.

We conducted this review to heighten the awareness and describe pathologic manifestations of hypophosphatemia. We present 3 cases of varied manifestations of hypophosphatemia where recognition was delayed. In certain settings, severe hypophosphatemia has significant morbidity and potential mortality. Appreciation of the pathophysiologic basis for organ dysfunction in severe hypophosphatemia should result in early recognition and treatment. We reviewed the English-language literature for reported cases and research studies dealing with pathophysiologic mechanisms subserving clinical manifestations. We observed that depletion of adenosine triphosphate (ATP) would explain most of the derangement noted in cellular functions. Phosphate plays a key role in the delivery of oxygen to the tissue. Lack of phosphate, therefore, leads to tissue hypoxia and hence disruption of cellular function. Severe hypophosphatemia becomes clinically significant when there is underlying phosphate depletion. Otherwise, short-term acute hypophosphatemia is not usually associated with any specific disorder. Chronic hypophosphatemia, on the other hand, results in hematologic, neuromuscular, and cardiovascular dysfunction, and unless corrected, the consequences can be grave. Most of the time hypophosphatemia results from renal loss of phosphate, diagnosed by a fractional secretion of phosphate > 5%. It is hard to provide precise estimates of how many patients are seen with hypophosphatemia annually at academic medical centers. This is complicated by use of chemistry panels that do not measure inorganic phosphate unless specifically ordered. This often leads to delay in correct diagnosis, and, therefore, additional delay in providing appropriate management. A high index of suspicion alone avoids the unnecessary withholding of treatment that can be life saving.

Acute Disease↗
PubMed1997

Syndromes of posttraumatic neurological deterioration in children with no focal lesions revealed by cerebral imaging: evidence for a trigeminovascular pathophysiology.

PURPOSE: To explain the pathophysiology of the neurological deterioration that occurs after trivial head injuries in children and that is not caused by focal structural brain damage. Symptoms and/or signs include headache, confusion, drowsiness, vomiting, hemiparesis, cortical blindness, and seizures. CONCEPT: We propose that children who are susceptible to such neurological attacks have an unstable "trigeminovascular reflex," which is activated by craniofacial trauma. RATIONALE: After posttraumatic mechanical stimulation and activation of a defective or immature "excitable" trigeminovascular system, release of perivascular vasodilatory peptides causes cerebral hyperemia, which underlies the neurological deterioration. DISCUSSION: The original assumption that underlying cerebral edema was responsible for these phenomena has been proven incorrect by computed tomography. Subsequent proposed pathophysiological mechanisms include cortical spreading depression and trauma-triggered migraine. Recent research has implicated the trigeminovascular pathways in both these conditions and documented that head trauma can be associated with noncongestive cerebral hyperemia (i.e., not causing swelling). Thus, we propose that head trauma activates trigeminal nerve endings in face, scalp, dura, or cortex and, via a reflex, causes intracranial vasodilation and cerebral hyperemia. Drugs that block trigeminovascular activation might offer a benefit.

Blindness, Cortical↗
PubMed1998

Trigeminal neuropathic pain: pathophysiological mechanisms examined by quantitative assessment of abnormal pain and sensory perception.

OBJECTIVE: This study was undertaken to examine the pathophysiological characteristics of trigeminal neuropathic pain. METHODS: The study included 23 consecutive patients with trigeminal neuropathic pain (15 patients with pain after nerve injury and 8 patients with pain of spontaneous origin). For each patient, quantitative examination of sensory and pain perception was performed in the painful facial skin area, and results were compared with the findings for the contralateral nonpainful facial skin area. RESULTS: In the painful facial skin area of patients with neuropathic pain after nerve injury, we demonstrated increased temperature and tactile thresholds, as well as abnormal temporal summation of pain (i.e., repetitive nonpainful skin stimulation produced an abnormal progressive increase of pain intensity, with abnormal radiation of pain and aftersensation). In the painful skin area of patients with pain of spontaneous origin, temperature and tactile thresholds were not increased, but heat pain and cold pain thresholds were significantly reduced, indicating heat and cold hyperalgesia. The characteristics of temporal summation of pain were not significantly altered in the painful facial skin area in this group of patients. CONCLUSION: This clinical study provides evidence that the pathophysiological mechanisms of trigeminal neuropathic pain after nerve injury involve impaired function of both small unmyelinated fibers and large myelinated fibers. An explanation for the finding of abnormal temporal summation of pain may involve hyperexcitability of central wide-dynamic range neurons. The results suggest that other mechanisms are involved in trigeminal neuropathic pain of spontaneous origin. Reduced heat and cold pain thresholds indicate heat and cold hyperalgesia, which possibly may be explained by sensitization of peripheral C nociceptors.

Adult↗
PubMed2002

Preeclampsia. Part 1: clinical and pathophysiologic considerations.

Preeclampsia-eclampsia is still one of the leading causes of maternal and fetal morbidity and mortality. Despite active research for many years, the etiology of this disorder exclusive to human pregnancy is an enigma. Recent evidence suggests there may be several underlying causes or predispositions leading to the signs of hypertension, proteinuria, and edema, findings that allow us to make the diagnosis of the "syndrome" of preeclampsia. Despite improved prenatal care, severe preeclampsia and eclampsia still occur. Although understanding of the pathophysiology of these disorders has improved, treatment has not changed significantly in over 50 years. Although postponement of delivery in selected women with severe preeclampsia improves fetal outcome to a degree, this is not done without risk to the mother. In the United States, magnesium sulfate and hydralazine are the most commonly used medications for seizure prophylaxis and hypertension in the intrapartum period. The search for the underlying cause of this disorder and for a clinical marker to predict those women who will develop preeclampsia-eclampsia is ongoing, with its prevention the ultimate goal. This review begins with the clinical and pathophysiologic aspects of preeclampsia-eclampsia (Part 1). In Part 2, the experimental observations, the search for predictive factors, and the genetics of this disorder will be reviewed.

Diagnosis, Differential↗
PubMedDate not supplied

First-line treatment for osteoarthritis. Part 1: Pathophysiology, assessment, and pharmacologic interventions.

While surgical interventions often relieve severe pain for those with osteoarthritis (OA), there are thousands of patients with this common and disabling condition who do not receive surgery. Pharmacologic and nonpharmacologic interventions may offer a reduction in pain and improvement in physical functioning. To help patients with OA, nurses should conduct thorough assessments based on pathophysiology, and plan appropriate care with the patient. In this first article of a two-part series, the pathophysiology and classification of OA are presented. Assessment factors are discussed, and pharmacologic interventions are presented. Part 2 of this series, to run in the November/December issue, will focus on nonpharmacologic interventions and evaluation.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1987

Clinical characteristics, pathophysiology, and management of hydrocarbon ingestion: case report and review of the literature.

Accidental ingestion of hydrocarbons is an important cause of childhood poisoning. Due to the number of hydrocarbon products available as solvents, fuels, and cleaning agents, increased awareness is necessary on the part of health caretakers. The scope of complications involving the respiratory system in petroleum products ingestion is frequently overlooked. Physicians may thus apply standard therapeutic modalities used in treating common poisonings to the child who drank a petroleum distillate. Prompt recognition of presenting symptoms and understanding of pathophysiology are important to planning and providing treatment. The two cases of hydrocarbon ingestion reported in this paper illustrate the wide spectrum of problems associated with this condition. The pathophysiology, current management, and a review of the literature of hydrocarbon ingestion are presented.

Accidents, Home↗
PubMed1995

Pulmonary sarcoidosis: population differences and pathophysiology.

Sarcoidosis is characterized as a hyperimmune response to an unknown agent(s) at the lesion sites. Regarding pulmonary lesions, macrophage-T lymphocyte alveolitis precedes an epithelioid cell granuloma formation. In the 35 years since the first International Conference on Sarcoidosis, the definition of sarcoidosis has been revised several times, and many new pathophysiologic mechanisms have been proposed. In this review, we focused on four important issues: (1) possible population differences, (2) possible causative agent(s) and the current problems of disease susceptibility or resistance, (3) recent data on pathogenesis (including a genetic approach) and pathophysiologic processes, and (4) monitoring of disease activity.

Adult↗
PubMed1996

Spinal dural arteriovenous malformations. Intraoperative evoked potential evidence for pathophysiology. A case report.

STUDY DESIGN: This case report details intraoperative evoked potential changes during surgical removal of a T8 dural arteriovenous malformation. OBJECTIVES: The pattern of changes in somatosensory-evoked responses during surgical correction of spinal dural at arteriovenous malformation can illuminate the pathophysiologic process behind the clinical symptoms. SUMMARY OF BACKGROUND DATA: Arteriovenous malformation of the spinal dura can manifest with multiple symptoms, including progressive myelopathy and pain. The pathophysiologic process behind these symptoms could be either direct compression of the spinal cord by the arteriovenous malformation, ischemia resulting from the cord, or increased venous pressure. METHODS: To investigate these hypotheses further, the results of posterior tibial evoked potentials obtained during surgical removal of a T8 dural arteriovenous malformation were analyzed. RESULTS: At baseline, the cortical (P40) potential was markedly prolonged bilaterally. During surgery, just after the dura was opened, a marked increase was observed in the latencies of the P40 and P60 components of the evoked response on the right, which began to resolve as soon as the arteriovenous malformation was occluded. Only minimal changes were seen on the left. CONCLUSIONS: These results are most consistent with the increased venous pressure hypothesis for the pathogenesis of neurologic symptoms in dural arteriovenous malformations.

Aged↗
PubMed1998

A review of the pathophysiology of cervical spondylotic myelopathy with insights for potential novel mechanisms drawn from traumatic spinal cord injury.

Cervical spondylotic myelopathy (CSM) is the most common cause of spinal cord dysfunction. Despite advances in diagnosis and surgical treatment, many patients still have severe permanent neurologic deficits caused by this condition. An improved understanding of the pathophysiology of cervical spondylotic myelopathy, particularly at a cellular and molecular level, may allow improved treatments in the future. A detailed review of articles in the literature pertaining to cervical spondylotic myelopathy was supplemented by an analysis of relevant mechanisms of spinal cord injury. The pathologic course of cervical spondylotic myelopathy is characterized by early involvement of the corticospinal tracts and later destruction of anterior horn cells, demyelination of lateral and dorsolateral tracts, and relative preservation of anterior columns. Static and mechanical factors and ischemia are critical to the development of cervical spondylotic myelopathy. Free radical-and cation-mediated cell injury, glutamatergic toxicity, and apoptosis may be of relevance to the pathophysiology of cervical spondylotic myelopathy. To date, research in cervical spondylotic myelopathy has focused exclusively on the role of mechanical factors and ischemia. Fundamental research at a cellular and molecular level, particularly in the areas of glutamatergic toxicity and apoptosis may result in clinically relevant treatments for this condition.

Cervical Vertebrae↗