[Physiology and pathophysiology of the heart as muscle and as pump; pathophysiology of heart insufficiency].
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Heart↗
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[Report of the 40th meeting of the work group on the pathophysiology of breathing of the Society for Pathophysiology and the Society for Bronchopneumonology and Tuberculosis of the DDR. Animal experimental models of acute and chronic lung diseases].
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Acute Disease↗
Pathophysiology of renal disease. Symposium on Pathophysiology of renal disease, Heidelberg, Aug. 30-Sept. 1, 1982.
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Humans↗
[Contemporary view on pathophysiology and pathogenesis of diabetic nephropathy. I. Pathophysiology of diabetic nephropathy].
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Child↗
Past and present in Romanian pathophysiology teaching: Iaşi experience.
Discipline of Pathophysiology is now a division of the University of Medicine and Pharmacy of Ia,si and it is included as a separate discipline for the third-year undergraduate students. Changes have occurred in the curricula of different disciplines that have progressively weakened the position of pathophysiology. The medical system is the most affected because the basic course in pathophysiology for undergraduate students is not completely satisfactory. A recent questionnaire is illustrative in the concern of pathophysiology both as a science and as a medical discipline. A coherent educational system regarding pathophysiology should include a basic course in pathophysiology, lectures and stages of clinical pathophysiology and postgraduate courses in different medical domains as well, all to take place in an integrated department of experimental and clinical pathophysiology.
Curriculum↗
Disseminated intravascular coagulation. clinical and pathophysiological mechanisms and manifestations.
Disseminated intravascular coagulation (DIC) is a complex disorder, with pathophysiology being variable and highly dependent upon the triggering event(s), host response(s) and comorbid conditions. As a result of these complicated interactions, the clinical expression and laboratory findings are varied, thereby affecting the specifics of diagnosis and therapeutic approaches. The highly complex and variable pathophysiology of DIC often results in a lack of uniformity in clinical manifestations, a lack of consensus in the specific appropriate laboratory criteria of diagnosis, and a lack of specific therapeutic modalities. Indeed, recommendations for therapy are often difficult because the morbidity and survival is more dependent on the specific cause of DIC and because the generally used specific therapeutic approaches, which include for example heparin, low-molecular-weight-heparin antithrombin concentrate and protein C concentrate, have never been subjected to objective prospective randomized trials, except antithrombin concentrates. An analysis of the complex and varied pathophysiological events in DIC provide objective guidelines and criteria for the clinical diagnosis, the laboratory diagnosis, and the definition of severity. These data compounded by an understanding of complex and varied pathophysiology can be used for objective evaluation of therapeutic responses and results. DIC is an intermediary mechanism of disease usually seen in association with well-defined clinical disorders. The pathophysiology of DIC serves as an intermediary mechanism in many disease processes, which sometimes remain organ specific. This catastrophic syndrome spans all areas of medicine and presents a broad clinical spectrum that is confusing to many. Most physicians consider DIC to be a systemic hemorrhagic syndrome; however, this is only because hemorrhage is evident and often impressive. Less commonly appreciated is the profound microvascular thrombosis and sometimes, large vessel thrombosis. The hemorrhage is often simple to contend with in patients with fulminant DIC, but it is the small- and large-vessel thrombosis, with impairment in blood flow, ischemia, and associated end-organ damage that usually leads to irreversible morbidity and mortality. In conclusion, the pathophysiological mechanisms, clinical, and laboratory manifestations of DIC are complex in part due to interrelationships within the hemostasis system. Only by clearly understanding these extraordinarily complex pathophysiological interrelationships can the clinician and laboratory scientist appreciate the divergent and wide spectrum of often confusing clinical and laboratory findings in patients with DIC. Many therapeutic decisions to be made are controversial and lack validation. Nevertheless, newer antithrombotic agents, and agents which can block, blunt or modify cytokine activity and the activity of vasoactive substances appear to be of value. The complexity and variable degree of clinical expression suggests that therapy should be individualized depending on the nature of DIC, age, etiology of DIC, site and severity of hemorrhage or thrombosis and hemodynamics and other appropriate clinical parameters.
Disseminated Intravascular Coagulation↗
[Constituent Congress of the International Society for Pathophysiology].
Pathophysiology began from general pathology due to a necessity of experimental analysis of pathological processes. Its origins date back to the works of Magenndie and Claude Bernard who introduced the concept of "experimental pathology". It is noteworthy that the founder of cellular pathology, Rudolph Virchow, emphasized the crucial importance of regulation disturbance for physiological processes as an essential mechanism of disease pathogenesis and used the term "pathological physiology". In Russia this term was defined by V.V. Pashutin in his lectures on pathological physiology (1878). In this country, in the thirties of this century pathophysiology acquired the significance of a medical discipline and was included in the medical education curricula. I. P. Pavlov, who designated pathophysiology as experimental pathology, greatly contributed to this end. In 1819, Galliot published a manual in general pathology and pathological physiology. But the first textbook in pathophysiology seems to have been written 200 years ago, as early as 1790, by professor A. F. Hecker, from the Erfurt University, who read lectures in "Physiologia pathologica". Thus, pathophysiology originated independently in various countries which testifies to the objective necessity for its origination due to medicine development. However, contemporary pathophysiology appreciably differs from that at its earlier stages of development, and even from that of several decades ago. Modern pathophysiology ceased to be just experimental pathology, it has acquired a new quality, having become an integrative biomedical science. This feature is due to medicine development, growing differentiation of medicine, and to an ever increasing body of diverse information about different pathological processes. All this brought about a necessity for the birth of an integrative medical science.(ABSTRACT TRUNCATED AT 250 WORDS)
History, 18th Century↗
Pathophysiology of bacteremia.
Despite the frequency and importance of both nosocomial and "community-acquired" bacteremia, definitive information concerning crucial pathophysiologic events in human bacteremia remains sparse. An extensive variety of clinical manifestations, such as fever, rigors, shock, altered circulatory dynamics, cutaneous manifestations changes in the coagulation, complement, and other mediator systems, and effects on the lungs, heart, kidney, liver, and other end organs, have been described, but it is difficult to determine the relative frequency of these events in bacteremia caused by different species. The extensive number of bacterial species capable of producing bacteremia and variations in the type of presentation, such as acute, asymptomatic, and chronic, even when bacteremia is produced by the same species, undoubtedly contribute to this difficulty and suggest that a variety of pathophysiologic mechanisms occur in various bacteremias. In contrast, the relative frequency of various manifestations and some pathophysiologic mechanisms have been better delineated in Gram-negative bacteremia. The development of bacteremia enhances the lethality of most types of localized infection and several studies have demonstrated a relation between the magnitude of bacteremia and the outcome of the disease. Among various pathophysiologic alterations, mechanisms involved in the production of fever have been delineated most clearly. Fever appears to reflect a "common pathway" with almost all infectious agents and results from release of endogenous pyrogen from phagocytic cells. Endogenous pyrogen regulates the thermostatic setting of the body through its effect on the anterior hypothalamus. Endogenous pyrogen seems identical with Interleukin 1 and exerts a variety of other biologic activities. An extensive number of bacterial components have been proposed as "effectors" and an equally large number of endogenous substances proposed as "mediators" of the pathophysiologic events in bacteremia. The importance of many of these effectors and mediators has been postulated largely on the basis of in vitro and animal studies. The lack of critical clinical studies hampers extrapolation of these experimental studies to human bacteremia. The development of more effective therapy for the complications of bacteremia, such as shock, will continue to be hampered until the mechanisms involved in the production of those pathophysiologic events that are crucial determinants of outcome have been delineated more precisely in human disease.
Bacterial Toxins↗
Pathophysiology and pharmacologic treatment of acute spinal cord injury.
BACKGROUND CONTEXT: The past three decades have witnessed increasing interest in strategies to improve neurologic function after spinal cord injury. As progress is made in our understanding of the pathophysiologic events that occur after acute spinal cord injury, neuroprotective agents are being developed. PURPOSE: Clinicians who treat acute spinal cord injuries should have a basic understanding of the pathophysiologic processes that are initiated after the spinal cord has been injured. A familiarity with the literature on which the current use of methylprednisolone is based is also essential. STUDY DESIGN/SETTING: Literature review. METHODS: Literature review of animal data on pathophysiologic mechanisms, and of both animal and human trials of neuroprotective agents. RESULTS: The mechanical forces imparted to the spinal cord cause primary damage to the neural tissue, but a complex cascade of pathophysiologic processes that imperil adjacent, initially spared tissue to secondary damage rapidly follows this. Attenuating this secondary damage with neuroprotective strategies requires an understanding of these pathophysiologic processes. Many researchers are investigating the role of such processes as ischemia, inflammation, ionic homeostasis and apoptotic cell death in the secondary injury cascade, with hopes of developing specific therapies to diminish their injurious effects. Beyond methylprednisolone, a number of other pharmacologic treatments have been investigated for the acute treatment of spinal cord injury, and even more are on the horizon as potential therapies. CONCLUSIONS: This review summarizes some of the important pathophysiologic processes involved in secondary damage after spinal cord injury and discusses a number of pharmacologic therapies that have either been studied or have future potential for this devastating injury.
Acute Disease↗
Differential effects of physiological versus pathophysiological plasma concentrations of epinephrine and norepinephrine on ketone body metabolism and hepatic portal blood flow in man.
Few studies that have examined the effects of catecholamines on ketogenesis have considered the effects of catecholamines on hepatic portal blood flow. Since hepatic blood flow is a major determinant of hepatic ketogenesis (via modification of free fatty acid availability), interpretation of these studies is difficult. To better define the relative contributions of these variables, we studied the effects of physiological and pathophysiological plasma concentrations of epinephrine and norepinephrine on plasma ketone body concentrations and hepatic portal blood flow in controlled paired studies in young healthy male volunteers. To assess the effects of physiological catecholamine concentrations, each of eight subjects received 60-minute sequential infusions of epinephrine (10 ng/kg/min) and norepinephrine (32.5 ng/kg/min) together with a control infusion of heparin (0.4 U/kg/min) separated by 60-minute washout periods. Similar increments in plasma nonesterified fatty acid ([NEFA] to approximately 1 mmol/L) were observed during each infusion. The ketotic ratios, calculated as the ratio of plasma ketone bodies to fatty acids integrated above baseline for 90 and 120 minutes, respectively, for epinephrine and norepinephrine infusions were both significantly greater (P < .005 for each) than for the heparin control infusion. To assess the effects of pathophysiological plasma catecholamine concentrations, each of eight subjects also received sequential 60-minute infusions of epinephrine 60 ng/kg/min, norepinephrine 80 ng/kg/min (plus heparin 0.1 U/kg/min), and a separate control infusion of heparin with or without Intralipid (KabiVitrum, Alameda, CA). Whereas integrated plasma fatty acid levels were approximately twofold greater than those observed in the physiological protocol, the absolute integrated ketone body response to the pathophysiological concentration of epinephrine was significantly lower than that observed for the physiological dose of the hormone (P < .05). In contrast, the ketotic ratio for norepinephrine was significantly greater (P < .005) than for both epinephrine and the control infusion of heparin with or without Intralipid. Significant (P < .01) increases above baseline fasting levels were observed in plasma glucose and immunoreactive insulin concentrations during infusion of pathophysiological concentrations of epinephrine. Because of the technical difficulties of simultaneously measuring portal blood and sampling blood frequently, studies were repeated in six additional subjects using noninvasive image-guided flowmetry to measure percentage changes in hepatic portal blood flow during catecholamine infusion. Norepinephrine reduced hepatic portal blood flow significantly at the low-physiological concentration by 12% (P < .05) and at the pathophysiological concentration by 18% (P < .05). In summary, (1) both epinephrine and norepinephrine were associated with significant ketotic effects at physiological plasma concentrations; and (2) when infused at pathophysiological concentrations, only norepinephrine exerted a significant additional ketotic effect. Since norepinephrine has a significant simultaneous effect of reducing hepatic portal blood flow, we conclude that previous studies may have underestimated the effect of norepinephrine on hepatic ketogenesis.
Adult↗
[Pathophysiology of acute pancreatitis].
Recent experiments in different animal models of acute pancreatitis have improved our understanding of the pathophysiology of this disease. The present review discusses the individual steps and mechanisms and puts them into a pathophysiologic concept for the two most important forms of acute pancreatitis (alcoholic and biliary form). In biliary acute pancreatitis a temporary occlusion of the common channel by impacted stones may be followed by a reflux into the pancreatic duct. This reflux results in an increase of ductal permeability and extravasation of cytotoxic agents into the surrounding tissue. As consequences, disturbances of compartimentation and faulty activation of enzymes occur in pancreatic cells. Long-term cellular damage, obstruction of pancreatic ducts and increase of ductal permeability with leakage of noxious agents play a substantial role in pathophysiology of alcoholic pancreatitis. Sustained abuse of alcohol usually leads to chronic pancreatitis. Additional, as yet unknown factors are necessary to induce acute alcoholic pancreatitis. Following its initiation by different etiological sources, pathophysiology of acute pancreatitis may take a similar course. Digestive enzymes are activated and set free into intracellular, intraductal and interstitial spaces. Trypsin as the trigger-enzyme of activation cascade is thought to play a major role. In addition, lipolytic enzymes may be involved in the pathophysiologic process. Phospholipase A is known to release lysolecithin which causes membrane damage. Recent studies indicate that the release of fatty acids by lipase causes acinar cell necrosis. New insights into the pathophysiology may lead to a rational and more successful therapy of acute pancreatitis.
Acute Disease↗
Differentiating primary pathophysiologic from secondary adaptational processes.
The following manuscript is mainly conceptual in nature. It should be read with reservation since the relevance of its suggestions have yet to be proven. Basically it proposes two rules for the differentiation between primary illness-related pathophysiological vs. secondary adaptational processes. These rules may guide hypotheses generation for further research that is aimed at understanding psychiatric disorders and their shared and unshared mechanisms. For example, in the case of anxiety disorders and depression, it may be of interest to learn if their shared properties are of primary pathophysiological or secondary adaptational significance. We first present some historical observations on the development of the concept of "secondary adaptational processes." We assume such adaptational processes are generated by the organism in order to compensate for primary pathophysiological malfunction or impairment. Next, we propose rules that may enable the dissection of secondary adaptational from primary pathophysiological processes. We also discuss the possible implications of designing studies to sort out these processes, suggesting that the understanding of adaptational processes, may explain the effects of "placebo treatment." Finally we illustrate the application of these rules by two examples: a) amygdala activation, a biological alteration shared by anxiety disorders and major depression and b) elevated plasma soluble interleukin 2 receptor, an unshared property by anxiety disorders and major depression. Also, the first example relates to a biological perturbation associated with a primary pathophysiological mechanism, while the second represents a biological alteration associated with secondary adaptational processes.
Adaptation, Psychological↗
Sepsis and septic shock. I. Definitions and pathophysiology.
Mortality from septic shock is considerable despite the advantages of cardiovascular support and antibiotic therapy. Understanding the pathophysiology of sepsis enables clinicians to institute rational intervention directed towards the pathophysiological mechanisms. This article reviews definitions of sepsis and offers a brief overview of ist pathophysiology. Current knowledge on the pathophysiological mechanism of cytokines and modulation of systemic cytokine levels during sepsis and septic shock is discussed. The important role of cytokines in sepsis and septic shock may require more detailed investigations of the cytokine pathophysiological network.
Cytokines↗
Association of the predominant symptom with clinical characteristics and pathophysiological mechanisms in functional dyspepsia.
BACKGROUND & AIMS: Functional dyspepsia (FD) is considered a heterogeneous disorder with different pathophysiological mechanisms contributing to the symptom pattern. The Rome II committee proposed that subdividing patients with FD into groups with predominant pain versus discomfort might identify subgroups with homogeneous pathophysiological and clinical properties. The aim of this study was to analyze the relationship of predominant pain or discomfort with pathophysiological mechanisms and to evaluate whether considering individual predominant symptoms yields better results. METHODS: Consecutive FD patients (n = 720; 489 women; mean age, 41.3 +/- 0.6 years) filled out a dyspepsia questionnaire and identified a single most bothersome symptom. We analyzed the association of this predominant symptom with demographic, clinical, and pathophysiological features (Helicobacter pylori status, gastric emptying in 592 patients, and gastric sensitivity and accommodation testing in 332 patients). RESULTS: According to Rome II criteria, 22% were pain predominant and 78% discomfort predominant. Patients with predominant pain had a higher prevalence of hypersensitivity (44% vs 25%) and delayed gastric emptying was observed less frequently in these patients (16% vs 26%), but there was major overlap. Detailed analysis showed that any of 8 dyspeptic symptoms could be predominant. Predominant early satiety or vomiting was associated with significantly higher prevalences of weight loss (89% and 75%, respectively) and of acute onset (61% and 60%, respectively). Impaired accommodation was found in 79% of patients with predominant early satiety. The highest prevalence of delayed emptying was found in predominant fullness (38%) and of hypersensitivity in predominant pain (44%). CONCLUSIONS: Subdividing FD patient groups according to the predominant symptom does not reliably identify subgroups with a homogeneous underlying pathophysiological mechanism.
Adult↗
Patent foramen ovale: anatomy versus pathophysiology--which determines stroke risk?
This study investigated anatomic and pathophysiologic variables that may determine which patent foramen ovale (PFO) are associated with cerebrovascular accidents (CVAs). Anatomic features of a PFO have been identified as risk factors that predispose certain people to cryptogenic strokes (strokes of unknown cause). However, potential pathophysiologic variables that can determine the pressure gradient between left and right atria, which could influence the right-to-left shunt through a PFO, have not been examined. A retrospective study included 78 consecutive patients in whom PFOs were detected during routine transesophageal echocardiography examination. Group I included 36 patients with CVAs of unknown cause (cryptogenic stroke). Group II included 42 patients without CVAs whose PFOs were incidental findings. Anatomic features measured included separation and overlap between septum primum and septum secundum, interatrial septal motion, and the relative size of the right-to-left shunt with peripheral saline solution contrast injections. Pathophysiologic variables considered were those that could cause elevated left atrial pressure, thereby minimizing the right-to-left shunt.Patients with a clinical neurologic event (group I) had a larger right-to-left shunt volume of contrast bubbles than did patients with asymptomatic PFO (group II; P =.004). The size of the overlap between septum primum and septum secundum was less in patients from group I as compared with patients from group II (7.5 +/- 3.4 mm versus 9.9 +/- 6.0 mm; P =.026). However, other anatomic features of PFO that are determinants of the "opening" were not significantly different between the 2 groups. No statistically significant difference was found in the distance of the separation between septum primum and septum secundum (2.5 +/- 2.0 mm versus 1.9 +/- 1.6 mm; P = not significant). The prevalence of interatrial septal aneurysm was also similar between the 2 groups (28% versus 21%; P = not significant). However, the prevalence of variables that could potentially raise left atrial pressure was greater in patients without CVA as compared with those with a CVA (48% versus 14%; P =.01). In our study, anatomic features alone did not determine interatrial shunt size and pathophysiologic variables that could raise left atrial pressures did differentiate between patients with a PFO with a CVA/transient ischemic attack and those without it. Thus, both anatomic and pathophysiologic mechanisms should be considered in determination of the potential clinical significance of a PFO.
Adult↗
Prevention of renovascular and cardiac pathophysiological changes in hypertension by angiotensin II type 1 receptor antisense gene therapy.
Hypertension produces pathophysiological changes that are often responsible for the mortality associated with the disease. However, it is unclear whether normalizing blood pressure (BP) with conventional therapy is effective in reversing the pathophysiological damage. The duration and initiation of treatment, site of administration, and agent used all appear to influence the reversal of the pathophysiological alterations associated with hypertension. We have previously established that retrovirally mediated delivery of angiotensin II type 1 receptor antisense (AT1R-AS) attenuates the development of high BP in the spontaneously hypertensive (SH) rat model of human essential hypertension. Our objective was to determine whether this attenuation of high BP is associated with prevention of other pathophysiological changes induced by the hypertensive state. Intracardiac delivery of AT1R-AS in neonates prevented the development of hypertension in SH rats for at least 120 days. Contractile experiments demonstrated an impaired endothelium-dependent vascular relaxation (acetylcholine) and an enhanced contractile response to vasoactive agents (phenylephrine and KCl) in the SH rat renal vasculature. In addition, the voltage-dependent K+ current density, which is believed to contribute to smooth muscle resting membrane potential and basal tone, was decreased in renal resistance artery cells of the SH rat. AT1R-AS treatment prevented each of these renal vascular alterations. Finally, AT1R-AS delivery prevented the pathological alterations observed in the SH rat myocardium, including left ventricular hypertrophy, multifocal fibrosis, and perivascular fibrosis. These observations demonstrate that viral-mediated delivery of AT1R-AS attenuates the development of hypertension on a long term basis, and this is associated with prevention of pathophysiological changes in SH rats.
Acetylcholine↗
Pathophysiology of priapism: dysregulatory erection physiology thesis.
PURPOSE: While a modest amount of medical literature has been written on the topic of priapism, reports heretofore have focused predominantly on diagnostic and management related aspects of the disorder, providing meager information in regard to its pathophysiology. Accordingly the intent of this review was to explore the etiological and pathogenic factors involved in priapism. MATERIALS AND METHODS: The review entailed an overview of traditional and modern concepts that have been applied to the pathophysiology of priapism and an evaluation of assorted observational and experimental data relating to this field of study. The basic exercise consisted of a literature search using the National Library of Medicine PubMed Services, index referencing provided through the Historical Collection of the Institute of Medicine of The Johns Hopkins University and a survey of abstract proceedings from national meetings relevant to priapism. RESULTS: Insight into the pathophysiology of priapism was derived from a synthesis of evolutionary clinical experiences, mythical beliefs, clinical variants and scientific advances associated with the field of priapism. The results can be summarized. 1) Clinicopathological manifestations of priapism support its basic classification into low flow (ischemic) and high flow (nonischemic) hemodynamic categories, commonly attributed to venous outflow occlusion and unregulated arterial overflow of the penis, respectively. 2) Factual information is insufficient to substantiate etiological roles for urethral infection, bladder distention, failed ejaculation, satyriasis and sleep apnea in priapism. 3) Features of the variant forms of priapism invoke changes in nervous system control of erection and penile vascular homeostasis as having pathogenic roles in the disorder. 4) Clinical therapeutic and basic science investigative studies have revealed various effector mechanisms of the erectile tissue response that may act in dysregulated fashion to subserve priapism. CONCLUSIONS: This exercise suggested that, while priapism is commonly defined in terms of adverse mechanical contexts affecting penile circulation, it may also be viewed at least in some situations as an unbalanced erectile response involving derangements in possibly diverse systems of regulatory control. An integrative scientific approach that encompasses tissular, cellular and molecular levels of investigation may allow further understanding of the pathophysiology of the disorder. Ongoing elucidation of this pathophysiology can be expected to promote the development of new priapism therapies.
Greece, Ancient↗
Pathophysiology and treatment of functional dyspepsia.
Functional dyspepsia is a highly prevalent symptom complex and a heterogenous disorder. Recent studies showed potential associations between specific pathophysiologic disturbances and dyspeptic symptoms. Delayed gastric emptying reported in about 30% of patients with functional dyspepsia is associated with the symptoms of postprandial fullness, nausea, and vomiting. Impaired gastric accommodation present in 40% of functional dyspepsia patients is found to be associated with early satiety. Hypersensitivity to gastric distension is observed in 37% of functional dyspepsia patients and associated with the symptoms of postprandial pain, belching, and weight loss. Psychosocial factors and altered response to duodenal lipids or acid have also been identified as pathophysiologic mechanisms. Therapeutic options are still limited but targeted therapy directed at the underlying pathophysiology seems desirable. Thus, efforts to further elucidate underlying pathophysiologic mechanisms and identify the appropriate patient population using some type of pathophysiologic testing will be required.
Dyspepsia↗