Intrinsic pathophysiology

There are typically three categories of ARF prerenal, intrinsic, and postrenal ARF. The pathophysiologic mechanisms differ for each of the categories. 

The pathophysiology of hemophilia is based on the factor VIII or IX deficiency resulting in inadequate thrombin generation and an impaired intrinsic-pathway coagulation cascade (see... 

Magnesium ions are also involved in biological processes and occur in cells at millimolar concentrations [315]. Magnesium can be estimated based on the chemical shift difference of the resonances of adenosine triphosphate (ATP) using P NMR [316-318], though P NMR has intrinsically low signal-to-noise, exacerbated under many pathophysiological conditions, such as ischemia. 

Lewis DA, Gonzalez-Burgos G. 2000. Intrinsic excitatory connections in the prefrontal cortex and the pathophysiology of schizophrenia. Brain Res Bull 52 309-317. 

A prerenal mechanism secondary to the vascular leak syndrome is commonly involved in the pathophysiology of acute renal insufficiency. In addition it has been suggested that a direct intrinsic intrarenal effect of aldesleukin with a higher than expected reduction in glomerular filtration rate or tubular dysfunction (85,89) is involved. Several isolated cases of acute interstitial or tubulointerstitial nephritis with predominant T lymphocjde infiltration of the kidneys (90-92) and the exacerbation of a subchnical IgA glomerulonephritis (93) suggested altered cell-mediated immunity. 

In human, the pathophysiology of inferleukin-2 induced renal dysfunction is still poorly understood. Interleukin-2 may act directly on the vascular tonus and endothelial integrity or may stimulate generation of other cytokines, which in turn would increase vascular permeability. Occurrence of an intrinsic renal lesion has been suggested by Shalmi et ah [194] who showed that glomerular filtration rate is altered in 90% of the patients [mean decrease of 43%] whereas renal plasma flow decreases is only slightly altered [mean decrease 5%] in 50% of the patients. 

The pathophysiology of isoimmune hemolysis is the same for all antigens. The differences in severity of disease are due to differences in the expression of the antigen on the surface of the cells, the intrinsic immunogenicity of the antigen, and peculiarities of the immune response of the mother. Destruction of the fetal erythrocytes, which is the central problem, produces several other problems. Fetal anemia imposes an extra burden on the fetal heart to provide adequate oxygen supply to fetal tissues. Anemia stimulates the fetal marrow and extramedullary erythropoiesis in the liver and spleen to replace the destroyed erythrocytes. Extramedullary erythropoiesis destroys hepatocytes and leads to decreased production of serum albumin and decreased oncotic pressure in tire intravascular space. 

Intrinsic defects in these renal adaptive mechanisms could lead to plasma volume expansion and increased blood flow to peripheral tissues, even when BP is normal. Local tissue autoregulatory processes that vasoconstrict then would be activated to offset the increased blood flow. This effect would result in increased peripheral vascular resistance and, if sustained, also would result in thickening of the arteriolar walls. This pathophysiologic component is plausible because increased total peripheral vascular resistance is a common underlying finding in patients with essential hypertension. 

Hepatorenal syndrome, functional renal failure in the setting of cirrhosis in the absence of intrinsic renal disease, occurs in patients with cirrhosis as a result of intense vasoconstriction within the renal cortical vasculature. It is common and develops in approximately 40% of patients with cirrhosis and ascites within 5 years. The resultant reduction in blood supply to the kidneys causes avid sodium retention and oliguria. The vasoconstriction that occurs in the kidneys is in stark contrast to the state of systemic vasodilation that is characteristic of chronic liver failure. The pathophysiologic mechanism responsible for these effects is unknown, but is linked to the systemic vasodilation, hypovolemia, and hyperkinetic circulation seen in chronic liver failure. ... 

It is generally thought that these four canonical mechanisms of IgE-mediated activation of human FceRI + cells are responsible for the pathophysiological involvement of these cells in the majority of patients with allergic disorders [34], However, there is evidence that a significant percentage of allergic diseases (e.g. certain cases of intrinsic asthma and chronic idiopathic urticaria) cannot be explained by the four classical mechanisms of FceRI + cell activation. 

Our metabolism consists of a huge number of biochemical processes which are generally in a state of dynamic equilibrium called homeostasis. Whenever stressors in the form of extrinsic or intrinsic forces are applied, the state of homeostasis is challenged, and the stress system in our body is activated. Normal stress is essential for maintenance of mental and physical health. The hypothalamic-pituitary-adrenal (HPA) axis is the main constituent of the stress system because it serves as a key junction for neuro, immuno and endocrine (hormonal) systems [7]. Acute or chronic stress causes dysregulation of the stress system. This situation leads to various pathophysiologic states that include psychiatric, endocrine/metabolic, and immunologic disorders. 

Thus, GH pitlse responsiveness is in part determined by intrinsic sex-specific factors, which may resnlt from prior hormone exposme (epigenetic mechartisms) or genetic factors that are pituitary irrdependent and could contribute to sex differences in the predisposition to liver cancer or other hepatic pathophysiologies [125]. 

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